@article {pmid38748594,
year = {2024},
author = {Liu, S and Luo, X and Zhou, L and Xie, RH and He, Y},
title = {Microbiota transplantation in restoring cesarean-related infant dysbiosis: a new frontier.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2351503},
doi = {10.1080/19490976.2024.2351503},
pmid = {38748594},
issn = {1949-0984},
mesh = {Humans ; *Dysbiosis/microbiology ; Female ; *Cesarean Section/adverse effects ; *Gastrointestinal Microbiome ; Pregnancy ; *Fecal Microbiota Transplantation ; Infant, Newborn ; Vagina/microbiology ; Infant ; },
abstract = {C-section is crucial in reducing maternal and neonatal mortality when medically indicated, but one of its side effects could be the disruption of vertical transmission of maternal-infant microbiota during delivery, potentially leading to gut dysbiosis and increased disease risks in C-section infants. To address such dysbiosis, it seems reasonable to supplement "what is missing" during C-section procedure. This idea has prompted several clinical trials, including proof-of-concept, investigating interventions like vaginal microbial seeding, oral administration of maternal vaginal microbes and even oral administration of maternal fecal materials. Hereby, we have summarized these trials to help understand the current state of these researches, highlighting the predominantly pilot nature of most of these studies and emphasizing the need for well-designed studies with larger sample to guide evidence-based medicine in the future.},
}

Humans
*Dysbiosis/microbiology
Female
*Cesarean Section/adverse effects
*Gastrointestinal Microbiome
Pregnancy
*Fecal Microbiota Transplantation
Infant, Newborn
Vagina/microbiology
Infant

@article {pmid38746249,
year = {2024},
author = {Ke, S and Villafuerte Gálvez, JA and Sun, Z and Cao, Y and Pollock, NR and Chen, X and Kelly, CP and Liu, YY},
title = {Rational Design of Live Biotherapeutic Products for the Prevention of Clostridioides difficile Infection.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.04.30.591969},
pmid = {38746249},
abstract = {Clostridioides difficile infection (CDI) is one of the leading causes of healthcare- and antibiotic-associated diarrhea. While fecal microbiota transplantation (FMT) has emerged as a promising therapy for recurrent CDI, its exact mechanisms of action and long-term safety are not fully understood. Defined consortia of clonal bacterial isolates, known as live biotherapeutic products (LBPs), have been proposed as an alternative therapeutic option. However, the rational design of LBPs remains challenging. Here, we employ a computational pipeline and three independent metagenomic datasets to systematically identify microbial strains that have the potential to inhibit CDI. We first constructed the CDI-related microbial genome catalog, comprising 3,741 non-redundant metagenome-assembled genomes (nrMAGs) at the strain level. We then identified multiple potential protective nrMAGs that can be candidates for the design of microbial consortia targeting CDI, including strains from Dorea formicigenerans , Oscillibacter welbionis , and Faecalibacterium prausnitzii . Importantly, some of these potential protective nrMAGs were found to play an important role in the success of FMT, and the majority of the top protective nrMAGs can be validated by various previously reported findings. Our results demonstrate a computational framework for the rational selection of microbial strains targeting CDI, paving the way for the computational design of microbial consortia against other enteric infections.},
}

@article {pmid38743445,
year = {2024},
author = {Cafaro, G and Cruciani, G and Bruno, L and Dal Pozzolo, R and Colangelo, A and Tromby, F and Nicchi, M and Pianese, B and Perricone, C and Gerli, R and Bartoloni, E},
title = {Microbiota and arthritis: cause or consequence?.},
journal = {Clinical and experimental rheumatology},
volume = {42},
number = {5},
pages = {1097-1103},
doi = {10.55563/clinexprheumatol/f6q4dc},
pmid = {38743445},
issn = {0392-856X},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Dysbiosis ; Animals ; Probiotics/therapeutic use ; Arthritis/microbiology ; Fecal Microbiota Transplantation ; Host-Pathogen Interactions ; Risk Factors ; },
abstract = {The relationship between intestinal microbiota and arthritis has garnered significant attention, with emerging evidence suggesting a potential association between dysbiosis and various forms of inflammatory arthropathies. While observational studies have provided valuable insights into microbiota alterations in patients with arthritis, establishing causality remains challenging. Observational data, influenced by multiple confounders such as environmental factors, medication effects, and dietary habits, are insufficient to conclusively determine whether microbiota changes are somehow causally linked to arthritis. The heterogeneity of results across independent studies further complicates interpretation. To further support this hypothesis, interventional randomised trials are deemed necessary, yet their implementation in this area presents significant technical limitations. Experimental animal models offer insights into potential pathogenic mechanisms linking dysbiosis to arthritis, including compromised intestinal barrier function, the role of microbiota-derived metabolites and molecular mimicry. However, conflicting findings underscore the complexity of hostmicrobiota interactions and the challenges in establishing causality.Efforts to modulate the microbiota for arthritis treatment or prevention have shown promise, yet efficacy and applicability remains uncertain. Antibacterial drugs, dietary interventions, probiotics, and faecal microbiota transplantation have been explored, but their clinical utility awaits further validation. In conclusion, while the association between intestinal microbiota and arthritis is increasingly recognised, establishing causality remains elusive.},
}

Humans
*Gastrointestinal Microbiome
*Dysbiosis
Animals
Probiotics/therapeutic use
Arthritis/microbiology
Fecal Microbiota Transplantation
Host-Pathogen Interactions
Risk Factors

@article {pmid38743047,
year = {2024},
author = {Namasivayam, S and Tilves, C and Ding, H and Wu, S and Domingue, JC and Ruiz-Bedoya, C and Shah, A and Bohrnsen, E and Schwarz, B and Bacorn, M and Chen, Q and Levy, S and Dominguez Bello, MG and Jain, SK and Sears, CL and Mueller, NT and Hourigan, SK},
title = {Fecal transplant from vaginally seeded infants decreases intraabdominal adiposity in mice.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2353394},
pmid = {38743047},
issn = {1949-0984},
mesh = {Animals ; Humans ; Female ; Mice ; *Adiposity ; *Gastrointestinal Microbiome ; Male ; *Vagina/microbiology ; *Fecal Microbiota Transplantation ; *Feces/microbiology/chemistry ; Double-Blind Method ; Intra-Abdominal Fat/metabolism ; Infant ; Infant, Newborn ; },
abstract = {Exposing C-section infants to the maternal vaginal microbiome, coined "vaginal seeding", partially restores microbial colonization. However, whether vaginal seeding decreases metabolic disease risk is unknown. Therefore, we assessed the effect of vaginal seeding of human infants on adiposity in a murine model. Germ-free mice were colonized with transitional stool from human infants who received vaginal seeding or control (placebo) seeding in a double-blind randomized trial. There was a reduction in intraabdominal adipose tissue (IAAT) volume in male mice that received stool from vaginally seeded infants compared to control infants. Higher levels of isoleucine and lower levels of nucleic acid metabolites were observed in controls and correlated with increased IAAT. This suggests that early changes in the gut microbiome and metabolome caused by vaginal seeding have a positive impact on metabolic health.},
}

Animals
Humans
Female
Mice
*Adiposity
*Gastrointestinal Microbiome
Male
*Vagina/microbiology
*Fecal Microbiota Transplantation
*Feces/microbiology/chemistry
Double-Blind Method
Intra-Abdominal Fat/metabolism
Infant
Infant, Newborn

@article {pmid38739944,
year = {2024},
author = {Zhu, M and Huang, Y and Wang, Z and Jin, Z and Cao, J and Zhong, Q and Xiong, Z},
title = {Fecal Microbiota Transplantation Attenuates Frailty via Gut-Muscle Axis in Old Mice.},
journal = {Aging and disease},
volume = {},
number = {},
pages = {},
doi = {10.14336/AD.2024.0321},
pmid = {38739944},
issn = {2152-5250},
abstract = {Targeting adverse pathogenic gut microbiota regulation through fecal microbiota transplantation (FMT) may restore health and has been validated in some aging-related diseases. However, the mechanisms of the gut microbiota's role in frailty and whether modulation of the gut microbiota can treat age-related frailty remain largely unknown. To assess the effects of FMT on frailty, we used bidirectional fecal microbiota transplantation in young and old mice. We demonstrated that fecal bacteria transplanted from old mice into young mice reduced body weight and grip strength (p=0.002), and led to elevated inflammatory factors in young mice, but had no significant effect on intestinal barrier function. Notably, FMT treatment in older mice not only improved frailty (grip strength: p=0.036, low physical activity: p=0.020, running speed: p=0.048, running time: p=0.058, frailty score: p=0.027) and muscle mass, but also improved intestinal ecological imbalances, intestinal barrier function, and systemic inflammation (serum TNF-α: p=0.002, and IL-6: p<0.001). KEGG enrichment analysis of fecal metabolites showed that FMT may ameliorate frailty through the sphingolipid metabolism pathway. In addition, aged mice given FMT treatment showed a significant increase in the abundance of SCFA-producing bacteria and increased levels of short-chain fatty acids (butyric acid: p=0.084, propionic acid: p=0.028). Subsequent further verification found that FMT ameliorating frailty may be achieved through SCFAs metabolism. Another mechanism study found that FMT reduces lipopolysaccharide levels (p<0.001), thereby inhibiting the TLR4/NF-κB signaling pathway and its downstream pro-inflammatory products. Therefore, regulating SCFAs metabolism by altering gut microbial composition and targeting the gut-muscle axis with LPS/TLR4 pathways may be potential strategies to treat frailty in older adults.},
}

@article {pmid38739837,
year = {2024},
author = {Herbin, SR and Crum, H and Gens, K},
title = {Breaking the Cycle of Recurrent Clostridioides difficile Infections: A Narrative Review Exploring Current and Novel Therapeutic Strategies.},
journal = {Journal of pharmacy practice},
volume = {},
number = {},
pages = {8971900241248883},
doi = {10.1177/08971900241248883},
pmid = {38739837},
issn = {1531-1937},
abstract = {Clostridioides difficile is a toxin-producing bacteria that is a main cause of antibiotic-associated diarrhea. Clostridioides difficile infections (CDI) are associated with disruptions within the gastrointestinal (GI) microbiota which can be further exacerbated by CDI-targeted antibiotic treatment thereby causing recurrent CDI (rCDI) and compounding the burden placed on patients and the healthcare system. Treatment of rCDI consists of antibiotics which can be paired with preventative therapeutics, such as bezlotoxumab or fecal microbiota transplants (FMTs), if sustained clinical response is not obtained. Newer preventative strategies have been recently approved to assist in restoring balance within the GI system with the goal of preventing recurrent infections.},
}

@article {pmid38738157,
year = {2024},
author = {Shimodaira, Y and Fukuda, S and Okubo, R and Onochi, K and Iijima, K},
title = {A Report of Ulcerative Colitis With Relapse on the Rectal Side of the Loop Sigmoid Colostomy and Not on the Oral Side.},
journal = {Cureus},
volume = {16},
number = {4},
pages = {e57941},
pmid = {38738157},
issn = {2168-8184},
abstract = {A patient who received a loop sigmoid colostomy was diagnosed with ulcerative colitis (pancolitis type) and treated with infliximab. Thereafter, he relapsed with intestinal inflammation only on the rectal side of the loop sigmoid colostomy and not on the oral side. Autologous fecal microbiota transplantation from the proximal intestine to the distal intestine was performed to treat the inflammation but was ineffective. He was treated with oral prednisolone and induced into remission. After analyzing fecal samples from the patient, we observed an alteration of the composition of the intestinal microbiota with intestinal inflammation, including a reduction of phylum Firmicutes in the inflamed distal intestine, whereas Firmicutes was conserved in the proximal non-inflamed intestine and recovered in the distal intestine after induction of remission. Thus, our results indicated that the inflammation was associated with an alteration of the intestinal microbiota.},
}

@article {pmid38737692,
year = {2024},
author = {Sang, Y and Zheng, K and Zhao, Y and Liu, Y and Zhu, S and Xie, X and Shang, L and Liu, J and Li, L},
title = {Efficacy and regulatory strategies of gut microbiota in immunotherapy: a narrative review.},
journal = {Translational cancer research},
volume = {13},
number = {4},
pages = {2043-2063},
pmid = {38737692},
issn = {2219-6803},
abstract = {BACKGROUND AND OBJECTIVE: With advances in gut microbiome research, it has been recognized that the gut microbiome has an important and far-reaching impact on many human diseases, including cancer. Therefore, more and more researchers are focusing on the treatment of gut flora in tumors. In this article, we present a review of the mechanisms of gut microbes in tumor immunotherapy and related studies to provide reference for further research and insights into the clinical application of gut microbes.

METHODS: Between April 25, 2023, and November 25, 2023, we searched for articles published only in English between 1984 and 2023 using the databases PubMed, American Medical Association and Elsevier ScienceDirect using the keywords "gut microbiology" and "tumor" or "immunotherapy".

KEY CONTENT AND FINDINGS: The gastrointestinal tract contains the largest number of microorganisms in the human body. Microorganisms are involved in regulating many physiological activities of the body. Studies have shown that gut microbes and their derivatives are involved in the occurrence and development of a variety of inflammations and tumors, and changes in their abundance and proportion affect the degree of cancer progression and sensitivity to immunotherapy. Gut microbiota-based drug research is ongoing, and some anti-tumor studies have entered the clinical trial stage.

CONCLUSIONS: The abundance and proportion of intestinal microorganisms influence the susceptibility of tumors to tumor immunotherapy. This article reviewed the effects and mechanisms of gut microbes on tumor immunotherapy to further explore the medical value of gut microbes in tumor immunotherapy.},
}

@article {pmid38734322,
year = {2024},
author = {Liu, X and Li, S and Wang, L and Ma, K},
title = {Microecological regulation in HCC therapy: Gut microbiome enhances ICI treatment.},
journal = {Biochimica et biophysica acta. Molecular basis of disease},
volume = {1870},
number = {6},
pages = {167230},
doi = {10.1016/j.bbadis.2024.167230},
pmid = {38734322},
issn = {1879-260X},
abstract = {The exploration of the complex mechanisms of cancer immunotherapy is rapidly evolving worldwide, and our focus is on the interaction of hepatocellular carcinoma (HCC) with immune checkpoint inhibitors (ICIs), particularly as it relates to the regulatory role of the gut microbiome. An important basis for the induction of immune responses in HCC is the presence of specific anti-tumor cells that can be activated and reinforced by ICIs, which is why the application of ICIs results in sustained tumor response rates in the majority of HCC patients. However, mechanisms of acquired resistance to immunotherapy in unresectable HCC result in no long-term benefit for some patients. The significant heterogeneity of inter-individual differences in the gut microbiome in response to treatment with ICIs makes it possible to target modulation of specific gut microbes to assist in augmenting checkpoint blockade therapies in HCC. This review focuses on the complex relationship between the gut microbiome, host immunity, and HCC, and emphasizes that manipulating the gut microbiome to improve response rates to cancer ICI therapy is a clinical strategy with unlimited potential.},
}

@article {pmid38734214,
year = {2024},
author = {Quan, M and Zhang, X and Fang, Q and Lv, X and Wang, X and Zong, Z},
title = {Fighting against Clostridioides difficile infection: Current medications.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107198},
doi = {10.1016/j.ijantimicag.2024.107198},
pmid = {38734214},
issn = {1872-7913},
abstract = {Clostridioides difficile (formerly Clostridium difficile) has been regarded as an "urgent threat" and a significant global health problem, as life-threatening diarrhea and refractory recurrence are common in patients with C. difficile infection (CDI). Unfortunately, the available anti-CDI drugs are limited. Recent guidelines recommend fidaxomicin and vancomycin as first-line drugs to treat CDI, bezlotoxumab to prevent recurrence, and fecal microbiota transplantation (FMT) for rescue treatment. Currently, researchers are investigating therapeutic antibacterial drugs (e.g., teicoplanin, ridinilazole, ibezapolstat, surotomycin, cadazolid, and LFF571), preventive medications against recurrence (e.g., Rebyota, Vowst, VP20621, VE303, RBX7455, and MET-2), primary prevention strategies (e.g., vaccine, ribaxamase, and DAV132) and other anti-CDI medications in the preclinical stage (e.g., Raja 42, Myxopyronin B, and bacteriophage). This narrative review summarizes current medications, including newly marketed drugs and products in development against CDI, to help clinicians treat CDI appropriately and to call for more research on innovation.},
}

@article {pmid38733907,
year = {2024},
author = {Ruan, Y and Ren, G and Wang, M and Lv, W and Shimizu, K and Zhang, C},
title = {The dual role of 20(S)-protopanaxadiol in alleviating pulmonary fibrosis through the gut-lung axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {129},
number = {},
pages = {155699},
doi = {10.1016/j.phymed.2024.155699},
pmid = {38733907},
issn = {1618-095X},
abstract = {BACKGROUND: Pulmonary Fibrosis (PF) is a progressive lung disease characterized by the diffuse interstitial tissue, leading to severe breathing difficulties. The existing treatment methods are primarily aimed at slowing the progression of the disease, underscoring the urgent need to discover new drug interventions targeting novel sites. The "gut-lung axis" represents a complex bidirectional communication system where the gut microbiota not only influences lung immunity but also responds to lung-derived signals. Recent advances have uncovered that alterations in gut microbiota composition can significantly impact respiratory diseases, offering new insights into their pathogenesis and potential therapeutic approaches.

METHODS: This study is based on the fundamental concepts of the lung-gut axis and our previous research, further exploring the potential mechanisms of 20(S)-Protopanaxadiol (PPD) in ginseng against PF. We utilized a bleomycin-induced mouse model of PF and employed metabolomics and 16S rRNA sequencing to investigate the pathways through which PPD regulates the pulmonary fibrosis process via the gut-lung axis. Finally, we employed strategies such as antibiotic-induced microbiota disruption and fecal microbiota transplantation (FMT) to provide a comprehensive perspective on how PPD regulates pulmonary fibrosis through gut microbiota.

RESULTS: The results of the bleomycin (BLM) mouse model of PF proved that PPD can directly act on the glycolysis- related metabolic reprogramming process in lung and the AMPK/STING pathway to improve PF. Combined the analysis of gut microbiota and related metabolites, we found that PPD can regulate the process of PF through the gut-lung axis target points G6PD and SPHK1. FMT and antibiotic-induced microbiota disruption further confirmed intermediate effect of gut microbiota in PF process and the treatment of PPD. Our study suggests that PPD can alleviate the process of pulmonary fibrosis either by directly acting on the lungs or by regulating the gut microbiota.

CONCLUSION: This study positions PPD as a vanguard in the therapeutic landscape for pulmonary fibrosis, offering a dual mechanism of action that encompasses both modulation of gut microbiota and direct intervention at molecular targets. These insights highlight the immense therapeutic potential of harnessing the gut-lung axis.},
}

@article {pmid38733623,
year = {2024},
author = {Ishikawa, D and Zhang, X and Nomura, K and Shibuya, T and Hojo, M and Yamashita, M and Koizumi, S and Yamazaki, F and Iwamoto, S and Saito, M and Kunigo, K and Nakano, R and Honma, N and Urakawa, I and Nagahara, A},
title = {Anti-inflammatory Effects of Bacteroidota Strains Derived From Outstanding Donors of Fecal Microbiota Transplantation for the Treatment of Ulcerative Colitis.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izae080},
pmid = {38733623},
issn = {1536-4844},
support = {JP22ae0121038//Japan Agency for Medical Research and Development/ ; },
abstract = {BACKGROUND: The proportion of certain Bacteroidota species decreased in patients with ulcerative colitis, and the recovery of Bacteroidota is associated with the efficacy of fecal microbiota transplantation therapy. We hypothesized that certain Bacteroidota may advance ulcerative colitis treatment. Accordingly, we aimed to evaluate the anti-inflammatory effects of Bacteroidota strains isolated from donors.

METHODS: Donors with proven efficacy of fecal microbiota transplantation for ulcerative colitis were selected, and Bacteroidota strains were isolated from their stools. The immune function of Bacteroidota isolates was evaluated through in vitro and in vivo studies.

RESULTS: Twenty-four Bacteroidota strains were isolated and identified. Using an in vitro interleukin (IL)-10 induction assay, we identified 4 Bacteroidota strains with remarkable IL-10-induction activity. Of these, an Alistipes putredinis strain exhibited anti-inflammatory effects in a mouse model of colitis induced by sodium dextran sulfate and oxazolone. However, 16S rRNA gene-based sequencing analysis of A. putredinis cultures in the in vivo study revealed unexpected Veillonella strain contamination. A second in vitro study confirmed that the coculture exhibited an even more potent IL-10-inducing activity. Furthermore, the production of A. putredinis-induced IL-10 was likely mediated via toll-like receptor 2 signaling.

CONCLUSIONS: This study demonstrated that A. putredinis, a representative Bacteroidota species, exhibits anti-inflammatory effects in vivo and in vitro; however, the effects of other Bacteroidota species remain unexplored. Our fecal microbiota transplantation-based reverse translation approach using promising bacterial species may represent a breakthrough in microbiome drug development for controlling dysbiosis during ulcerative colitis.},
}

@article {pmid38732527,
year = {2024},
author = {Ouyang, Q and Li, X and Liang, Y and Liu, R},
title = {Sea Buckthorn Polysaccharide Ameliorates Colitis.},
journal = {Nutrients},
volume = {16},
number = {9},
pages = {},
pmid = {38732527},
issn = {2072-6643},
mesh = {Animals ; *Hippophae/chemistry ; *Polysaccharides/pharmacology ; *Gastrointestinal Microbiome/drug effects ; Mice ; Colitis/drug therapy/chemically induced/microbiology ; Colitis, Ulcerative/microbiology/drug therapy ; Disease Models, Animal ; Male ; Mice, Inbred C57BL ; Oxidative Stress/drug effects ; Fecal Microbiota Transplantation ; Colon/drug effects/microbiology/metabolism ; Dextran Sulfate ; Anti-Inflammatory Agents/pharmacology ; Antioxidants/pharmacology ; Fruit/chemistry ; Fatty Acids, Volatile/metabolism ; },
abstract = {Ulcerative colitis (UC) is characterized by chronic inflammation and ulceration of the intestinal inner lining, resulting in various symptoms. Sea buckthorn berries contain a bioactive compound known as sea buckthorn polysaccharide (SBP). However, the precise mechanisms underlying the impact of SBP on UC remain unclear. In this study, we investigated the effects of pretreatment with SBP on colitis induced by DSS. Our findings demonstrate that SBP pretreatment effectively reduces inflammation, oxidative stress, and intestinal barrier damage associated with colitis. To further elucidate the role of SBP-modulated gut microbiota in UC, we performed fecal microbiota transplantation (FMT) on DSS-treated mice. The microbiota from SBP-treated mice exhibits notable anti-inflammatory and antioxidant effects, improves colonic barrier integrity, and increases the abundance of beneficial bacteria, as well as enhancing SCFA production. Collectively, these results strongly indicate that SBP-mediated amelioration of colitis is attributed to its impact on the gut microbiota, particularly through the promotion of SCFA-producing bacteria and subsequent elevation of SCFA levels. This study provides compelling evidence supporting the efficacy of pre-emptive SBP supplementation in alleviating colitis symptoms by modulating the gut microbiota, thereby offering novel insights into the potential of SBP as a regulator of the gut microbiota for colitis relief.},
}

Animals
*Hippophae/chemistry
*Polysaccharides/pharmacology
*Gastrointestinal Microbiome/drug effects
Mice
Colitis/drug therapy/chemically induced/microbiology
Colitis, Ulcerative/microbiology/drug therapy
Disease Models, Animal
Male
Mice, Inbred C57BL
Oxidative Stress/drug effects
Fecal Microbiota Transplantation
Colon/drug effects/microbiology/metabolism
Dextran Sulfate
Anti-Inflammatory Agents/pharmacology
Antioxidants/pharmacology
Fruit/chemistry
Fatty Acids, Volatile/metabolism

@article {pmid38530358,
year = {2024},
author = {Pal, S and Morgan, X and Dar, HY and Gacasan, CA and Patil, S and Stoica, A and Hu, YJ and Weitzmann, MN and Jones, RM and Pacifici, R},
title = {Gender-affirming hormone therapy preserves skeletal maturation in young mice via the gut microbiome.},
journal = {The Journal of clinical investigation},
volume = {134},
number = {10},
pages = {},
pmid = {38530358},
issn = {1558-8238},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; Female ; Male ; *T-Lymphocytes, Regulatory/immunology/drug effects ; Bone Development/drug effects ; Osteogenesis/drug effects ; Bacteroides ; Fecal Microbiota Transplantation ; Humans ; },
abstract = {Gender-affirming hormone therapy (GAHT) is often prescribed to transgender (TG) adolescents to alleviate gender dysphoria, but the effect of GAHT on the growing skeleton is unclear. We found GAHT to improve trabecular bone structure via increased bone formation in young male mice and not to affect trabecular structure in female mice. GAHT modified gut microbiome composition in both male and female mice. However, fecal microbiota transfers (FMTs) revealed that GAHT-shaped gut microbiome was a communicable regulator of bone structure and turnover in male, but not in female mice. Mediation analysis identified 2 species of Bacteroides as significant contributors to the skeletal effects of GAHT in male mice, with Bacteroides supplementation phenocopying the effects of GAHT on bone. Bacteroides have the capacity to expand Treg populations in the gut. Accordingly, GAHT expanded intestinal Tregs and stimulated their migration to the bone marrow (BM) in male but not in female mice. Attesting to the functional relevance of Tregs, pharmacological blockade of Treg expansion prevented GAHT-induced bone anabolism. In summary, in male mice GAHT stimulated bone formation and improved trabecular structure by promoting Treg expansion via a microbiome-mediated effect, while in female mice, GAHT neither improved nor impaired trabecular structure.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
Female
Male
*T-Lymphocytes, Regulatory/immunology/drug effects
Bone Development/drug effects
Osteogenesis/drug effects
Bacteroides
Fecal Microbiota Transplantation
Humans

@article {pmid38732276,
year = {2024},
author = {Boicean, A and Ichim, C and Todor, SB and Anderco, P and Popa, ML},
title = {The Importance of Microbiota and Fecal Microbiota Transplantation in Pancreatic Disorders.},
journal = {Diagnostics (Basel, Switzerland)},
volume = {14},
number = {9},
pages = {},
pmid = {38732276},
issn = {2075-4418},
abstract = {The role of the intestinal microbiota in the diagnosis and treatment of pancreatic diseases is increasingly significant. Consequently, fecal microbiota transplantation (FMT) is emerging as a promising therapeutic avenue for various pancreatic disorders, including cancer, pancreatitis, and type 1 diabetes (T1D). This innovative procedure entails transferring gut microbiota from healthy donors to individuals affected by pancreatic ailments with the potential to restore intestinal balance and alleviate associated symptoms. FMT represents a pioneering approach to improve patient outcomes in pancreatic diseases, offering tailored treatments customized to individual microbiomes and specific conditions. Recent research highlights the therapeutic benefits of targeting the gut microbiota for personalized interventions in pancreatic disorders. However, a comprehensive understanding of the intricate interplay between gut microbiota and pancreatic physiology warrants further investigation. The necessity for additional studies and research endeavors remains crucial, especially in elucidating both adult and pediatric cases affected by pathological pancreatic conditions.},
}

@article {pmid38729481,
year = {2024},
author = {Xia, T and He, W and Luo, Z and Wang, K and Tan, X},
title = {Achyranthes bidentata polysaccharide ameliorates type 2 diabetes mellitus by gut microbiota-derived short-chain fatty acids-induced activation of the GLP-1/GLP-1R/cAMP/PKA/CREB/INS pathway.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {132256},
doi = {10.1016/j.ijbiomac.2024.132256},
pmid = {38729481},
issn = {1879-0003},
abstract = {Gut microbiota variances reflecting the severity type 2 diabetes mellitus (T2DM). Achyranthes bidentata polysaccharide (ABP) can regulate gut microbiota. However, the hypoglycemic effect and underlying mechanism of ABP remain unclear. Herein, we characterized the structure of ABP and revealed the hypoglycemic effect of ABP in mice with T2DM. ABP repaired the intestinal barrier in T2DM mice and regulated the composition and abundance of gut microbiota, especially increasing bacteria which producing short-chain fatty acids (SCFAs), then increasing glucagon-like peptide-1 (GLP-1) level. The abundance of these bacteria was positively correlated with blood lipid and INS levels, negatively correlated with FBG levels. Colon transcriptome data and immunohistochemistry demonstrated that the alleviating T2DM effect of ABP was related to activation of the GLP-1/GLP-1 receptor (GLP-1R)/cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-response element binding protein (CREB)/INS pathway. Fecal microbiota transplantation (FMT) confirmed the transmissible efficacy of ABPs through gut microbiota. Overall, our research shows that ABP plays a hypoglycemic role by increasing gut microbiota-derived SCFAs levels, and activating the GLP-1/GLP-1R/cAMP/PKA/CREB/INS pathway, emphasizing ABP as promising T2DM therapeutic candidates.},
}

@article {pmid38728472,
year = {2024},
author = {Ugwu, OP and Alum, EU and Okon, MB and Obeagu, EI},
title = {Mechanisms of microbiota modulation: Implications for health, disease, and therapeutic interventions.},
journal = {Medicine},
volume = {103},
number = {19},
pages = {e38088},
pmid = {38728472},
issn = {1536-5964},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/physiology ; Anti-Bacterial Agents/therapeutic use ; Probiotics/therapeutic use ; Gastrointestinal Diseases/therapy/microbiology ; },
abstract = {Microbiota modulation, the intentional change in the structure and function of the microbial community, is an emerging trajectory that holds the promise to mitigate an infinite number of health issues. The present review illustrates the underlying principles of microbiota modulation and the various applications of this fundamental process to human health, healthcare management, and pharmacologic interventions. Different strategies, directing on dietary interventions, fecal microbiota transplantation, treatment with antibiotics, bacteriophages, microbiome engineering, and modulation of the immune system, are described in detail. This therapeutic implication is reflected in clinical applications to gastrointestinal disorders and immune-mediated diseases for microbiota-modulating agents. In addition to this, the review outlines the challenges of translating researched outcomes into clinical practice to consider safety and provides insights into future research directions of this rapidly developing area.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/physiology
Anti-Bacterial Agents/therapeutic use
Probiotics/therapeutic use
Gastrointestinal Diseases/therapy/microbiology

@article {pmid38727248,
year = {2024},
author = {Hao, QY and Yan, J and Wei, JT and Zeng, YH and Feng, LY and Que, DD and Li, SC and Guo, JB and Fan, Y and Ding, YF and Zhang, XL and Yang, PZ and Gao, JW and Li, ZH},
title = {Prevotella copri promotes vascular calcification via lipopolysaccharide through activation of NF-κB signaling pathway.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2351532},
doi = {10.1080/19490976.2024.2351532},
pmid = {38727248},
issn = {1949-0984},
mesh = {Animals ; *Vascular Calcification/metabolism/pathology ; *NF-kappa B/metabolism ; *Lipopolysaccharides/metabolism ; Rats ; *Renal Insufficiency, Chronic/metabolism/microbiology/chemically induced/pathology ; *Signal Transduction ; Humans ; Male ; *Toll-Like Receptor 4/metabolism/genetics ; *Gastrointestinal Microbiome ; *Prevotella/metabolism ; Rats, Sprague-Dawley ; Myocytes, Smooth Muscle/metabolism ; Osteogenesis/drug effects ; Muscle, Smooth, Vascular/metabolism/pathology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/genetics ; Feces/microbiology ; Inflammasomes/metabolism ; },
abstract = {Emerging evidence indicates that alteration of gut microbiota plays an important role in chronic kidney disease (CKD)-related vascular calcification (VC). We aimed to investigate the specific gut microbiota and the underlying mechanism involved in CKD-VC. We identified an increased abundance of Prevotella copri (P. copri) in the feces of CKD rats (induced by using 5/6 nephrectomy followed by a high calcium and phosphate diet) with aortic calcification via amplicon sequencing of 16S rRNA genes. In patients with CKD, we further confirmed a positive correlation between abundance of P. copri and aortic calcification scores. Moreover, oral administration of live P. copri aggravated CKD-related VC and osteogenic differentiation of vascular smooth muscle cells in vivo, accompanied by intestinal destruction, enhanced expression of Toll-like receptor-4 (TLR4), and elevated lipopolysaccharide (LPS) levels. In vitro and ex vivo experiments consistently demonstrated that P. copri-derived LPS (Pc-LPS) accelerated high phosphate-induced VC and VSMC osteogenic differentiation. Mechanistically, Pc-LPS bound to TLR4, then activated the nuclear factor κB (NF-κB) and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome signals during VC. Inhibition of NF-κB reduced NLRP3 inflammasome and attenuated Pc-LPS-induced VSMC calcification. Our study clarifies a novel role of P. copri in CKD-related VC, by the mechanisms involving increased inflammation-regulating metabolites including Pc-LPS, and activation of the NF-κB/NLRP3 signaling pathway. These findings highlight P. copri and its-derived LPS as potential therapeutic targets for VC in CKD.},
}

Animals
*Vascular Calcification/metabolism/pathology
*NF-kappa B/metabolism
*Lipopolysaccharides/metabolism
Rats
*Renal Insufficiency, Chronic/metabolism/microbiology/chemically induced/pathology
*Signal Transduction
Humans
Male
*Toll-Like Receptor 4/metabolism/genetics
*Gastrointestinal Microbiome
*Prevotella/metabolism
Rats, Sprague-Dawley
Myocytes, Smooth Muscle/metabolism
Osteogenesis/drug effects
Muscle, Smooth, Vascular/metabolism/pathology
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/genetics
Feces/microbiology
Inflammasomes/metabolism

@article {pmid38726585,
year = {2024},
author = {Yakout, A and Bi, Y and Harris, DM},
title = {Clostridioides Difficile: A Concise Review of Best Practices and Updates.},
journal = {Journal of primary care & community health},
volume = {15},
number = {},
pages = {21501319241249645},
pmid = {38726585},
issn = {2150-1327},
mesh = {Humans ; *Clostridium Infections/prevention & control/diagnosis/therapy ; *Anti-Bacterial Agents/therapeutic use ; *Clostridioides difficile ; Fecal Microbiota Transplantation ; Cross Infection/prevention & control ; Practice Guidelines as Topic ; Fidaxomicin/therapeutic use ; Metronidazole/therapeutic use ; },
abstract = {Clostridioides difficile infection (CDI) is one of the most common and severe nosocomial infections worldwide. It can also affect healthy individuals in the community. The incidence of CDI has been on the rise globally for the past decade, necessitating a proactive approach to combat its spread; new strategies are being developed to enhance diagnostic accuracy and optimize treatment outcomes. Implementing the 2-step testing has increased diagnostic specificity, reducing the usage of CD-specific antibiotics with no concomitant increase in surgical complication rates. In 2021, the Infectious Diseases Society of America/Society for Healthcare Epidemiology of America (IDSA/SHEA) shifted its preference for initial treatment to fidaxomicin over vancomycin and metronidazole due to its lower recurrence rate. It also prioritized fidaxomicin for the treatment of recurrent CDI. There are new developments on the frontiers of fecal microbiota therapies, with RBX2660 and SER-109 approved recently by the FDA for prevention, with other microbiome-based therapies in various development and clinical trials. This review offers providers an updated and practical guide for CDI management.},
}

Humans
*Clostridium Infections/prevention & control/diagnosis/therapy
*Anti-Bacterial Agents/therapeutic use
*Clostridioides difficile
Fecal Microbiota Transplantation
Cross Infection/prevention & control
Practice Guidelines as Topic
Fidaxomicin/therapeutic use
Metronidazole/therapeutic use

@article {pmid38724904,
year = {2024},
author = {Wang, L and Guo, G and Xu, Y and Li, L and Yang, B and Zhao, D and Tian, H and Ye, C and Lin, Z and Cui, J and Li, N and Huang, L and Chen, Q},
title = {The effect of fecal microbiota transplantation on antibiotic-associated diarrhea and its impact on gut microbiota.},
journal = {BMC microbiology},
volume = {24},
number = {1},
pages = {160},
pmid = {38724904},
issn = {1471-2180},
mesh = {Humans ; *Diarrhea/microbiology/therapy ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Female ; Male ; Middle Aged ; *Anti-Bacterial Agents/adverse effects ; *Feces/microbiology ; Adult ; *RNA, Ribosomal, 16S/genetics ; Aged ; Treatment Outcome ; Bacteria/classification/isolation & purification/genetics ; },
abstract = {BACKGROUND: Antibiotic-associated diarrhea (AAD) refers to symptoms of diarrhea that cannot be explained by other causes after the use of antibiotics. AAD is thought to be caused by a disruption of intestinal ecology due to antibiotics. Fecal Microbiota Transplantation (FMT) is a treatment method that involves transferring microbial communities from the feces of healthy individuals into the patient's gut.

METHOD: We selected 23 AAD patients who received FMT treatment in our department. Before FMT, we documented patients' bowel movement frequency, abdominal symptoms, routine blood tests, and inflammatory markers, and collected fecal samples for 16S rRNA sequencing to observe changes in the intestinal microbiota. Patients' treatment outcomes were followed up 1 month and 3 months after FMT.

RESULTS: Out of the 23 AAD patients, 19 showed a clinical response to FMT with alleviation of abdominal symptoms. Among them, 82.61% (19/23) experienced relief from diarrhea, 65% (13/20) from abdominal pain, 77.78% (14/18) from abdominal distension, and 57.14% (4/7) from bloody stools within 1 month after FMT. Inflammatory markers IL-8 and CRP significantly decreased after FMT, but there were no noticeable changes in WBC, IL-6, and TNF-α before and after transplantation. After FMT, the abundance of Bacteroides and Faecalibacterium increased in patients' fecal samples, while the abundance of Escherichia-Shigella and Veillonella decreased.

CONCLUSION: FMT has a certain therapeutic effect on AAD, and can alleviate abdominal symptoms and change the intestinal microbiota of patients.},
}

Humans
*Diarrhea/microbiology/therapy
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Female
Male
Middle Aged
*Anti-Bacterial Agents/adverse effects
*Feces/microbiology
Adult
*RNA, Ribosomal, 16S/genetics
Aged
Treatment Outcome
Bacteria/classification/isolation & purification/genetics

@article {pmid38722758,
year = {2024},
author = {Imamura, Y and Motooka, D and Nakajima, Y and Ito, S and Kitakaze, M and Iida, T and Nakamura, S},
title = {Turicibacter faecis sp. nov., isolated from faeces of heart failure mouse model.},
journal = {International journal of systematic and evolutionary microbiology},
volume = {74},
number = {5},
pages = {},
doi = {10.1099/ijsem.0.006379},
pmid = {38722758},
issn = {1466-5034},
mesh = {Animals ; *RNA, Ribosomal, 16S/genetics ; *Feces/microbiology ; *Phylogeny ; Mice ; *Base Composition ; *DNA, Bacterial/genetics ; *Bacterial Typing Techniques ; *Sequence Analysis, DNA ; *Heart Failure/microbiology ; *Disease Models, Animal ; Genome, Bacterial ; Male ; Fatty Acids ; },
abstract = {Strain TC023[T], a Gram-positive, long, rod-shaped, spore-forming anaerobe, was isolated from the faeces of a heart failure mouse model. The strain formed greyish-white coloured colonies with a convex elevation on brain-heart infusion medium supplemented with 0.1 % sodium taurocholate, incubated at 37 °C for 2 days. Taxonomic analysis based on the 16S rRNA gene sequence showed that TC023[T] belonged to the genus Turicibacter, and was closely related to Turicibacter bilis MMM721[T] (97.6 %) and Turicibacter sanguinis MOL361[T] (97.4 %). The whole genome of the strain has a G+C content of 37.3 mol%. The average nucleotide identity and genome-to-genome distance between TC023[T] and Turicibacter bilis MMM721[T] were 77.6 % and 24.3 %, respectively, and those with Turicibacter sanguinis MOL361[T] were 75.4 % and 24.3 %, respectively. These genotypic, phenotypic, and biochemical analyses indicated that the isolate represents a novel species in the genus Turicibacter, and the name Turicibacter faecis sp. nov. is proposed. The type strain is TC023[T] (RIMD 2002001[T]=TSD 372[T]).},
}

Animals
*RNA, Ribosomal, 16S/genetics
*Feces/microbiology
*Phylogeny
Mice
*Base Composition
*DNA, Bacterial/genetics
*Bacterial Typing Techniques
*Sequence Analysis, DNA
*Heart Failure/microbiology
*Disease Models, Animal
Genome, Bacterial
Male
Fatty Acids

@article {pmid38720628,
year = {2024},
author = {Leibovitzh, H and Sarbagili Shabat, C and Hirsch, A and Zittan, E and Mentella, MC and Petito, V and Cohen, NA and Ron, Y and Fliss Isakov, N and Pfeffer, J and Yaakov, M and Fanali, C and Turchini, L and Masucci, L and Quaranta, G and Kolonimos, N and Godneva, A and Weinberger, A and Scaldaferri, F and Maharshak, N},
title = {Fecal transplantation for ulcerative colitis from diet conditioned donors followed by dietary intervention results in favorable gut microbial profile compared to fecal transplantation alone.},
journal = {Journal of Crohn's & colitis},
volume = {},
number = {},
pages = {},
doi = {10.1093/ecco-jcc/jjae062},
pmid = {38720628},
issn = {1876-4479},
abstract = {BACKGROUND AND AIMS: Several fecal microbial transplantation (FMT) approaches for ulcerative colitis (UC) have been investigated with conflicting results. We have recently published the clinical outcomes from the CRAFT-UC Trial using FMT with the UC Exclusion Diet (UCED), compared with FMT alone. Here we aimed to compare the two FMT strategies in terms of microbial profile and function.

METHODS: Subjects recruited to the CRAFT-UC study with available pre- and post-intervention fecal samples were included. Donors received diet conditioning for 14 days based on the UCED principles. Group-1 received single FMT by colonoscopy (Day 1) and enemas (Days 2 and 14) without donors' dietary conditioning (N=11). Group-2 received FMT but with donors' dietary pre-conditioning and UCED for the patients (N=10). Fecal samples were assessed by DNA shotgun metagenomic sequencing.

RESULTS: Following diet conditioning, donors had depletion in metabolic pathways involved in sulfur-containing amino acids biosynthesis. Only Group-2 showed significant shifts towards the donors' microbial composition (ADONIS: R2=0.15, p=0.008) and significant increased Eubacterium_sp_AF228LB post-intervention (β-coefficient 2.66, 95%CI 2.1-3.3, q<0.05) which was inversely correlated with fecal calprotectin (rho=-0.52, p=0.035). Moreover, pathways involved in gut inflammation and barrier function including branched chain amino acids were enriched post intervention in Group-2 and were significantly inversely correlated with fecal calprotectin.

CONCLUSION: FMT from diet conditioned donors followed by the UCED led to microbial alterations associated with favorable microbial profile which correlated with decreased fecal calprotectin. Our findings support further exploration of additive benefit of dietary intervention for both donors and patients undergoing FMT as a potential treatment of UC.},
}

@article {pmid38720499,
year = {2023},
author = {Ramakrishna, BS and Patankar, R},
title = {Antibiotic-associated Gut Dysbiosis.},
journal = {The Journal of the Association of Physicians of India},
volume = {71},
number = {11},
pages = {62-68},
doi = {10.59556/japi.71.0381},
pmid = {38720499},
issn = {0004-5772},
mesh = {*Dysbiosis/chemically induced ; Humans ; *Anti-Bacterial Agents/adverse effects ; *Gastrointestinal Microbiome/drug effects ; *Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Phage Therapy/methods ; },
abstract = {The human gut microbiota plays a crucial role in maintaining overall health. However, the widespread use of antibiotics has raised concerns about its impact on the microbial ecosystem. This review explores the multifaceted relationship between antibiotics and gut dysbiosis, highlighting the mechanisms underlying these interactions and their implications for human health. Antibiotics, while invaluable in treating infections, disrupt the gut microbiota by indiscriminately targeting both harmful and beneficial microorganisms. This disturbance leads to a reduction in microbial diversity, altered metabolite production, and compromised immune responses, resulting in a state referred to as dysbiosis. Broad-spectrum antibiotics tend to induce more severe dysbiosis compared to narrow-spectrum agents. Antibiotic-induced dysbiosis has been linked to the onset and progression of these disorders, emphasizing the far-reaching consequences of microbial imbalance. The review highlights various strategies to mitigate the adverse effects of antibiotics on gut health, like probiotics, fecal microbiota transplantation (FMT), and phage therapy, as promising approaches to restore and maintain a balanced gut microbiota. How to cite this article: Ramakrishna BS, Patankar R. Antibiotic-associated Gut Dysbiosis. J Assoc Physicians India 2023;71(11):62-68.},
}

*Dysbiosis/chemically induced
Humans
*Anti-Bacterial Agents/adverse effects
*Gastrointestinal Microbiome/drug effects
*Fecal Microbiota Transplantation
Probiotics/therapeutic use
Phage Therapy/methods

@article {pmid38720361,
year = {2024},
author = {Huang, C and Li, X and Li, H and Chen, R and Li, Z and Li, D and Xu, X and Zhang, G and Qin, L and Li, B and Chu, XM},
title = {Role of gut microbiota in doxorubicin-induced cardiotoxicity: from pathogenesis to related interventions.},
journal = {Journal of translational medicine},
volume = {22},
number = {1},
pages = {433},
pmid = {38720361},
issn = {1479-5876},
support = {82172574//National Natural Science Foundation of China/ ; 81871231//National Natural Science Foundation of China/ ; ZR2020MH016//Natural Science Foundation of Shandong Province/ ; ZR202209280042//Natural Science Foundation of Shandong Province/ ; YJKT202171//Project of Shandong Province Higher Educational Science and Technology Program/ ; tsqn202103056//Taishan Scholar Foundation of Shandong Province/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects ; Humans ; *Doxorubicin/adverse effects ; *Cardiotoxicity/etiology ; Animals ; Dysbiosis ; Fecal Microbiota Transplantation ; },
abstract = {Doxorubicin (DOX) is a broad-spectrum and highly efficient anticancer agent, but its clinical implication is limited by lethal cardiotoxicity. Growing evidences have shown that alterations in intestinal microbial composition and function, namely dysbiosis, are closely linked to the progression of DOX-induced cardiotoxicity (DIC) through regulating the gut-microbiota-heart (GMH) axis. The role of gut microbiota and its metabolites in DIC, however, is largely unelucidated. Our review will focus on the potential mechanism between gut microbiota dysbiosis and DIC, so as to provide novel insights into the pathophysiology of DIC. Furthermore, we summarize the underlying interventions of microbial-targeted therapeutics in DIC, encompassing dietary interventions, fecal microbiota transplantation (FMT), probiotics, antibiotics, and natural phytochemicals. Given the emergence of microbial investigation in DIC, finally we aim to point out a novel direction for future research and clinical intervention of DIC, which may be helpful for the DIC patients.},
}

*Gastrointestinal Microbiome/drug effects
Humans
*Doxorubicin/adverse effects
*Cardiotoxicity/etiology
Animals
Dysbiosis
Fecal Microbiota Transplantation

@article {pmid38719790,
year = {2024},
author = {Grodin, EN and Burnette, EM and Rodriguez, C and Fulcher, JA and Ray, LA},
title = {The gut microbiome in alcohol use disorder and alcohol-associated liver disease: A systematic review of clinical studies.},
journal = {Alcohol, clinical & experimental research},
volume = {},
number = {},
pages = {},
doi = {10.1111/acer.15338},
pmid = {38719790},
issn = {2993-7175},
support = {K08 AI124979/AI/NIAID NIH HHS/United States ; 2019086/DDCF/Doris Duke Charitable Foundation/United States ; F31 AA028976/AA/NIAAA NIH HHS/United States ; K01 AA029712/AA/NIAAA NIH HHS/United States ; K24 AA025704/AA/NIAAA NIH HHS/United States ; },
abstract = {Evidence suggests that a relationship exists between the gut microbiome and the pathogenesis of alcohol use disorder (AUD) and alcohol-associated liver disease (AALD). This systematic review identified studies that investigated the gut microbiome in individuals with an AUD or an AALD. A search was conducted on October 27, 2022, in PubMed, Web of Science, and Embase databases. Fifty studies satisfied eligibility criteria. Most studies found evidence for gut dysbiosis in individuals with AUD and AALD. Microbiome intervention studies have mostly been conducted in AALD patients; fecal microbial transplant interventions show the most promise. Because most studies were conducted cross-sectionally, the causal relationship between the gut microbiome and alcohol use is unknown. Furthermore, almost all studies have been conducted in predominantly male populations, leaving critical questions regarding sex differences and generalizability of the findings. The study summaries and recommendations provided in this review seek to identify areas for further research and to highlight potential gut microbial interventions for treating AUD and AALD.},
}

@article {pmid38718729,
year = {2024},
author = {Gu, T and Kong, M and Duan, M and Chen, L and Tian, Y and Xu, W and Zeng, T and Lu, L},
title = {Cu exposure induces liver inflammation via regulating gut microbiota/LPS/liver TLR4 signaling axis.},
journal = {Ecotoxicology and environmental safety},
volume = {278},
number = {},
pages = {116430},
doi = {10.1016/j.ecoenv.2024.116430},
pmid = {38718729},
issn = {1090-2414},
abstract = {Copper (Cu) serves as an essential cofactor in all organisms, yet excessive Cu exposure is widely recognized for its role in inducing liver inflammation. However, the precise mechanism by which Cu triggers liver inflammation in ducks, particularly in relation to the interplay in gut microbiota regulation, has remained elusive. In this investigation, we sought to elucidate the impact of Cu exposure on liver inflammation through gut-liver axis in ducks. Our findings revealed that Cu exposure markedly elevated liver AST and ALT levels and induced liver inflammation through upregulating pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and triggering the LPS/TLR4/NF-κB signaling pathway. Simultaneously, Cu exposure induced alterations in the composition of intestinal flora communities, notably increasing the relative abundance of Sphingobacterium, Campylobacter, Acinetobacter and reducing the relative abundance of Lactobacillus. Cu exposure significantly decreased the protein expression related to intestinal barrier (Occludin, Claudin-1 and ZO-1) and promoted the secretion of intestinal pro-inflammatory cytokines. Furthermore, correlation analysis was observed that intestinal microbiome and gut barrier induced by Cu were closely related to liver inflammation. Fecal microbiota transplantation (FMT) experiments further demonstrated the microbiota-depleted ducks transplanting fecal samples from Cu-exposed ducks disturbed the intestinal dysfunction, which lead to impaire liver function and activate the liver inflammation. Our study provided insights into the mechanism by which Cu exposure induced liver inflammation in ducks through the regulation of gut-liver axis. These results enhanced our comprehension of the potential mechanisms driving Cu-induced hepatotoxicity in avian species.},
}

@article {pmid38717124,
year = {2024},
author = {Yadegar, A and Bar-Yoseph, H and Monaghan, TM and Pakpour, S and Severino, A and Kuijper, EJ and Smits, WK and Terveer, EM and Neupane, S and Nabavi-Rad, A and Sadeghi, J and Cammarota, G and Ianiro, G and Nap-Hill, E and Leung, D and Wong, K and Kao, D},
title = {Fecal microbiota transplantation: current challenges and future landscapes.},
journal = {Clinical microbiology reviews},
volume = {},
number = {},
pages = {e0006022},
doi = {10.1128/cmr.00060-22},
pmid = {38717124},
issn = {1098-6618},
abstract = {SUMMARYGiven the importance of gut microbial homeostasis in maintaining health, there has been considerable interest in developing innovative therapeutic strategies for restoring gut microbiota. One such approach, fecal microbiota transplantation (FMT), is the main "whole gut microbiome replacement" strategy and has been integrated into clinical practice guidelines for treating recurrent Clostridioides difficile infection (rCDI). Furthermore, the potential application of FMT in other indications such as inflammatory bowel disease (IBD), metabolic syndrome, and solid tumor malignancies is an area of intense interest and active research. However, the complex and variable nature of FMT makes it challenging to address its precise functionality and to assess clinical efficacy and safety in different disease contexts. In this review, we outline clinical applications, efficacy, durability, and safety of FMT and provide a comprehensive assessment of its procedural and administration aspects. The clinical applications of FMT in children and cancer immunotherapy are also described. We focus on data from human studies in IBD in contrast with rCDI to delineate the putative mechanisms of this treatment in IBD as a model, including colonization resistance and functional restoration through bacterial engraftment, modulating effects of virome/phageome, gut metabolome and host interactions, and immunoregulatory actions of FMT. Furthermore, we comprehensively review omics technologies, metagenomic approaches, and bioinformatics pipelines to characterize complex microbial communities and discuss their limitations. FMT regulatory challenges, ethical considerations, and pharmacomicrobiomics are also highlighted to shed light on future development of tailored microbiome-based therapeutics.},
}

@article {pmid38716216,
year = {2024},
author = {Tetali, B and Suresh, S},
title = {Management of irritable bowel syndrome: a narrative review.},
journal = {Translational gastroenterology and hepatology},
volume = {9},
number = {},
pages = {26},
pmid = {38716216},
issn = {2415-1289},
abstract = {BACKGROUND AND OBJECTIVE: As our understanding of the pathophysiology of irritable bowel syndrome (IBS) has advanced, so too has the therapeutic landscape, offering a myriad of approaches to alleviate symptoms and enhance the well-being of patients. This review paper is dedicated to a comprehensive exploration of the diverse therapeutic modalities available for managing IBS. By delving into the complexities of IBS therapeutics, our aim is to contribute to the enhancement of patient care and the overall quality of life for patients grappling with this complex condition.

METHODS: This review utilized information from PubMed/MEDLINE using the key search term "irritable bowel syndrome" as well as the 2020 American College of Gastroenterology (ACG) and 2022 American Gastroenterological Association (AGA) society guidelines on IBS. The search was restricted to articles in the English language only and included peer-reviewed observational studies and randomized controlled trials (RCTs) in adult patients from April 22, 2020 to October 16, 2023.

KEY CONTENT AND FINDINGS: This review will start with an overview of the current guidelines for pharmacologic therapies for IBS as recommended by the ACG and the AGA, with an emphasis on clinical trials published after the most recent guidelines. It will then delve into the literature on dietary modifications, probiotics, fecal microbiota transplant, behavioral therapy, and complementary and alternative medicine approaches to IBS.

CONCLUSIONS: It is evident that the management of IBS has transcended a one-size-fits-all approach. As the field of IBS management continues to evolve, it is imperative for physicians to stay informed and receptive to the array of therapeutic options available, ultimately providing patients with the most effective and personalized care.},
}

@article {pmid38098430,
year = {2024},
author = {Neubauer, J and Kaiser, A and Hohmann, S},
title = {[Gut Microbiota and Autism Spectrum Disorders: An Overview of Correlations and Potential Implications for Therapeutic Interventions].},
journal = {Zeitschrift fur Kinder- und Jugendpsychiatrie und Psychotherapie},
volume = {52},
number = {3},
pages = {151-165},
doi = {10.1024/1422-4917/a000962},
pmid = {38098430},
issn = {1422-4917},
mesh = {*Autism Spectrum Disorder/therapy/microbiology/diagnosis/psychology ; Humans ; *Gastrointestinal Microbiome ; Child ; *Probiotics/therapeutic use ; *Brain-Gut Axis ; *Fecal Microbiota Transplantation ; *Prebiotics ; Dysbiosis ; Correlation of Data ; },
abstract = {Gut Microbiota and Autism Spectrum Disorders: An Overview of Correlations and Potential Implications for Therapeutic Interventions Abstract: At the beginning of research on microbiota, researchers focused mainly on the role of microbiota dysbiosis in the development of gastrointestinal diseases. However, over the last years, researchers have also identified correlations with other physical processes and neuropsychiatric diseases such as autism spectrum disorder. These correlations are believed to be at least partly mediated through the brain-gut-microbiome axis. An altered composition of microbiota in patients with autism spectrum disorder was detected compared to healthy controls. Today, the discussion centers around a possible systemic impact of the metabolites of some microbiota or microbiota-induced chronic inflammatory processes on the brain (mediated through the brain-gut-microbiome axis) as an underlying mechanism. Still, the specific underlying mechanisms remain largely unknown, so conclusions on therapeutic implications are difficult to determine. Here, we describe some promising approaches to improving autistic behavior through dietary changes, the use of prebiotics and probiotics, stool transplantation from healthy controls, and restricted absorbance of certain metabolites. We need further clinical studies of high quality to fully understand the pathophysiology of autism spectrum disorder and to improve diagnostic and therapeutic strategies.},
}

*Autism Spectrum Disorder/therapy/microbiology/diagnosis/psychology
Humans
*Gastrointestinal Microbiome
Child
*Probiotics/therapeutic use
*Brain-Gut Axis
*Fecal Microbiota Transplantation
*Prebiotics
Dysbiosis
Correlation of Data

@article {pmid38715916,
year = {2024},
author = {Hazan, S and Haroon, J and Jordan, S and Walker, SJ},
title = {Improvements in Gut Microbiome Composition and Clinical Symptoms Following Familial Fecal Microbiota Transplantation in a Nineteen-Year-Old Adolescent With Severe Autism.},
journal = {Journal of medical cases},
volume = {15},
number = {4-5},
pages = {82-91},
pmid = {38715916},
issn = {1923-4163},
abstract = {This case report describes a novel therapy for patients with severe autism spectrum disorder (ASD) that is worth further investigation. A 19-year-old male adolescent with ASD, who was not responding to standard treatment received fecal microbiota transplant (FMT) using donor material from his typically developing female sibling. The patient's ASD symptoms were assessed by assessors who were blind to the patient's past ASD symptomatology. Assessors used the Childhood Autism Rating Scale (CARS), an observation-based rating scale to assess developmental delay in children with autism (range of CARS scores is 15 - 60; a score > 28 is indicative of autism; higher score is positively correlated with degree of severity), at baseline and again at six timepoints post-FMT. The patient experienced marked improvements in microbiome diversity and composition over the year and a half period that followed the FMT procedure. Additionally, the patient who was previously nonverbal said his first two words and experienced a reduction in aggression 1-month post-FMT. To the authors' knowledge, this is the first report to demonstrate the use of familial FMT in an adolescent patient with ASD. Given that ASD symptom improvements post-FMT tend to occur in younger patients, the authors hypothesize that the use of a familial donor may be an important factor that contributed to the improved outcomes experienced by this older child.},
}

@article {pmid38713722,
year = {2024},
author = {Yang, M and Zheng, X and Fan, J and Cheng, W and Yan, TM and Lai, Y and Zhang, N and Lu, Y and Qi, J and Huo, Z and Xu, Z and Huang, J and Jiao, Y and Liu, B and Pang, R and Zhong, X and Huang, S and Luo, GZ and Lee, G and Jobin, C and Eren, AM and Chang, EB and Wei, H and Pan, T and Wang, X},
title = {Antibiotic-Induced Gut Microbiota Dysbiosis Modulates Host Transcriptome and m[6]A Epitranscriptome via Bile Acid Metabolism.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2307981},
doi = {10.1002/advs.202307981},
pmid = {38713722},
issn = {2198-3844},
support = {K22CA234399/NH/NIH HHS/United States ; },
abstract = {Gut microbiota can influence host gene expression and physiology through metabolites. Besides, the presence or absence of gut microbiome can reprogram host transcriptome and epitranscriptome as represented by N[6]-methyladenosine (m[6]A), the most abundant mammalian mRNA modification. However, which and how gut microbiota-derived metabolites reprogram host transcriptome and m[6]A epitranscriptome remain poorly understood. Here, investigation is conducted into how gut microbiota-derived metabolites impact host transcriptome and m[6]A epitranscriptome using multiple mouse models and multi-omics approaches. Various antibiotics-induced dysbiotic mice are established, followed by fecal microbiota transplantation (FMT) into germ-free mice, and the results show that bile acid metabolism is significantly altered along with the abundance change in bile acid-producing microbiota. Unbalanced gut microbiota and bile acids drastically change the host transcriptome and the m[6]A epitranscriptome in multiple tissues. Mechanistically, the expression of m[6]A writer proteins is regulated in animals treated with antibiotics and in cultured cells treated with bile acids, indicating a direct link between bile acid metabolism and m[6]A biology. Collectively, these results demonstrate that antibiotic-induced gut dysbiosis regulates the landscape of host transcriptome and m[6]A epitranscriptome via bile acid metabolism pathway. This work provides novel insights into the interplay between microbial metabolites and host gene expression.},
}

@article {pmid38712927,
year = {2024},
author = {Zhang, S and Swarte, JC and Gacesa, R and Knobbe, TJ and Kremer, D and Jansen, BH and de Borst, MH and , and Harmsen, HJM and Erasmus, ME and Verschuuren, EAM and Bakker, SJL and Gan, CT and Weersma, RK and Björk, JR},
title = {The gut microbiome in end-stage lung disease and lung transplantation.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0131223},
doi = {10.1128/msystems.01312-23},
pmid = {38712927},
issn = {2379-5077},
abstract = {Gut dysbiosis has been associated with impaired outcomes in liver and kidney transplant recipients, but the gut microbiome of lung transplant recipients has not been extensively explored. We assessed the gut microbiome in 64 fecal samples from end-stage lung disease patients before transplantation and 219 samples from lung transplant recipients after transplantation using metagenomic sequencing. To identify dysbiotic microbial signatures, we analyzed 243 fecal samples from age-, sex-, and BMI-matched healthy controls. By unsupervised clustering, we identified five groups of lung transplant recipients using different combinations of immunosuppressants and antibiotics and analyzed them in relation to the gut microbiome. Finally, we investigated the gut microbiome of lung transplant recipients in different chronic lung allograft dysfunction (CLAD) stages and longitudinal gut microbiome changes after transplantation. We found 108 species (58.1%) in end-stage lung disease patients and 139 species (74.7%) in lung transplant recipients that were differentially abundant compared with healthy controls, with several species exhibiting sharp longitudinal increases from before to after transplantation. Different combinations of immunosuppressants and antibiotics were associated with specific gut microbial signatures. We found that the gut microbiome of lung transplant recipients in CLAD stage 0 was more similar to healthy controls compared to those in CLAD stage 1. Finally, the gut microbial diversity of lung transplant recipients remained lower than the average gut microbial diversity of healthy controls up to more than 20 years post-transplantation. Gut dysbiosis, already present before lung transplantation was exacerbated following lung transplantation.IMPORTANCEThis study provides extensive insights into the gut microbiome of end-stage lung disease patients and lung transplant recipients, which warrants further investigation before the gut microbiome can be used for microbiome-targeted interventions that could improve the outcome of lung transplantation.},
}

@article {pmid38711648,
year = {2024},
author = {Yi, C and Chen, J and She, X},
title = {The emerging role of the gut virome in necrotizing enterocolitis.},
journal = {Heliyon},
volume = {10},
number = {9},
pages = {e30496},
pmid = {38711648},
issn = {2405-8440},
abstract = {Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in neonates, particularly preterm infants. Many factors can lead to NEC, but microbial dysbiosis is one of the most important risk factors that can induce this disease. Given the major role of the gut virome in shaping bacterial homeostasis, virome research is a fledgling but rapidly evolving area in the field of microbiome that is increasingly connected to human diseases, including NEC. This review provides an overview of the development of the gut virome in newborns, discusses its emerging role in NEC, and explores promising therapeutic applications, including phage therapy and fecal virome transplantation.},
}

@article {pmid38711536,
year = {2024},
author = {Tuniyazi, M and Tang, R and Hu, X and Fu, Y and Zhang, N},
title = {Carbonate buffer mixture and fecal microbiota transplantation hold promising therapeutic effects on oligofructose-induced diarrhea in horses.},
journal = {Frontiers in veterinary science},
volume = {11},
number = {},
pages = {1388227},
pmid = {38711536},
issn = {2297-1769},
abstract = {Diarrhea is a common gastrointestinal disorder in horses, with diet-induced diarrhea being an emerging challenge. This study aimed to investigate the gut microbiota differences in healthy and diet-induced diarrheic horses and evaluate the effectiveness of fecal microbiota transplantation (FMT) and carbonate buffer mixture (CBM) as potential therapeutic approaches. Twenty healthy horses were included in the study, with four groups: Control, Diarrhea, CBM, and FMT. Diarrhea was induced using oligofructose, and fecal samples were collected for microbiota analysis. FMT and CBM treatments were administered orally using donor fecal matter, and formula mixture, respectively. Clinical parameters, serum levels, intestinal tissue histopathology, and fecal microbiota profiles were evaluated. The results showed that diarrhea induction disbalanced the gut microbiota with decreased diversity and richness, affected clinical parameters including elevated body temperature and diarrhea score, and decreased fecal pH, increased inflammatory responses such as increased serum LPS, IL-17A, lactic acid and total protein, and caused damage in the colon tissue. CBM and FMT treatments altered the gut microbiota composition, restoring it towards a healthier profile compared to diarrheic, restored the gut microbiota composition to healthier states, improved clinical symptoms including decreased body temperature and diarrhea score, and increased fecal pH, decreased inflammatory responses such as increased serum LPS, IL-17A, lactic acid and total protein, and repaired tissue damage. CBM and FMT Spearman correlation analysis identified specific bacterial taxa associated with host parameters and inflammation. FMT and CBM treatments showed promising therapeutic effects in managing oligofructose-induced diarrhea in horses. The findings provide valuable insights into the management and treatment of diarrhea in horses and suggest the potential of combined CBM and FMT approaches for optimal therapeutic outcomes.},
}

@article {pmid38709933,
year = {2024},
author = {Chen, J and Liu, X and Zou, Y and Gong, J and Ge, Z and Lin, X and Zhang, W and Huang, H and Zhao, J and Saw, PE and Lu, Y and Hu, H and Song, E},
title = {A high-fat diet promotes cancer progression by inducing gut microbiota-mediated leucine production and PMN-MDSC differentiation.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {121},
number = {20},
pages = {e2306776121},
doi = {10.1073/pnas.2306776121},
pmid = {38709933},
issn = {1091-6490},
support = {2019BT02Y198//Program for Guangdong Introducing Innovative and Enterpreneurial Teams/ ; 82330056//Natural Science Foundation of China/ ; 81730077//National Natural Science Foundation of China/ ; 92159303//National Natural Science Foundation of China/ ; 81930081//National Natural Science Foundation of China/ ; 82025026//National Natural Science Foundation of China/ ; 2022A1515110069//GDSTC | Basic and Applied Basic Research Foundation of Guangdong Province ()/ ; 2023B1212060013//Guangdong Science and Technology Department/ ; 20212200003//Bureau of Science and Technology of Guangzhou/ ; E2018096//Guang Dong Cheung Kong philanthropy Foundation/ ; },
mesh = {*Gastrointestinal Microbiome ; Animals ; *Diet, High-Fat/adverse effects ; *Leucine/metabolism ; Female ; Humans ; Mice ; *Myeloid-Derived Suppressor Cells/metabolism ; *Breast Neoplasms/pathology/microbiology/metabolism ; *Cell Differentiation ; *Disease Progression ; Obesity/microbiology/metabolism/pathology ; Cell Line, Tumor ; },
abstract = {A high-fat diet (HFD) is a high-risk factor for the malignant progression of cancers through the disruption of the intestinal microbiota. However, the role of the HFD-related gut microbiota in cancer development remains unclear. This study found that obesity and obesity-related gut microbiota were associated with poor prognosis and advanced clinicopathological status in female patients with breast cancer. To investigate the impact of HFD-associated gut microbiota on cancer progression, we established various models, including HFD feeding, fecal microbiota transplantation, antibiotic feeding, and bacterial gavage, in tumor-bearing mice. HFD-related microbiota promotes cancer progression by generating polymorphonuclear myeloid-derived suppressor cells (PMN-MDSCs). Mechanistically, the HFD microbiota released abundant leucine, which activated the mTORC1 signaling pathway in myeloid progenitors for PMN-MDSC differentiation. Clinically, the elevated leucine level in the peripheral blood induced by the HFD microbiota was correlated with abundant tumoral PMN-MDSC infiltration and poor clinical outcomes in female patients with breast cancer. These findings revealed that the "gut-bone marrow-tumor" axis is involved in HFD-mediated cancer progression and opens a broad avenue for anticancer therapeutic strategies by targeting the aberrant metabolism of the gut microbiota.},
}

*Gastrointestinal Microbiome
Animals
*Diet, High-Fat/adverse effects
*Leucine/metabolism
Female
Humans
Mice
*Myeloid-Derived Suppressor Cells/metabolism
*Breast Neoplasms/pathology/microbiology/metabolism
*Cell Differentiation
*Disease Progression
Obesity/microbiology/metabolism/pathology
Cell Line, Tumor

@article {pmid38708959,
year = {2024},
author = {Kousgaard, SJ and Cold, F and Halkjær, SI and Petersen, AM and Kjeldsen, J and Møller Hansen, J and Dall, SM and Albertsen, M and Nielsen, HL and Kirk, KF and Duch, K and Sønderkær, M and Thorlacius-Ussing, O},
title = {The effect of non-pooled multi-donor faecal microbiota transplantation for inducing clinical remission in patients with chronic pouchitis: Results from a multicentre randomised double-blinded placebo-controlled trial (MicroPouch).},
journal = {Journal of Crohn's & colitis},
volume = {},
number = {},
pages = {},
doi = {10.1093/ecco-jcc/jjae066},
pmid = {38708959},
issn = {1876-4479},
abstract = {BACKGROUND AND AIMS: To investigate if treatment with non-pooled multi-donor faecal microbiota transplantation (FMT) for four weeks was superior to placebo to induce clinical remission in patients with chronic pouchitis.

METHODS: The study was a randomised double-blinded placebo-controlled study with a 4-week intervention period and 12-month follow-up. Eligible patients with chronic pouchitis were recruited from five Danish hospitals. Participants were randomised to non-pooled multi-donor FMT derived from four faecal donors, or placebo. Treatment was delivered daily by enema for two weeks followed by every second day for two weeks. Disease severity was accessed at inclusion and 30-day follow-up, using the Pouchitis Disease Activity Index (PDAI); PDAI <7 was considered equivalent to clinical remission. Faecal samples from participants and donors were analysed by shotgun metagenomic sequencing.

RESULTS: Inclusion was stopped after inclusion of 30 participants who were randomised 1:1 for treatment with FMT or placebo. There was no difference in participants achieving clinical remission between the two groups at 30-day follow-up, relative risk 1.0 (95%CI(0.55;1.81)). Treatment with FMT resulted in a clinically relevant increase in adverse events compared to placebo, incidence rate ratio 1.67 (95%CI(1.10;2.52)); no serious adverse events within either group. Faecal microbiota transplantation statistically significantly increased the similarity of participant faecal microbiome to the faecal donor microbiome at 30-days follow-up (p=0.01), which was not seen after placebo.

CONCLUSIONS: Non-pooled multi-donor FMT was comparable to placebo in inducing clinical remission in patients with chronic pouchitis but showed a clinically relevant increase in adverse events compared to placebo.},
}

@article {pmid38708416,
year = {2024},
author = {Zoghi, S and Sadeghpour Heravi, F and Nikniaz, Z and Shirmohamadi, M and Moaddab, SY and Ebrahimzadeh Leylabadlo, H},
title = {Gut microbiota and childhood malnutrition: Understanding the link and exploring therapeutic interventions.},
journal = {Engineering in life sciences},
volume = {24},
number = {5},
pages = {2300070},
pmid = {38708416},
issn = {1618-0240},
abstract = {Childhood malnutrition is a metabolic condition that affects the physical and mental well-being of children and leads to resultant disorders in maturity. The development of childhood malnutrition is influenced by a number of physiological and environmental factors including metabolic stress, infections, diet, genetic variables, and gut microbiota. The imbalanced gut microbiota is one of the main environmental risk factors that significantly influence host physiology and childhood malnutrition progression. In this review, we have evaluated the gut microbiota association with undernutrition and overnutrition in children, and then the quantitative and qualitative significance of gut dysbiosis in order to reveal the impact of gut microbiota modification using probiotics, prebiotics, synbiotics, postbiotics, fecal microbiota transplantation, and engineering biology methods as new therapeutic challenges in the management of disturbed energy homeostasis. Understanding the host-microbiota interaction and the remote regulation of other organs and pathways by gut microbiota can improve the effectiveness of new therapeutic approaches and mitigate the negative consequences of childhood malnutrition.},
}

@article {pmid38707810,
year = {2024},
author = {León-Janampa, N and Boennec, N and Le Tilly, O and Ereh, S and Herbet, G and Moreau, A and Gatault, P and Longuet, H and Barbet, C and Büchler, M and Baron, C and Gaudy-Graffin, C and Brand, D and Marlet, J},
title = {Relevance of Tacrolimus Trough Concentration and Hepatitis E virus Genetic Changes in Kidney Transplant Recipients With Chronic Hepatitis E.},
journal = {Kidney international reports},
volume = {9},
number = {5},
pages = {1333-1342},
pmid = {38707810},
issn = {2468-0249},
abstract = {INTRODUCTION: Hepatitis E virus (HEV) can cause chronic infection (≥3 months) and cirrhosis in immunocompromised patients, especially kidney transplant recipients. Low alanine aminotransferase (ALT) levels and high HEV intrahost diversity have previously been associated with evolution toward chronicity in these patients. We hypothesized that additional clinical and viral factors could be associated with the risk of chronic HEV infection.

METHODS: We investigated a series of 27 kidney transplant recipients with HEV infection, including 20 patients with chronic hepatitis E.

RESULTS: High tacrolimus trough concentration at diagnosis was the most relevant marker associated with chronic hepatitis E (9.2 vs. 6.4 ng/ml, P = 0.04). Most HEV genetic changes selected during HEV infection were compartmentalized between plasma and feces.

CONCLUSION: This compartmentalization highlights the diversity and complexity of HEV replication compartments. Tacrolimus trough concentration at diagnosis of HEV infection could allow an early identification of patients at high risk of chronic hepatitis E and guide treatment initiation.},
}

@article {pmid38702466,
year = {2024},
author = {Ferreira, J},
title = {Effects of microbiome transplants on fly microbiome.},
journal = {Lab animal},
volume = {53},
number = {5},
pages = {109},
doi = {10.1038/s41684-024-01369-4},
pmid = {38702466},
issn = {1548-4475},
mesh = {Animals ; *Microbiota ; Drosophila melanogaster/microbiology ; Fecal Microbiota Transplantation ; Gastrointestinal Microbiome ; },
}

Animals
*Microbiota
Drosophila melanogaster/microbiology
Fecal Microbiota Transplantation
Gastrointestinal Microbiome

@article {pmid38701935,
year = {2024},
author = {Xiao, K and Li, H and Li, Y and Zhan, B and Fang, X and Zhao, B and Zhang, X and Wu, Y and Wang, F and Jia, Y},
title = {Protective effects and mechanism of Sangyu granule on acetaminophen-induced liver injury in mice.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {118282},
doi = {10.1016/j.jep.2024.118282},
pmid = {38701935},
issn = {1872-7573},
abstract = {The Sang Yu granule (SY), a traditional Chinese medicine prescription of Xijing Hospital, was developed based on the Guanyin powder in the classical prescription "Hong's Collection of Proven Prescriptions" and the new theory of modern Chinese medicine. It has been proved to have a certain therapeutic effect on drug-induced liver injury (DILI), but the specific mechanism of action is still unclear.

AIM OF STUDY: Aim of the study was to explore the effect of SangYu granule on treating drug-induced liver injury induced by acetaminophen in mice.

MATERIALS AND METHODS: The chemical composition of SY, serum, and liver tissue was analyzed using ultrahigh-performance liquid chromatography quadrupole time-of-flight mass spectrometry. To assess hepatic function, measurements were taken using kits for total bile acids, as well as serum AST, ALT, and ALP activity. Concentrations of IL-1β and TNF-α in serum were quantified using ELISA kits. Transcriptome Sequencing Analysis and 2bRAD-M microbial diversity analysis were employed to evaluate gene expression variance in liver tissue and fecal microbiota diversity among different groups, respectively. Western blotting was performed to observe differences in the activation levels of FXR, SHP, CYP7A1 and PPARα in the liver, and the levels of FXR and FGF-15 genes and proteins in the ileum of mice. Additionally, fecal microbiota transplantation (FMT) experiments were conducted to investigate the potential therapeutic effect of administering the intestinal microbial suspension from mice treated with SY on drug-induced liver injury.

RESULTS: SY treatment exhibited significant hepatoprotective effects in mice, effectively ameliorating drug-induced liver injury while concurrently restoring intestinal microbial dysbiosis. Furthermore, SY administration demonstrated a reduction in the concentration of total bile acids, the expression of FXR and SHP proteins in the liver was up-regulated, CYP7A1 protein was down-regulated, and the expressions of FXR and FGF-15 proteins in the ileum were up-regulated. However, no notable impact on PPARα was observed. Furthermore, results from FMT experiments indicated that the administration of fecal suspensions derived from mice treated with SY did not yield any therapeutic benefits in the context of drug-induced liver injury.

CONCLUSION: The aforementioned findings strongly suggest that SY exerts a pronounced ameliorative effect on drug-induced liver injury through its ability to modulate the expression of key proteins involved in bile acid secretion, thereby preserving hepato-enteric circulation homeostasis.},
}

@article {pmid38701724,
year = {2024},
author = {Chang, X and Shen, Y and Yang, M and Yun, L and Liu, Z and Feng, S and Yang, G and Meng, X and Su, X},
title = {Antipsychotic drug-induced behavioral abnormalities in common carp: The potential involvement of the gut microbiota-brain axis.},
journal = {Journal of hazardous materials},
volume = {472},
number = {},
pages = {134444},
doi = {10.1016/j.jhazmat.2024.134444},
pmid = {38701724},
issn = {1873-3336},
abstract = {The effects of antipsychotic drugs on aquatic organisms have received widespread attention owing to their widespread use and continued release in aquatic environments. The toxicological effects of antipsychotics on aquatic organisms, particularly fish, are unexplored, and the underlying mechanisms remain unelucidated. This study aimed to use common carp to explore the effects of antipsychotics (olanzapine [OLA] and risperidone [RIS]) on behavior and the potential mechanisms driving these effects. The fish were exposed to OLA (0.1 and 10 μg/L) and RIS (0.03 and 3 μg/L) for 60 days. Behavioral tests and neurological indicators showed that exposure to antipsychotics could cause behavioral abnormalities and neurotoxicity in common carp. Further, 16 S rRNA sequencing revealed gut microbiota alteration and decreased relative abundance of some strains related to SCFA production after OLA and RIS exposure. Subsequently, a pseudo-sterile common carp model was successfully constructed, and transplantation of the gut microbiota from antipsychotic-exposed fish caused behavioral abnormalities and neurotoxicity in pseudo-sterile fish. Further, SCFA supplementation demonstrated that SCFAs ameliorated the behavioral abnormalities and neurological damage caused by antipsychotic exposure. To our knowledge, the present study is the first to investigate the effects of antipsychotics on various complex behaviors (swimming performance and social behavior) in common carp, highlighting the potential health risks associated with antipsychotic drug-induced neurotoxicity in fish. Although these results do not fully elucidate the mechanisms underlying the effects of antipsychotic drugs on fish behavior, they serve as a valuable initial investigation and form the basis for future research.},
}

@article {pmid38700306,
year = {2023},
author = {Abraham, P and Pratap, N},
title = {Dysbiosis in Irritable Bowel Syndrome.},
journal = {The Journal of the Association of Physicians of India},
volume = {71},
number = {9},
pages = {75-81},
doi = {10.59556/japi.71.0353},
pmid = {38700306},
issn = {0004-5772},
mesh = {*Irritable Bowel Syndrome/microbiology/therapy ; *Dysbiosis/therapy ; Humans ; *Gastrointestinal Microbiome/physiology ; Anti-Bacterial Agents/therapeutic use ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation/methods ; Prebiotics/administration & dosage ; },
abstract = {The human gut microbiota fosters the development of a dynamic group of microorganisms impacted by diverse variables that include genetics, diet, infection, stress, ingested drugs, such as antibiotics and small intestine bacterial overgrowth (SIBO) as well as the gut microbiota itself. These factors may influence the change in microbial composition, which results in dysbiosis (microbial imbalance) and exposes the gut to pathogenic insults. Dysbiosis is incidental to the etiology of inflammatory diseases such as irritable bowel syndrome (IBS) and metabolic diseases, including type 2 diabetes and obesity. IBS exhibits different symptoms like abdominal pain or discomfort, distention/bloating, and flatulence. To treat IBS, modification of dysregulated gut microbiota can be done using treatment strategies like a low-fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (FODMAP) diet, antibiotics that cannot be absorbed like rifaximin and neomycin, probiotics and prebiotics, and fecal microbiota transplantation (FMT). The remedial modalities in the existing literature have been demonstrated to be efficacious in the prevention and mitigation of IBS. Additionally, newer curative approaches with serum-derived bovine immunoglobulin (SBI) are an effective option. The focal point of the review paper is the pathophysiology of IBS, mainly due to dysbiosis and the various factors that advance dysbiosis. Here, we have also discussed the different treatment strategies targeting dysbiosis that effectively treat IBS. How to cite this article: Abraham P, Pratap N. Dysbiosis in Irritable Bowel Syndrome. J Assoc Physicians India 2023;71(9):75-81.},
}

*Irritable Bowel Syndrome/microbiology/therapy
*Dysbiosis/therapy
Humans
*Gastrointestinal Microbiome/physiology
Anti-Bacterial Agents/therapeutic use
Probiotics/therapeutic use
Fecal Microbiota Transplantation/methods
Prebiotics/administration & dosage

@article {pmid38699545,
year = {2024},
author = {Lamas-Paz, A and Mesquita, M and Garcia-Lacarte, M and Estévez-Vázquez, O and Benedé-Ubieto, R and Gutierrez, AH and Wu, H and Leal Lasalle, H and Vaquero, J and Bañares, R and Martínez-Naves, E and Roa, S and Nevzorova, YA and Jorquera, G and Cubero, FJ},
title = {Fecal microbiota transplantation from female donors restores gut permeability and reduces liver injury and inflammation in middle-aged male mice exposed to alcohol.},
journal = {Frontiers in nutrition},
volume = {11},
number = {},
pages = {1393014},
pmid = {38699545},
issn = {2296-861X},
abstract = {BACKGROUND: Alcohol misuse, binge drinking pattern, and gender-specific effects in the middle-aged population has been clearly underestimated. In the present study, we focused on understanding gender-specific effects of alcohol exposure on the gut-liver axis and the role of gut microbiota in modulating gender-specific responses to alcohol consumption.

METHODS: Fifty-two-week-old female and male C57BL/6 mice were fasted for 12 h, and then administered a single oral dose of ethanol (EtOH) (6 g/kg). Controls were given a single dose of PBS. Animals were sacrificed 8 h later. Alternatively, fecal microbiota transplantation (FMT) was performed in 52-week-old male mice from female donors of the same age. Permeability of the large intestine (colon), gut microbiota, liver injury, and inflammation was thoroughly evaluated in all groups.

RESULTS: Middle-aged male mice exposed to EtOH showed a significant increase in gut permeability in the large intestine, evaluated by FITC-dextran assay and ZO-1, OCCLUDIN and MUCIN-2 immuno-staining, compared to PBS-treated animals, whilst female mice of the same age also increased their gut permeability, but displayed a partially maintained intestinal barrier integrity. Moreover, there was a significant up-regulation of TLRs and markers of hepatocellular injury, cell death (AST, TUNEL-positive cells) and lipid accumulation (ORO) in male mice after EtOH exposure. Interestingly, FMT from female donors to male mice reduced gut leakiness, modified gut microbiota composition, ameliorated liver injury and inflammation, TLR activation and the senescence phenotype of middle-aged mice.

CONCLUSION: Our findings highlighted the relevance of gender in middle-aged individuals who are exposed to alcohol in the gut-liver axis. Moreover, our study revealed that gender-specific microbiota transplantation might be a plausible therapy in the management of alcohol-related disorders during aging.},
}

@article {pmid38698178,
year = {2024},
author = {Liao, C and Rolling, T and Djukovic, A and Fei, T and Mishra, V and Liu, H and Lindberg, C and Dai, L and Zhai, B and Peled, JU and van den Brink, MRM and Hohl, TM and Xavier, JB},
title = {Oral bacteria relative abundance in faeces increases due to gut microbiota depletion and is linked with patient outcomes.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {38698178},
issn = {2058-5276},
support = {U54 CA209975/CA/NCI NIH HHS/United States ; R01 AI093808/AI/NIAID NIH HHS/United States ; P30 CA008748/CA/NCI NIH HHS/United States ; R21 AI156157/AI/NIAID NIH HHS/United States ; R01 AI137269/AI/NIAID NIH HHS/United States ; K08 HL143189/HL/NHLBI NIH HHS/United States ; },
abstract = {The detection of oral bacteria in faecal samples has been associated with inflammation and intestinal diseases. The increased relative abundance of oral bacteria in faeces has two competing explanations: either oral bacteria invade the gut ecosystem and expand (the 'expansion' hypothesis), or oral bacteria transit through the gut and their relative increase marks the depletion of other gut bacteria (the 'marker' hypothesis). Here we collected oral and faecal samples from mouse models of gut dysbiosis (antibiotic treatment and DSS-induced colitis) and used 16S ribosomal RNA sequencing to determine the abundance dynamics of oral bacteria. We found that the relative, but not absolute, abundance of oral bacteria increases, reflecting the 'marker' hypothesis. Faecal microbiome datasets from diverse patient cohorts, including healthy individuals and patients with allogeneic haematopoietic cell transplantation or inflammatory bowel disease, consistently support the 'marker' hypothesis and explain associations between oral bacterial abundance and patient outcomes consistent with depleted gut microbiota. By distinguishing between the two hypotheses, our study guides the interpretation of microbiome compositional data and could potentially identify cases where therapies are needed to rebuild the resident microbiome rather than protect against invading oral bacteria.},
}

@article {pmid38697851,
year = {2024},
author = {Wu, T and Li, L and Zhou, W and Bi, G and Jiang, X and Guo, M and Yang, X and Fang, J and Pang, J and Fan, S and Bi, H},
title = {Gut microbiota affects mPXR agonist PCN-induced hepatomegaly by regulating PXR and YAP activation.},
journal = {Drug metabolism and disposition: the biological fate of chemicals},
volume = {},
number = {},
pages = {},
doi = {10.1124/dmd.123.001604},
pmid = {38697851},
issn = {1521-009X},
abstract = {Pregnane X receptor (PXR) is essential in the regulation of liver homeostasis and the gut microbiota is closely linked to liver physiological and pathological status. We previously found that activation of PXR significantly promotes liver enlargement through interaction with yes-associated protein (YAP). However, whether gut microbiota is contributed to PXR-induced hepatomegaly and the involved mechanisms remain unclear. In this study, C57BL/6 mice were administered the mouse-specific agonist PCN for 5 days. Depletion of gut microbiota was achieved using broad-spectrum antibiotics (ABX) and fecal microbiota transplantation (FMT) was performed to restore the gut microbial. The composition of gut microbiota was analyzed by 16S rRNA sequencing, while the expression of PXR, YAP and their downstream target genes and proteins were assessed. The results indicated that PCN treatment altered the composition and abundance of specific bacterial taxa. Furthermore, depletion of gut microbiota using ABX significantly attenuated PCN-induced hepatomegaly. FMT experiment further demonstrated that the fecal microbiota from PCN-treated mice could induce liver enlargement. Mechanistic studies revealed that ABX treatment impeded the PXR and YAP activation induced by PCN, as evidenced by decreased expression of PXR, YAP, and their downstream targets. Moreover, alterations in PXR and YAP activation were likely contributing to hepatomegaly in recipient mice following FMT from PCN-treated mice. Collectively, the current study demonstrated that gut microbiota is involved in PCN-induced hepatomegaly via regulating PXR and YAP activation, providing potential novel insights into the involvement of gut microbiota in PXR-mediated hepatomegaly. Significance Statement This work describes that the composition of gut microbiota is altered in mPXR agonist PCN-induced hepatomegaly. The treatment with an antibiotic cocktail (ABX) depletes the intestinal microbiota, leading to the impairment of liver enlargement caused by PCN. Besides, fecal microbiota transplantation (FMT) from PCN-treated mice induces liver enlargement. Further study revealed that gut microbiota is involved in hepatomegaly via regulating PXR and YAP activation.},
}

@article {pmid38697391,
year = {2024},
author = {Soueges, S and Cheynet, V and Briot, T and Merveilleux du Vignaux, C and Benech, N and Ader, F},
title = {Clinical remission after faecal microbiota transplantation in transplanted recipients with refractory chronic Norovirus infections: a retrospective case series.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2024.04.015},
pmid = {38697391},
issn = {1469-0691},
}

@article {pmid38697207,
year = {2024},
author = {Tapasco-Tapasco, O and González, CA and Letourneur, A},
title = {Phase angle and impedance ratio as meta-inflammation biomarkers after a colon cleansing protocol in a group of overweight young women.},
journal = {Physiological measurement},
volume = {},
number = {},
pages = {},
doi = {10.1088/1361-6579/ad46df},
pmid = {38697207},
issn = {1361-6579},
abstract = {Blood C-reactive protein (CRP) and the electrical bioimpedance (EBI) variables phase angle (PhA) and impedance ratio (IR) have been proposed as biomarkers of metainflammation in overweight/obesity. CRP involves taking blood samples, while PhA and IR imply a less-than-2-minute-non-invasive procedure. In this study, values for these variables and percent body fat mass (PBFM) were obtained and compared immediately before and immediately after a colon cleansing protocol (CCP), aimed at modulating intestinal microbiota, as well as along a period of 8 weeks after it. Methods: 20 female volunteers (20.9-24.9 years old) participated: 12 in an overweight group (OG), and 8 in a lean group (LG). The OG was divided in two subgroups (n=6, each): control (SCG) and experimental (SEG). The ESG underwent a 6-day colon cleansing protocol (CCP) at week 2, while 5 volunteers in the CSG underwent it at week 9. Results: Pre/post-CCP mean values for the variables in the OG were: PBF (34.3/31.3%), CRP (3.7/0.6 mg/dL), PhA (6.9/7.5°) and IR*10 (0.78/0.77). Calculated R2 correlation factors among these variables are all above 0.89). The favorable changes first seen in the SEG were still present 8 weeks after the CCP. Conclusion: a) the CCP drastically lowers meta-inflammation, b) EBIS can be used to measure metainflammation, before and after treatment, c) for microbiota modulation, CCP could be a good alternative to more drastic procedures like fecal microbiota transplantation; d) reestablishing eubiosis by CCP could be an effective coadjutant in the treatment of overweight young adult overweight women. .},
}

@article {pmid38355755,
year = {2024},
author = {Zhang, J and Hasty, J and Zarrinpar, A},
title = {Live bacterial therapeutics for detection and treatment of colorectal cancer.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {21},
number = {5},
pages = {295-296},
pmid = {38355755},
issn = {1759-5053},
support = {R01 EB030134/EB/NIBIB NIH HHS/United States ; UL1 TR001442/TR/NCATS NIH HHS/United States ; P30 DK120515/DK/NIDDK NIH HHS/United States ; P30 DK063491/DK/NIDDK NIH HHS/United States ; R01 AI163483/AI/NIAID NIH HHS/United States ; U01 CA265719/CA/NCI NIH HHS/United States ; P30 CA014195/CA/NCI NIH HHS/United States ; },
mesh = {*Colorectal Neoplasms/diagnosis/therapy ; Humans ; Probiotics/therapeutic use ; Gastrointestinal Microbiome ; },
abstract = {Live microorganisms can be manipulated and engineered for colorectal cancer detection and treatment through methods such as faecal microbiota transplantation, native bacteria engineering and synthetic circuit engineering. Although promising, substantial effort is required to translate these approaches for clinical use.},
}

*Colorectal Neoplasms/diagnosis/therapy
Humans
Probiotics/therapeutic use
Gastrointestinal Microbiome

@article {pmid38696921,
year = {2024},
author = {Mao, Q and Zhang, H and Zhang, Z and Lu, Y and Pan, J and Guo, D and Huang, L and Tian, H and Ma, K},
title = {Co-decoction of Lilii bulbus and Radix Rehmannia Recens and its key bioactive ingredient verbascoside inhibit neuroinflammation and intestinal permeability associated with chronic stress-induced depression via the gut microbiota-brain axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {129},
number = {},
pages = {155510},
doi = {10.1016/j.phymed.2024.155510},
pmid = {38696921},
issn = {1618-095X},
abstract = {BACKGROUND: Gut microbiota plays a critical role in the pathogenesis of depression and are a therapeutic target via maintaining the homeostasis of the host through the gut microbiota-brain axis (GMBA). A co-decoction of Lilii bulbus and Radix Rehmannia Recens (LBRD), in which verbascoside is the key active ingredient, improves brain and gastrointestinal function in patients with depression. However, in depression treatment using verbascoside or LBRD, mechanisms underlying the bidirectional communication between the intestine and brain via the GMBA are still unclear.

PURPOSE: This study aimed to examine the role of verbascoside in alleviating depression via gut-brain bidirectional communication and to study the possible pathways involved in the GMBA.

METHODS: Key molecules and compounds involved in antidepressant action were identified using HPLC and transcriptomic analyses. The antidepressant effects of LBRD and verbascoside were observed in chronic stress induced depression model by behavioural test, neuronal morphology, and synaptic dendrite ultrastructure, and their neuroprotective function was measured in corticosterone (CORT)-stimulated nerve cell injury model. The causal link between the gut microbiota and the LBRD and verbascoside antidepressant efficacy was evaluate via gut microbiota composition analysis and faecal microbiota transplantation (FMT).

RESULTS: LBRD and Verbascoside administration ameliorated depression-like behaviours and synaptic damage by reversing gut microbiota disturbance and inhibiting inflammatory responses as the result of impaired intestinal permeability or blood-brain barrier leakiness. Furthermore, verbascoside exerted neuroprotective effects against CORT-induced cytotoxicity in an in vitro depression model. FMT therapy indicated that verbascoside treatment attenuated gut inflammation and central nervous system inflammatory responses, as well as eliminated neurotransmitter and brain-gut peptide deficiencies in the prefrontal cortex by modulating the composition of gut microbiota. Lactobacillus, Parabacteroides, Bifidobacterium, and Ruminococcus might play key roles in the antidepressant effects of LBRD via the GMBA.

CONCLUSION: The current study elucidates the multi-component, multi-target, and multi-pathway therapeutic effects of LBRD on depression by remodeling GMBA homeostasis and further verifies the causality between gut microbiota and the antidepressant effects of verbascoside and LBRD.},
}

@article {pmid38694925,
year = {2024},
author = {Elford, JD and Becht, N and Garssen, J and Kraneveld, AD and Perez-Pardo, P},
title = {Buty and the beast: the complex role of butyrate in Parkinson's disease.},
journal = {Frontiers in pharmacology},
volume = {15},
number = {},
pages = {1388401},
pmid = {38694925},
issn = {1663-9812},
abstract = {Parkinson's disease (PD) is a complex neurodegenerative disease which is often associated with gastrointestinal (GI) dysfunction. The GI tract is home to a wide range of microorganisms, among which bacteria, that can influence the host through various mechanisms. Products produced by these bacteria can act in the gut but can also exert effects in the brain via what is now well established to be the microbiota-gut-brain axis. In those with PD the gut-bacteria composition is often found to be different to that of non-PD individuals. In addition to compositional changes, the metabolic activity of the gut-microbiota is also changed in PD. Specifically, it is often reported that key producers of short chain fatty acids (SCFAs) as well as the concentration of SCFAs themselves are altered in the stool and blood of those with PD. These SCFAs, among which butyrate, are essential nutrients for the host and are a major energy source for epithelial cells of the GI tract. Additionally, butyrate plays a key role in regulating various host responses particularly in relation to inflammation. Studies have demonstrated that a reduction in butyrate levels can have a critical role in the onset and progression of PD. Furthermore, it has been shown that restoring butyrate levels in those with PD through methods such as probiotics, prebiotics, sodium butyrate supplementation, and fecal transplantation can have a beneficial effect on both motor and non-motor outcomes of the disease. This review presents an overview of evidence for the altered gut-bacteria composition and corresponding metabolite production in those with PD, with a particular focus on the SCFA butyrate. In addition to presenting current studies regarding SCFA in clinical and preclinical reports, evidence for the possibility to target butyrate production using microbiome based approaches in a therapeutic context is discussed.},
}

@article {pmid38694298,
year = {2024},
author = {Shariff, S and Kwan Su Huey, A and Parag Soni, N and Yahia, A and Hammoud, D and Nazir, A and Uwishema, O and Wojtara, M},
title = {Unlocking the gut-heart axis: exploring the role of gut microbiota in cardiovascular health and disease.},
journal = {Annals of medicine and surgery (2012)},
volume = {86},
number = {5},
pages = {2752-2758},
pmid = {38694298},
issn = {2049-0801},
abstract = {INTRODUCTION: Gut microbiota has emerged as a pivotal player in cardiovascular health and disease, extending its influence beyond the gut through intricate metabolic processes and interactions with the immune system. Accumulating evidence supports a significant association between gut microbiota and cardiovascular diseases such as atherosclerosis, hypertension, and heart failure. Dietary patterns have been identified as key factors shaping the composition of the gut microbiota and exerting notable impacts on cardiovascular health. Probiotics and prebiotics have shown promise in mitigating the risks of cardiovascular disease by modulating key cardiovascular parameters. Faecal microbiota transplantation (FMT) has recently emerged as a novel and intriguing therapeutic strategy.

AIM: This review paper aims to explore and elucidate the multifaceted role of gut microbiota in cardiovascular health. It will also address the prevailing challenges and limitations in gut microbiota studies, emphasizing the importance of future research in overcoming these obstacles to expand our understanding of the gut-heart axis.

MATERIALS AND METHODS: A comprehensive literature search was conducted using various databases including ClinicalTrials, Google Scholar, PubMed, ScienceDirect, MEDLINE, and Ovid Resources. The search strategy included utilizing keywords such as "Gut microbiota," "Randomized controlled trials (RCTs)," "Gut-heart axis," "Dysbiosis," "Diet," "Probiotics," "Prebiotics," "Faecal Microbiota transplantation," "cardiovascular disease," "Meta-analyses," and other compatible terms thereof. Only articles written in English were considered, and selection criteria included relevance to the research objectives, reasonable sample sizes, and robust methodology. In addition to the identified articles, meta-analyses, animal models and studies, and references from the selected articles were also examined to ensure a comprehensive review of the literature.

RESULTS: Dietary patterns exert a significant influence on the composition of the gut microbiota, and certain diets, such as the Mediterranean diet, have been associated with a favourable gut microbiota profile and a reduced risk of cardiovascular disease (CVD). Probiotics and prebiotics have emerged as potential interventions to mitigate CVD risks by modulating blood pressure, glycemic control, lipid profiles, and gut dysbiosis. Another innovative therapeutic approach is FMT, which involves transferring faecal material from a healthy donor to restore a balanced gut microbiota. FMT holds promise for improving cardiometabolic parameters in individuals with CVD, although further research is needed to elucidate its precise mechanisms and assess its effectiveness.

CONCLUSION: The gut microbiota is emerging as a potential therapeutic target for CVD prevention and management. However, current research has limitations, including the need for larger and more diverse studies, the challenges of establishing causality, and concerns regarding the long-term consequences and safety of gut microbiota modulation. Despite these limitations, understanding the gut-heart axis holds promise for the development of personalized therapies and interventions for cardiovascular health. Further research is needed to expand our knowledge and address the ethical and safety issues associated with gut microbiota modification.},
}

@article {pmid38691831,
year = {2024},
author = {Chen, H and Yu, Z and Qi, Z and Huang, X and Gao, J},
title = {Tongfu Lifei Decoction Attenuated Sepsis-Related Intestinal Mucosal Injury Through Regulating Th17/Treg Balance and Modulating Gut Microbiota.},
journal = {Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research},
volume = {44},
number = {5},
pages = {208-220},
doi = {10.1089/jir.2024.0001},
pmid = {38691831},
issn = {1557-7465},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Sepsis/immunology/drug therapy/complications ; *Th17 Cells/immunology/drug effects ; Rats ; *Drugs, Chinese Herbal/pharmacology ; *T-Lymphocytes, Regulatory/immunology/drug effects ; *Intestinal Mucosa/drug effects/immunology/pathology/microbiology ; Male ; Rats, Sprague-Dawley ; },
abstract = {Intestinal damage and secondary bacterial translocation are caused by the inflammatory response induced by sepsis. Tongfu Lifei (TLF) decoction has a protective effect on sepsis-related gastrointestinal function injury. However, the relation between gut microbiota, immune barrier, and sepsis under the treatment of TLF have not been well clarified yet. Here, rats were subjected to cecal ligation and puncture (CLP) to create a sepsis model. Subsequently, the TLF decoction was given to CLP rats by gavage, fecal microbiota transplantation (FMT), and antibiotic were used as positive control. TLF suppressed the inflammatory response and improved the pathological changes in the intestines of CLP rats. Besides, TLF promoted the balance of the percentage of the Th17 and Treg cells. Intestinal barrier function was also improved by TLF through enhancing ZO-1, and Occludin and Claudin 1 expression, preventing the secondary translocation of other gut microbiota. TLF dramatically boosted the gut microbiota's alpha- and beta-diversity in CLP rats. Moreover, it increased the relative abundance of anti-inflammatory gut microbiota and changed the progress of the glucose metabolism. In short, TLF regulated the gut microbiota to balance the ratio of Th17/Treg cells, reducing the inflammation in serum and intestinal mucosal injury in rats.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Sepsis/immunology/drug therapy/complications
*Th17 Cells/immunology/drug effects
Rats
*Drugs, Chinese Herbal/pharmacology
*T-Lymphocytes, Regulatory/immunology/drug effects
*Intestinal Mucosa/drug effects/immunology/pathology/microbiology
Male
Rats, Sprague-Dawley

@article {pmid38690290,
year = {2024},
author = {Paudel, D and Nair, DVT and Joseph, G and Castro, R and Tiwari, AK and Singh, V},
title = {Gastrointestinal microbiota-directed nutritional and therapeutic interventions for inflammatory bowel disease: opportunities and challenges.},
journal = {Gastroenterology report},
volume = {12},
number = {},
pages = {goae033},
pmid = {38690290},
issn = {2052-0034},
abstract = {Evidence-based research has confirmed the role of gastrointestinal microbiota in regulating intestinal inflammation. These data have generated interest in developing microbiota-based therapies for the prevention and management of inflammatory bowel disease (IBD). Despite in-depth understanding of the etiology of IBD, it currently lacks a cure and requires ongoing management. Accumulating data suggest that an aberrant gastrointestinal microbiome, often referred to as dysbiosis, is a significant environmental instigator of IBD. Novel microbiome-targeted interventions including prebiotics, probiotics, fecal microbiota transplant, and small molecule microbiome modulators are being evaluated as therapeutic interventions to attenuate intestinal inflammation by restoring a healthy microbiota composition and function. In this review, the effectiveness and challenges of microbiome-centered interventions that have the potential to alleviate intestinal inflammation and improve clinical outcomes of IBD are explored.},
}

@article {pmid38690018,
year = {2024},
author = {Dai, C and Huang, YH and Jiang, M},
title = {Fecal microbiota transplantation for irritable bowel syndrome: Current evidence and perspectives.},
journal = {World journal of gastroenterology},
volume = {30},
number = {16},
pages = {2179-2183},
pmid = {38690018},
issn = {2219-2840},
mesh = {*Irritable Bowel Syndrome/therapy/microbiology ; *Fecal Microbiota Transplantation/methods ; Humans ; Treatment Outcome ; *Gastrointestinal Microbiome ; Feces/microbiology ; Randomized Controlled Trials as Topic ; Clostridioides difficile/pathogenicity ; Clostridium Infections/therapy/microbiology ; },
abstract = {In this editorial we comment on the article published in the recent issue of the World journal of Gastroenterology. We focus specifically on the mechanisms un-derlying the effects of fecal microbiota transplantation (FMT) for irritable bowel syndrome (IBS), the factors which affect the outcomes of FMT in IBS patients, and challenges. FMT has emerged as a efficacious intervention for clostridium difficile infection and holds promise as a therapeutic modality for IBS. The utilization of FMT in the treatment of IBS has undergone scrutiny in numerous randomized controlled trials, yielding divergent outcomes. The current frontier in this field seeks to elucidate these variations, underscore the existing knowledge gaps that necessitate exploration, and provide a guideline for successful FMT imple-mentation in IBS patients. At the same time, the application of FMT as a treatment for IBS confronts several challenges.},
}

*Irritable Bowel Syndrome/therapy/microbiology
*Fecal Microbiota Transplantation/methods
Humans
Treatment Outcome
*Gastrointestinal Microbiome
Feces/microbiology
Randomized Controlled Trials as Topic
Clostridioides difficile/pathogenicity
Clostridium Infections/therapy/microbiology

@article {pmid38689371,
year = {2024},
author = {Gooch, HCC and Labedan, M and Hall, LJ and Maxwell, A},
title = {Transplanting human infant gut microbiome species into Galleria mellonella.},
journal = {BMC research notes},
volume = {17},
number = {1},
pages = {123},
pmid = {38689371},
issn = {1756-0500},
support = {NC/R001782/1/NC3RS_/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom ; BB/P012523/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/P012523/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; BB/P012523/1/BB_/Biotechnology and Biological Sciences Research Council/United Kingdom ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Humans ; *Moths/microbiology ; *Larva/microbiology ; Infant ; *Feces/microbiology ; Bifidobacterium/isolation & purification ; Enterococcus/isolation & purification ; },
abstract = {OBJECTIVE: Study of the human infant gut microbiome requires the use of surrogate mammalian species such as mice. We sought to investigate the usefulness of the greater wax moth larva, Galleria mellonella, as an alternative.

RESULTS: We have analysed the native gut microbiome of Galleria and developed methods for clearing the native microbiome and introducing species from human infant faecal samples. We find that some species, e.g. enterococci, are more successful at recolonisation, but that others, e.g. Bifidobacterium, are less so. The work paves the way for using Galleria rather than mice in this and similar work.},
}

Animals
*Gastrointestinal Microbiome/physiology
Humans
*Moths/microbiology
*Larva/microbiology
Infant
*Feces/microbiology
Bifidobacterium/isolation & purification
Enterococcus/isolation & purification

@article {pmid38687096,
year = {2024},
author = {Song, XL and Liang, J and Lin, SZ and Xie, YW and Ke, CH and Ao, D and Lu, J and Chen, XM and He, YZ and Liu, XH and Li, W},
title = {Gut-lung axis and asthma: A historical review on mechanism and future perspective.},
journal = {Clinical and translational allergy},
volume = {14},
number = {5},
pages = {e12356},
pmid = {38687096},
issn = {2045-7022},
support = {32100602//National Natural Science Foundation of China/ ; 2023A1515012755//Guangdong Natural Science Foundation of China/ ; GCC2021009//Scientific Research Start-up Fund for High-level Talents of Affiliated Hospital of Guangdong Medical University/ ; },
abstract = {BACKGROUND: Gut microbiota are closely related to the development and regulation of the host immune system by regulating the maturation of immune cells and the resistance to pathogens, which affects the host immunity. Early use of antibiotics disrupts the homeostasis of gut microbiota and increases the risk of asthma. Gut microbiota actively interact with the host immune system via the gut-lung axis, a bidirectional communication pathway between the gut and lung. The manipulation of gut microbiota through probiotics, helminth therapy, and fecal microbiota transplantation (FMT) to combat asthma has become a hot research topic. BODY: This review mainly describes the current immune pathogenesis of asthma, gut microbiota and the role of the gut-lung axis in asthma. Moreover, the potential of manipulating the gut microbiota and its metabolites as a treatment strategy for asthma has been discussed.

CONCLUSION: The gut-lung axis has a bidirectional effect on asthma. Gut microecology imbalance contributes to asthma through bacterial structural components and metabolites. Asthma, in turn, can also cause intestinal damage through inflammation throughout the body. The manipulation of gut microbiota through probiotics, helminth therapy, and FMT can inform the treatment strategies for asthma by regulating the maturation of immune cells and the resistance to pathogens.},
}

@article {pmid38686220,
year = {2024},
author = {Bruggeman, A and Vandendriessche, C and Hamerlinck, H and De Looze, D and Tate, DJ and Vuylsteke, M and De Commer, L and Devolder, L and Raes, J and Verhasselt, B and Laukens, D and Vandenbroucke, RE and Santens, P},
title = {Safety and efficacy of faecal microbiota transplantation in patients with mild to moderate Parkinson's disease (GUT-PARFECT): a double-blind, placebo-controlled, randomised, phase 2 trial.},
journal = {EClinicalMedicine},
volume = {71},
number = {},
pages = {102563},
pmid = {38686220},
issn = {2589-5370},
abstract = {BACKGROUND: Dysregulation of the gut microbiome has been implicated in Parkinson's disease (PD). This study aimed to evaluate the clinical effects and safety of a single faecal microbiota transplantation (FMT) in patients with early-stage PD.

METHODS: The GUT-PARFECT trial, a single-centre randomised, double-blind, placebo-controlled trial was conducted at Ghent University Hospital between December 01, 2020 and December 12, 2022. Participants (aged 50-65 years, Hoehn and Yahr stage 2) were randomly assigned to receive nasojejunal FMT with either healthy donor stool or their own stool. Computer-generated randomisation was done in a 1:1 ratio through permutated-block scheduling. Treatment allocation was concealed for participants and investigators. The primary outcome measure at 12 months was the change in the Movement Disorders Society-Unified Parkinson's Disease Rating Scale (MDS-UPDRS) motor score obtained during off-medication evaluations. Intention-to-treat analysis was performed using a mixed model for repeated measures analysis. This completed trial is registered on ClinicalTrials.gov (NCT03808389).

FINDINGS: Between December 2020 and December 2021, FMT procedures were conducted on 46 patients with PD: 22 in the healthy donor group and 24 in the placebo group. Clinical evaluations were performed at baseline, 3, 6, and 12 months post-FMT. Full data analysis was possible for 21 participants in the healthy donor group and 22 in the placebo group. After 12 months, the MDS-UPDRS motor score significantly improved by a mean of 5.8 points (95% CI -11.4 to -0.2) in the healthy donor group and by 2.7 points (-8.3 to 2.9) in the placebo group (p = 0.0235). Adverse events were limited to temporary abdominal discomfort.

INTERPRETATION: Our findings suggested a single FMT induced mild, but long-lasting beneficial effects on motor symptoms in patients with early-stage PD. These findings highlight the potential of modulating the gut microbiome as a therapeutic approach and warrant a further exploration of FMT in larger cohorts of patients with PD in various disease stages.

FUNDING: Flemish PD patient organizations (VPL and Parkili), Research Foundation Flanders (FWO), Biocodex Microbiota Foundation.},
}

@article {pmid38685762,
year = {2024},
author = {Ishnaiwer, M and Le Bastard, Q and Naour, M and Zeman, M and Dailly, E and Montassier, E and Batard, E and Dion, M},
title = {Efficacy of an inulin-based treatment on intestinal colonization by multidrug-resistant E. coli: insight into the mechanism of action.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2347021},
pmid = {38685762},
issn = {1949-0984},
mesh = {Animals ; *Inulin/pharmacology/metabolism ; Mice ; *Gastrointestinal Microbiome/drug effects ; *Escherichia coli/drug effects/genetics ; *Feces/microbiology ; *Amoxicillin/pharmacology ; *Pantoprazole/pharmacology ; *Drug Resistance, Multiple, Bacterial ; beta-Lactamases/metabolism/genetics ; Dysbiosis/microbiology/drug therapy ; Anti-Bacterial Agents/pharmacology ; Escherichia coli Infections/drug therapy/microbiology ; Female ; Prebiotics/administration & dosage ; },
abstract = {Inulin, an increasingly studied dietary fiber, alters intestinal microbiota. The aim of this study was to assess whether inulin decreases intestinal colonization by multidrug resistant E. coli and to investigate its potential mechanisms of action. Mice with amoxicillin-induced intestinal dysbiosis mice were inoculated with extended spectrum beta-lactamase producing E. coli (ESBL-E. coli). The combination of inulin and pantoprazole (IP) significantly reduced ESBL-E. coli fecal titers, whereas pantoprazole alone did not and inulin had a delayed and limited effect. Fecal microbiome was assessed using shotgun metagenomic sequencing and qPCR. The efficacy of IP was predicted by increased abundance of 74 taxa, including two species of Adlercreutzia. Preventive treatments with A. caecimuris or A. muris also reduced ESBL-E. coli fecal titers. Fecal microbiota of mice effectively treated by IP was enriched in genes involved in inulin catabolism, production of propionate and expression of beta-lactamases. They also had increased beta-lactamase activity and decreased amoxicillin concentration. These results suggest that IP act through production of propionate and degradation of amoxicillin by the microbiota. The combination of pantoprazole and inulin is a potential treatment of intestinal colonization by multidrug-resistant E. coli. The ability of prebiotics to promote propionate and/or beta-lactamase producing bacteria may be used as a screening tool to identify potential treatments of intestinal colonization by multidrug resistant Enterobacterales.},
}

Animals
*Inulin/pharmacology/metabolism
Mice
*Gastrointestinal Microbiome/drug effects
*Escherichia coli/drug effects/genetics
*Feces/microbiology
*Amoxicillin/pharmacology
*Pantoprazole/pharmacology
*Drug Resistance, Multiple, Bacterial
beta-Lactamases/metabolism/genetics
Dysbiosis/microbiology/drug therapy
Anti-Bacterial Agents/pharmacology
Escherichia coli Infections/drug therapy/microbiology
Female
Prebiotics/administration & dosage

@article {pmid38685731,
year = {2024},
author = {Zhang, Z and Mocanu, V and Deehan, EC and Hotte, N and Zhu, Y and Wei, S and Kao, DH and Karmali, S and Birch, DW and Walter, J and Madsen, KL},
title = {Recipient microbiome-related features predicting metabolic improvement following fecal microbiota transplantation in adults with severe obesity and metabolic syndrome: a secondary analysis of a phase 2 clinical trial.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2345134},
pmid = {38685731},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Metabolic Syndrome/therapy/microbiology ; Male ; Female ; *Gastrointestinal Microbiome ; Adult ; Middle Aged ; *Feces/microbiology ; *Bile Acids and Salts/metabolism/blood ; *Bacteria/classification/isolation & purification/genetics/metabolism ; Obesity/therapy/microbiology ; Dietary Fiber/administration & dosage/metabolism ; Insulin Resistance ; Treatment Outcome ; },
abstract = {Microbial-based therapeutics in clinical practice are of considerable interest, and a recent study demonstrated fecal microbial transplantation (FMT) followed by dietary fiber supplements improved glucose homeostasis. Previous evidence suggests that donor and recipient compatibility and FMT protocol are key determinants, but little is known about the involvement of specific recipient factors. Using data from our recent randomized placebo-control phase 2 clinical trial in adults with obesity and metabolic syndrome, we grouped participants that received FMT from one of 4 donors with either fiber supplement into HOMA-IR responders (n = 21) and HOMA-IR non-responders (n = 8). We further assessed plasma bile acids using targeted metabolomics and performed subgroup analyzes to evaluate the effects of recipient parameters and gastrointestinal factors on microbiota engraftment and homeostatic model assessment of insulin resistance (HOMA2-IR) response. The baseline fecal microbiota composition at genus level of recipients could predict the improvements in HOMA2-IR at week 6 (ROC-AUC = 0.70). Prevotella was identified as an important predictor, with responders having significantly lower relative abundance than non-responders (p = .02). In addition, recipients displayed a highly individualized degree of microbial engraftment from donors. Compared to the non-responders, the responders had significantly increased bacterial richness (Chao1) after FMT and a more consistent engraftment of donor-specific bacteria ASVs (amplicon sequence variants) such as Faecalibacillus intestinalis (ASV44), Roseburia spp. (ASV103), and Christensenellaceae spp. (ASV140) (p < .05). Microbiota engraftment was strongly associated with recipients' factors at baseline including initial gut microbial diversity, fiber and nutrient intakes, inflammatory markers, and bile acid derivative levels. This study identified that responders to FMT therapy had a higher engraftment rate in the transplantation of specific donor-specific microbes, which were strongly correlated with insulin sensitivity improvements. Further, the recipient baseline gut microbiota and related factors were identified as the determinants for responsiveness to FMT and fiber supplementation. The findings provide a basis for the development of precision microbial therapeutics for the treatment of metabolic syndrome.},
}

Humans
*Fecal Microbiota Transplantation
*Metabolic Syndrome/therapy/microbiology
Male
Female
*Gastrointestinal Microbiome
Adult
Middle Aged
*Feces/microbiology
*Bile Acids and Salts/metabolism/blood
*Bacteria/classification/isolation & purification/genetics/metabolism
Obesity/therapy/microbiology
Dietary Fiber/administration & dosage/metabolism
Insulin Resistance
Treatment Outcome

@article {pmid38684800,
year = {2024},
author = {Liu, MT and Zhang, Y and Xiang, CG and Yang, T and Wang, XH and Lu, QK and Lu, HM and Fan, C and Feng, CL and Yang, XQ and Zou, DW and Li, H and Tang, W},
title = {Methionine-choline deficient diet deteriorates DSS-induced murine colitis through disturbance of gut microbes and infiltration of macrophages.},
journal = {Acta pharmacologica Sinica},
volume = {},
number = {},
pages = {},
pmid = {38684800},
issn = {1745-7254},
abstract = {Ulcerative colitis (UC) is associated with changed dietary habits and mainly linked with the gut microbiota dysbiosis, necroptosis of epithelial cells, and mucosal ulcerations. Liver dysfunction and abnormal level of liver metabolism indices were identified in UC patients, suggesting a close interaction between gut and liver disorders. Methionine-choline deficient diet (MCD) has been shown to induce persistent alterations of gut microbiota and metabolome during hepatitis. In this study we further explored the disease phenotypes in UC patients and investigated whether MCD functioned as a trigger for UC susceptibility. After assessing 88 serum specimens from UC patients, we found significant liver dysfunction and dyslipidemia including abnormal ALT, AST, TG, TC, LDL-c and HDL-c. Liver dysfunction and dyslipidemia were confirmed in DSS-induced colitis mice. We fed mice with MCD for 14 days to cause mild liver damage, and then treated with DSS for 7 days. We found that MCD intake significantly exacerbated the pathogenesis of mucosal inflammation in DSS-induced acute, progressive, and chronic colitis, referring to promotion of mucosal ulcers, colon shortening, diarrhea, inflammatory immune cell infiltration, cytokines release, and abnormal activation of inflammatory macrophages in colon and liver specimens. Intraperitoneal injection of clodronate liposomes to globally delete macrophages dramatically compromised the pathogenesis of MCD-triggering colitis. In addition, MCD intake markedly changed the production pattern of short-chain fatty acids (SCFAs) in murine stools, colons, and livers. We demonstrated that MCD-induced colitis pathogenesis largely depended on the gut microbes and the disease phenotypes could be transmissible through fecal microbiota transplantation (FMT). In conclusion, this study supports the concept that intake of MCD predisposes to experimental colitis and enhances its pathogenesis via modulating gut microbes and macrophages in mice.},
}

@article {pmid38682201,
year = {2024},
author = {Ayabe, RI and White, MG},
title = {Metastasis and the Microbiome: The Impact of Bacteria in Disseminated Colorectal Cancer.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {29},
number = {4},
pages = {152},
doi = {10.31083/j.fbl2904152},
pmid = {38682201},
issn = {2768-6698},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/pathology/therapy ; *Gastrointestinal Microbiome/physiology ; *Neoplasm Metastasis ; Dysbiosis/microbiology ; Bacteria/classification/genetics ; Fecal Microbiota Transplantation ; },
abstract = {Metastasis remains a leading cause of mortality for patients with solid tumors. An expanding body of literature suggests interplay between the host, gut, and tumoral microbiomes may play a role in cancer initiation and distant dissemination. These associations have been particularly well-studied in colorectal cancer, where gut dysbiosis and an endotoxin-induced inflammatory milieu foster premalignant polyp formation, setting the stage for carcinogenesis. Subsequent violation of the gut vascular barrier enables dissemination of bacterial agents to sites such as the liver, where they contribute to establishment of pre-metastatic niches, which promote tumor cell extravasation and metastatic outgrowth. Intriguingly, breakdown of this vascular barrier has been shown to be aided by the presence of tumoral bacteria. The presence of similar species, including Fusobacterium nucleatum and Escherichia Coli, in both primary and metastatic colorectal tumors, supports this hypothesis and their presence is associated with chemotherapy resistance and an overall poor prognosis. Specific gut microbial populations are also associated with differential response to immunotherapy, which has a growing role in microsatellite unstable colorectal cancers. Recent work suggests that modulation of gut microbiome using dietary modification, targeted antibiotics, or fecal microbiota transplantation may improve response to immunotherapy and oncologic outcomes. Elucidation of the precise mechanistic links between the microbiome and cancer dissemination will open the doors to additional therapeutic possibilities.},
}

Humans
*Colorectal Neoplasms/microbiology/pathology/therapy
*Gastrointestinal Microbiome/physiology
*Neoplasm Metastasis
Dysbiosis/microbiology
Bacteria/classification/genetics
Fecal Microbiota Transplantation

@article {pmid38680517,
year = {2024},
author = {Patel, P and Robinson, PD and Fisher, BT and Phillips, R and Morgan, JE and Lehrnbecher, T and Kuczynski, S and Koenig, C and Haeusler, GM and Esbenshade, A and Elgarten, C and Duong, N and Diorio, C and Castagnola, E and Beauchemin, MP and Ammann, RA and Dupuis, LL and Sung, L},
title = {Guideline for the management of Clostridioides difficile infection in pediatric patients with cancer and hematopoietic cell transplantation recipients: 2024 update.},
journal = {EClinicalMedicine},
volume = {72},
number = {},
pages = {102604},
pmid = {38680517},
issn = {2589-5370},
abstract = {Our objective was to update a clinical practice guideline for the prevention and treatment of Clostridioides difficile infection (CDI) in pediatric patients with cancer and hematopoietic cell transplantation recipients. We reconvened an international multi-disciplinary panel. A systematic review of randomized controlled trials (RCTs) for the prevention or treatment of CDI in any population was updated and identified 31 new RCTs. Strong recommendations were made to use either oral metronidazole or oral vancomycin for non-severe CDI treatment, and to use either oral vancomycin or oral fidaxomicin for severe CDI. A strong recommendation that fecal microbiota transplantation should not be routinely used to treat CDI was also made. The panel made two new good practice statements to follow infection control practices including isolation in patients experiencing CDI, and to minimize systemic antibacterial administration where feasible, especially in patients who have experienced CDI.},
}

@article {pmid38679396,
year = {2024},
author = {Benech, N and Cassir, N and Galperine, T and Alric, L and Scanzi, J and Sokol, H and , },
title = {Fecal microbiota transplantation for recurrent C. difficile infection can be the best therapeutic option in severely immunocompromised patients depending on a case-by-case assessment of the benefit/risk ratio.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2024.04.022},
pmid = {38679396},
issn = {1528-0012},
}

@article {pmid38679228,
year = {2024},
author = {Rondinella, D and Quaranta, G and Rozera, T and Dargenio, P and Fancello, G and Venturini, I and Guarnaccia, A and Porcari, S and Bibbò, S and Sanguinetti, M and Gasbarrini, A and Masucci, L and Cammarota, G and Ianiro, G},
title = {Donor screening for fecal microbiota transplantation with a direct stool testing-based strategy: a prospective cohort study.},
journal = {Microbes and infection},
volume = {},
number = {},
pages = {105341},
doi = {10.1016/j.micinf.2024.105341},
pmid = {38679228},
issn = {1769-714X},
abstract = {Fecal microbiota transplantation (FMT) is effective against recurrent Clostridioides difficile infection (rCDI), but its safety is jeopardized by the potential transmission of pathogens, so international guidelines recommend either a quarantine or a direct stool testing. Whereas reports of the quarantine-based approach are emerging, data on the direct testing-based approach are not available. Our aim is to report outcomes of a donor screening framework for FMT including direct stool testing. In this prospective cohort study, all donor candidates recruited at our FMT centre underwent a four-step screening process to be enrolled as actual donors. Each collected stool donation was then evaluated with a direct stool testing including a molecular assay for gut pathogens and a culture assay for multi-drug resistant organisms (MDRO). From January 2019 to June 2023, 72 of 227 candidates (32%) were considered eligible and provided 277 stool donations. Ninety-nine donations (36%) were discarded for positivity to intestinal pathogens, most commonly enteropathogenic Escherichia coli (n= 37) and Blastocystis hominis (n= 20). Overall, 337 stool aliquots were obtained from 165 approved donations. All suspensions were used for patients with rCDI, and no serious adverse events or clinically evident infections were observed at 12 weeks after procedures. In our study, screening of donor faeces including direct stool testing led to the discard of a considerable rate of stool donations but was also extremely safe. This approach may represent a reliable strategy to guarantee the safety of FMT programs, especially in countries with high prevalence of MDRO.},
}

@article {pmid38678155,
year = {2024},
author = {Corriero, A and Giglio, M and Soloperto, R and Inchingolo, F and Varrassi, G and Puntillo, F},
title = {Microbial Symphony: Exploring the Role of the Gut in Osteoarthritis-Related Pain. A Narrative Review.},
journal = {Pain and therapy},
volume = {},
number = {},
pages = {},
pmid = {38678155},
issn = {2193-8237},
abstract = {One of the most common musculoskeletal disorders, osteoarthritis (OA), causes worldwide disability, morbidity, and poor quality of life by degenerating articular cartilage, modifying subchondral bone, and inflaming synovial membranes. OA pathogenesis pathways must be understood to generate new preventative and disease-modifying therapies. In recent years, it has been acknowledged that gut microbiota (GM) can significantly contribute to the development of OA. Dysbiosis of GM can disrupt the "symphony" between the host and the GM, leading to a host immunological response that activates the "gut-joint" axis, ultimately worsening OA. This narrative review summarizes research supporting the "gut-joint axis" hypothesis, focusing on the interactions between GM and the immune system in its two main components, innate and adaptive immunity. Furthermore, the pathophysiological sequence of events that link GM imbalance to OA and OA-related pain is broken down and further investigated. We also suggest that diet and prebiotics, probiotics, nutraceuticals, exercise, and fecal microbiota transplantation could improve OA management and represent a new potential therapeutic tool in the light of the scarce panorama of disease-modifying osteoarthritis drugs (DMOADs). Future research is needed to elucidate these complex interactions, prioritizing how a particular change in GM, i.e., a rise or a drop of a specific bacterial strain, correlates with a certain OA subset to pinpoint the associated signaling pathway that leads to OA.},
}

@article {pmid38674860,
year = {2024},
author = {Wang, X and Jin, Y and Di, C and Zeng, Y and Zhou, Y and Chen, Y and Pan, Z and Li, Z and Ling, W},
title = {Supplementation of Silymarin Alone or in Combination with Salvianolic Acids B and Puerarin Regulates Gut Microbiota and Its Metabolism to Improve High-Fat Diet-Induced NAFLD in Mice.},
journal = {Nutrients},
volume = {16},
number = {8},
pages = {},
pmid = {38674860},
issn = {2072-6643},
support = {81973022//National Natural Science Foundation of China/ ; TY202101003//BYHEALTH Nutrition and Health Research Foundation/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Non-alcoholic Fatty Liver Disease/etiology/drug therapy ; *Diet, High-Fat/adverse effects ; *Mice, Inbred C57BL ; *Isoflavones/pharmacology ; Male ; Mice ; *Silymarin/pharmacology ; *Dietary Supplements ; Benzofurans/pharmacology ; Liver/metabolism/drug effects ; Disease Models, Animal ; Bile Acids and Salts/metabolism ; Plant Extracts/pharmacology ; *Depsides ; },
abstract = {Silymarin, salvianolic acids B, and puerarin were considered healthy food agents with tremendous potential to ameliorate non-alcoholic fatty liver disease (NAFLD). However, the mechanisms by which they interact with gut microbiota to exert benefits are largely unknown. After 8 weeks of NAFLD modeling, C57BL/6J mice were randomly divided into five groups and fed a normal diet, high-fat diet (HFD), or HFD supplemented with a medium or high dose of Silybum marianum extract contained silymarin or polyherbal extract contained silymarin, salvianolic acids B, and puerarin for 16 weeks, respectively. The untargeted metabolomics and 16S rRNA sequencing were used for molecular mechanisms exploration. The intervention of silymarin and polyherbal extract significantly improved liver steatosis and recovered liver function in the mice, accompanied by an increase in probiotics like Akkermansia and Blautia, and suppressed Clostridium, which related to changes in the bile acids profile in feces and serum. Fecal microbiome transplantation confirmed that this alteration of microbiota and its metabolites were responsible for the improvement in NAFLD. The present study substantiated that alterations of the gut microbiota upon silymarin and polyherbal extract intervention have beneficial effects on HFD-induced hepatic steatosis and suggested the pivotal role of gut microbiota and its metabolites in the amelioration of NAFLD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Non-alcoholic Fatty Liver Disease/etiology/drug therapy
*Diet, High-Fat/adverse effects
*Mice, Inbred C57BL
*Isoflavones/pharmacology
Male
Mice
*Silymarin/pharmacology
*Dietary Supplements
Benzofurans/pharmacology
Liver/metabolism/drug effects
Disease Models, Animal
Bile Acids and Salts/metabolism
Plant Extracts/pharmacology
*Depsides

@article {pmid38674803,
year = {2024},
author = {Arteaga-Muller, GY and Flores-Treviño, S and Bocanegra-Ibarias, P and Robles-Espino, D and Garza-González, E and Fabela-Valdez, GC and Camacho-Ortiz, A},
title = {Changes in the Progression of Chronic Kidney Disease in Patients Undergoing Fecal Microbiota Transplantation.},
journal = {Nutrients},
volume = {16},
number = {8},
pages = {},
pmid = {38674803},
issn = {2072-6643},
mesh = {Humans ; *Renal Insufficiency, Chronic/therapy/microbiology ; *Fecal Microbiota Transplantation ; Male ; Female ; *Disease Progression ; Middle Aged ; Double-Blind Method ; *Gastrointestinal Microbiome ; Aged ; *Feces/microbiology ; Dysbiosis/therapy ; Treatment Outcome ; Adult ; Creatinine/blood ; },
abstract = {Chronic kidney disease (CKD) is a progressive loss of renal function in which gut dysbiosis is involved. Fecal microbiota transplantation (FMT) may be a promising alternative for restoring gut microbiota and treating CKD. This study evaluated the changes in CKD progression in patients treated with FMT. Patients with diabetes and/or hypertension with CKD clinical stages 2, 3, and 4 in this single-center, double-blind, randomized, placebo-controlled clinical trial (NCT04361097) were randomly assigned to receive either FMT or placebo capsules for 6 months. Laboratory and stool metagenomic analyses were performed. A total of 28 patients were included (15 FMT and 13 placebo). Regardless of CKD stages, patients responded similarly to FMT treatment. More patients (53.8%) from the placebo group progressed to CKD than the FMT group (13.3%). The FMT group maintained stable renal function parameters (serum creatinine and urea nitrogen) compared to the placebo group. Adverse events after FMT treatment were mild or moderate gastrointestinal symptoms. The abundance of Firmicutes and Actinobacteria decreased whereas Bacteroidetes, Proteobacteria and Roseburia spp. increased in the FMT group. CKD patients showed less disease progression after FMT administration. The administration of oral FMT in patients with CKD is a safe strategy, does not represent a risk, and has potential benefits.},
}

Humans
*Renal Insufficiency, Chronic/therapy/microbiology
*Fecal Microbiota Transplantation
Male
Female
*Disease Progression
Middle Aged
Double-Blind Method
*Gastrointestinal Microbiome
Aged
*Feces/microbiology
Dysbiosis/therapy
Treatment Outcome
Adult
Creatinine/blood

@article {pmid38674209,
year = {2024},
author = {Abenavoli, L and Gambardella, ML and Scarlata, GGM and Lenci, I and Baiocchi, L and Luzza, F},
title = {The Many Faces of Metabolic Dysfunction-Associated Fatty Liver Disease Treatment: From the Mediterranean Diet to Fecal Microbiota Transplantation.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {60},
number = {4},
pages = {},
pmid = {38674209},
issn = {1648-9144},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Diet, Mediterranean ; *Non-alcoholic Fatty Liver Disease/therapy/microbiology ; Probiotics/therapeutic use/administration & dosage ; Gastrointestinal Microbiome/physiology ; },
abstract = {The gastrointestinal tract is inhabited by the gut microbiota. The main phyla are Firmicutes and Bacteroidetes. In non-alcoholic fatty liver disease, now renamed metabolic dysfunction-associated fatty liver disease (MAFLD), an alteration in Firmicutes and Bacteroidetes abundance promotes its pathogenesis and evolution into non-alcoholic steatohepatitis, liver cirrhosis, and hepatocellular carcinoma. For this reason, early treatment is necessary to counteract its progression. The aim of the present narrative review is to evaluate the different therapeutic approaches to MAFLD. The most important treatment for MAFLD is lifestyle changes. In this regard, the Mediterranean diet could be considered the gold standard in the prevention and treatment of MAFLD. In contrast, a Western diet should be discouraged. Probiotics and fecal microbiota transplantation seem to be valid, safe, and effective alternatives for MAFLD treatment. However, more studies with a longer follow-up and with a larger cohort of patients are needed to underline the more effective approaches to contrasting MAFLD.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Diet, Mediterranean
*Non-alcoholic Fatty Liver Disease/therapy/microbiology
Probiotics/therapeutic use/administration & dosage
Gastrointestinal Microbiome/physiology

@article {pmid38673510,
year = {2024},
author = {Bragazzi, MC and Pianigiani, F and Venere, R and Ridola, L},
title = {Dysbiosis in Inflammatory Bowel Disease and Spondyloarthritis: Still a Long Way to Go?.},
journal = {Journal of clinical medicine},
volume = {13},
number = {8},
pages = {},
pmid = {38673510},
issn = {2077-0383},
abstract = {The association between Inflammatory Bowel Disease (IBD) and Spondyloarthritis (SpA) has been known for years, as has the concept that IBD is associated with an altered intestinal bacterial composition, a condition known as "dysbiosis". Recently, a state of intestinal dysbiosis has also been found in SpA. Dysbiosis in the field of IBD has been well characterized so far, as well as in SpA. The aim of this review is to summarize what is known to date and to emphasize the similarities between the microbiota conditions in these two diseases: particularly, an altered distribution in the gut of Enterobacteriaceae, Streptococcus, Haemophilus, Clostridium, Akkermansia, Ruminococcus, Faecalibacterium Prausnitzii, Bacteroides Vulgatus, Dialister Invisus, and Bifidubacterium Adolescentis is common to both IBD and SpA. At the same time, little is known about intestinal dysbiosis in IBD-related SpA. Only a single recent study has found an increase in Escherichia and Shigella abundances and a decrease in Firmicutes, Ruminococcaceae, and Faecalibacterium abundances in an IBD-related SpA group. Based on what has been discovered so far about the altered distribution of bacteria that unite both pathologies, it is appropriate to carry out further studies aiming to improve the understanding of IBD-related SpA for the purpose of developing new therapeutic strategies.},
}

@article {pmid38672797,
year = {2024},
author = {Nayak, G and Dimitriadis, K and Pyrpyris, N and Manti, M and Kamperidis, N and Kamperidis, V and Ziakas, A and Tsioufis, K},
title = {Gut Microbiome and Its Role in Valvular Heart Disease: Not a "Gutted" Relationship.},
journal = {Life (Basel, Switzerland)},
volume = {14},
number = {4},
pages = {},
pmid = {38672797},
issn = {2075-1729},
abstract = {The role of the gut microbiome (GM) and oral microbiome (OM) in cardiovascular disease (CVD) has been increasingly being understood in recent years. It is well known that GM is a risk factor for various CVD phenotypes, including hypertension, dyslipidemia, heart failure and atrial fibrillation. However, its role in valvular heart disease (VHD) is less well understood. Research shows that, direct, microbe-mediated and indirect, metabolite-mediated damage as a result of gut dysbiosis and environmental factors results in a subclinical, chronic, systemic inflammatory state, which promotes inflammatory cell infiltration in heart valves and subsequently, via pro-inflammatory molecules, initiates a cascade of reaction, resulting in valve calcification, fibrosis and dysfunction. This relationship between GM and VHD adds a pathophysiological link to the pathogenesis of VHD, which can be aimed therapeutically, in order to prevent or regress any risk for valvular pathologies. Therapeutic interventions include dietary modifications and lifestyle interventions, in order to influence environmental factors that can promote gut dysbiosis. Furthermore, the combination of probiotics and prebiotics, as well as fecal m transplantation and targeted treatment with inducers or inhibitors of microbial enzymes have showed promising results in animal and/or clinical studies, with the potential to reduce the inflammatory state and restore the normal gut flora in patients. This review, thus, is going to discuss the pathophysiological links behind the relationship of GM, CVD and VHD, as well as explore the recent data regarding the effect of GM-altering treatment in CVD, cardiac function and systemic inflammation.},
}

@article {pmid38672155,
year = {2024},
author = {Shin, J and Baek, GH and Cha, B and Park, SH and Lee, JH and Kim, JS and Kwon, KS},
title = {Complementary Therapeutic Effect of Fecal Microbiota Transplantation in Ulcerative Colitis after the Response to Anti-Tumor Necrosis Factor Alpha Agent Was Lost: A Case Report.},
journal = {Biomedicines},
volume = {12},
number = {4},
pages = {},
pmid = {38672155},
issn = {2227-9059},
support = {2021R1G1A1095241//National Research Foundation of Korea/ ; },
abstract = {In patients with ulcerative colitis (UC), the development of an antidrug antibody (ADA) to anti-tumor necrosis factor (TNF)α agent is a crucial problem which aggravates the clinical course of the disease, being cited as one of the most common causes for discontinuing anti-TNFα treatment. This is due to ADA eventually causing secondary LOR, leading to discontinuation of anti-TNFα treatment. Recently, research on the microbiome and relationship between worsening UC and dysbiosis has been conducted. Further, investigations on the association between the microbiome and secondary LOR are increasing. Here, we present the therapeutic effect of fecal microbiota transplantation (FMT) on a 42-year-old man with secondary LOR and high ADA levels. FMT has recently been used for the treatment of, and for overcoming, drug resistance through microbiome modification. Stool samples were collected from the patient before and 4 weeks after FMT. Symptoms, including hematochezia and Mayo endoscopy sub-scores, improved after FMT, while ADA levels decreased by one-third to less than half the value (29 ng/mL) compared to before FMT (79 ng/mL). Additionally, the trough level of infliximab became measurable, which reflects the improvement in the area under the concentration (AUC). Butyricicoccus, Faecalibacterium, Bifidobacterium, Ligilactobacillus, Alistipes, and Odoribacter, which regulate immune responses and alleviate inflammation, also increased after FMT. We report a case in which microbiome modification by FMT increased the AUC of anti-TNFα in a patient who developed secondary LOR during anti-TNFα treatment, thereby improving symptoms and mucosal inflammation.},
}

@article {pmid38667013,
year = {2024},
author = {Losurdo, G and Mezzapesa, M and Ditonno, I and Piazzolla, M and Pricci, M and Girardi, B and Celiberto, F and Galeano, G and Riezzo, G and Russo, F and Iannone, A and Ierardi, E and Di Leo, A},
title = {Helicobacter pylori Secondary Antibiotic Resistance after One or More Eradication Failure: A Genotypic Stool Analysis Study.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {13},
number = {4},
pages = {},
pmid = {38667013},
issn = {2079-6382},
abstract = {Helicobacter pylori (H. pylori) antibiotic resistance is the leading cause for unsuccessful eradication therapy. After one or more failures, the chance of encountering secondary antibiotic resistance increases. The aim of this study was to characterize genotypic secondary resistance in a cohort of southern Italian H. pylori patients with at least one previous failure. Such patients collected stool samples using a dedicated kit (THD fecal test[TM]), and bacterial DNA was extracted and amplified using RT-PCR. Resistance to clarithromycin, amoxicillin, metronidazole, levofloxacin, and tetracycline was assessed using a high-resolution melting curve. We enrolled 50 patients. A total of 72% of patients failed one previous antibiotic course, 16% failed two, 10% failed three, and 2% failed four. The rate of secondary antibiotic resistance was 16% for clarithromycin, 18% for metronidazole, 14% for amoxicillin, 14% for levofloxacin, and 2% for tetracycline. Among the eight clarithromycin-resistant patients, five (62.5%) previously received a clarithromycin-based regimen. The same rate was 33.3% (3/9) for metronidazole. The only tetracycline-resistant patient had received Pylera. In conclusion, our data seem to show that, even though secondary resistance is not very high, resistance to clarithromycin could be very likely related to previous exposure to this antibiotic.},
}

@article {pmid38666855,
year = {2024},
author = {Long, C and Zhou, X and Xia, F and Zhou, B},
title = {Intestinal Barrier Dysfunction and Gut Microbiota in Non-Alcoholic Fatty Liver Disease: Assessment, Mechanisms, and Therapeutic Considerations.},
journal = {Biology},
volume = {13},
number = {4},
pages = {},
pmid = {38666855},
issn = {2079-7737},
support = {2022A1515010833//Natural Science Foundation of Guangdong Province/ ; 82074078//National Natural Science Foundation of China/ ; 81803816//National Natural Science Foundation of China/ ; ZDSYS20220606100801003//Shenzhen Key Laboratory of Chinese Medicine Active Substance Screening and Translational Re-search/ ; },
abstract = {Non-alcoholic fatty liver disease (NAFLD) is a type of metabolic stress liver injury closely related to insulin resistance (IR) and genetic susceptibility without alcohol consumption, which encompasses a spectrum of liver disorders ranging from simple hepatic lipid accumulation, known as steatosis, to the more severe form of steatohepatitis (NASH). NASH can progress to cirrhosis and hepatocellular carcinoma (HCC), posing significant health risks. As a multisystem disease, NAFLD is closely associated with systemic insulin resistance, central obesity, and metabolic disorders, which contribute to its pathogenesis and the development of extrahepatic complications, such as cardiovascular disease (CVD), type 2 diabetes mellitus, chronic kidney disease, and certain extrahepatic cancers. Recent evidence highlights the indispensable roles of intestinal barrier dysfunction and gut microbiota in the onset and progression of NAFLD/NASH. This review provides a comprehensive insight into the role of intestinal barrier dysfunction and gut microbiota in NAFLD, including intestinal barrier function and assessment, inflammatory factors, TLR4 signaling, and the gut-liver axis. Finally, we conclude with a discussion on the potential therapeutic strategies targeting gut permeability and gut microbiota in individuals with NAFLD/NASH, such as interventions with medications/probiotics, fecal transplantation (FMT), and modifications in lifestyle, including exercise and diet.},
}

@article {pmid38664425,
year = {2024},
author = {Chui, ZSW and Chan, LML and Zhang, EWH and Liang, S and Choi, EPH and Lok, KYW and Tun, HM and Kwok, JYY},
title = {Effects of microbiome-based interventions on neurodegenerative diseases: a systematic review and meta-analysis.},
journal = {Scientific reports},
volume = {14},
number = {1},
pages = {9558},
pmid = {38664425},
issn = {2045-2322},
mesh = {Humans ; *Neurodegenerative Diseases/microbiology/therapy ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation/methods ; Probiotics/therapeutic use ; Microbiota ; },
abstract = {Neurodegenerative diseases (NDDs) are characterized by neuronal damage and progressive loss of neuron function. Microbiome-based interventions, such as dietary interventions, biotics, and fecal microbiome transplant, have been proposed as a novel approach to managing symptoms and modulating disease progression. Emerging clinical trials have investigated the efficacy of interventions modulating the GM in alleviating or reversing disease progression, yet no comprehensive synthesis have been done. A systematic review of the literature was therefore conducted to investigate the efficacy of microbiome-modulating methods. The search yielded 4051 articles, with 15 clinical trials included. The overall risk of bias was moderate in most studies. Most microbiome-modulating interventions changed the GM composition. Despite inconsistent changes in GM composition, the meta-analysis showed that microbiome-modulating interventions improved disease burden (SMD, - 0.57; 95% CI - 0.93 to - 0.21; I[2] = 42%; P = 0.002) with a qualitative trend of improvement in constipation. However, current studies have high methodological heterogeneity and small sample sizes, requiring more well-designed and controlled studies to elucidate the complex linkage between microbiome, microbiome-modulating interventions, and NDDs.},
}

Humans
*Neurodegenerative Diseases/microbiology/therapy
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation/methods
Probiotics/therapeutic use
Microbiota

@article {pmid38664378,
year = {2024},
author = {Holmberg, SM and Feeney, RH and Prasoodanan P K, V and Puértolas-Balint, F and Singh, DK and Wongkuna, S and Zandbergen, L and Hauner, H and Brandl, B and Nieminen, AI and Skurk, T and Schroeder, BO},
title = {The gut commensal Blautia maintains colonic mucus function under low-fiber consumption through secretion of short-chain fatty acids.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {3502},
pmid = {38664378},
issn = {2041-1723},
support = {2018-02095//Vetenskapsrådet (Swedish Research Council)/ ; SMK-1959//Kempestiftelserna (Kempe Foundations)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Dietary Fiber/metabolism ; *Fatty Acids, Volatile/metabolism ; Mice ; *Colon/metabolism/microbiology ; Humans ; *Intestinal Mucosa/metabolism/microbiology ; Male ; Receptors, G-Protein-Coupled/metabolism/genetics ; Female ; Mice, Inbred C57BL ; Mucus/metabolism ; Fecal Microbiota Transplantation ; Symbiosis ; Propionates/metabolism ; Clostridiales/metabolism ; Acetates/metabolism ; Adult ; *Receptors, Cell Surface ; },
abstract = {Beneficial gut bacteria are indispensable for developing colonic mucus and fully establishing its protective function against intestinal microorganisms. Low-fiber diet consumption alters the gut bacterial configuration and disturbs this microbe-mucus interaction, but the specific bacteria and microbial metabolites responsible for maintaining mucus function remain poorly understood. By using human-to-mouse microbiota transplantation and ex vivo analysis of colonic mucus function, we here show as a proof-of-concept that individuals who increase their daily dietary fiber intake can improve the capacity of their gut microbiota to prevent diet-mediated mucus defects. Mucus growth, a critical feature of intact colonic mucus, correlated with the abundance of the gut commensal Blautia, and supplementation of Blautia coccoides to mice confirmed its mucus-stimulating capacity. Mechanistically, B. coccoides stimulated mucus growth through the production of the short-chain fatty acids propionate and acetate via activation of the short-chain fatty acid receptor Ffar2, which could serve as a new target to restore mucus growth during mucus-associated lifestyle diseases.},
}

Animals
*Gastrointestinal Microbiome
*Dietary Fiber/metabolism
*Fatty Acids, Volatile/metabolism
Mice
*Colon/metabolism/microbiology
Humans
*Intestinal Mucosa/metabolism/microbiology
Male
Receptors, G-Protein-Coupled/metabolism/genetics
Female
Mice, Inbred C57BL
Mucus/metabolism
Fecal Microbiota Transplantation
Symbiosis
Propionates/metabolism
Clostridiales/metabolism
Acetates/metabolism
Adult
*Receptors, Cell Surface

@article {pmid38663650,
year = {2024},
author = {Fang, H and Hou, Q and Zhang, W and Su, Z and Zhang, J and Li, J and Lin, J and Wang, Z and Yu, X and Yang, Y and Wang, Q and Li, X and Li, Y and Hu, L and Li, S and Wang, X and Liao, L},
title = {Fecal Microbiota Transplantation Improves Clinical Symptoms of Fibromyalgia: An open-label, Randomized, Nonplacebo-Controlled Study.},
journal = {The journal of pain},
volume = {},
number = {},
pages = {104535},
doi = {10.1016/j.jpain.2024.104535},
pmid = {38663650},
issn = {1528-8447},
abstract = {Fibromyalgia (FM) is a complex and poorly understood disorder characterized by chronic and widespread musculoskeletal pain, of which the etiology remains unknown. Now, the disorder of the gut microbiome is considered as one of the main causes of FM. This study was aimed to investigate the potential benefits of fecal microbiota transplantation (FMT) in patients with FM. A total of 45 patients completed this open-label randomized, nonplacebo-controlled clinical study. The Numerical Rating Scale (NRS) scores in the FMT group were slightly lower than the control group at 1 month (P> 0.05), and they decreased significantly at 2, 3, 6, and 12 months after treatment (P < 0.001). Besides, compared with the control group, the Widespread Pain Index (WPI), Symptom Severity (SS), Hospital Anxiety and Depression Scale (HADS) and Pittsburgh Sleep Quality Index (PSQI) scores were significantly lower in the FMT group at different time points (P < 0.001). After 6 months of treatment, there was a significant increase in serotonin (5-HT) and gamma-aminobutyric acid (GABA) levels (P < 0.001), while glutamate levels significantly decreased in the FMT group (P < 0.001). The total effective rate was higher in the FMT group (90.9%) compared to the control group (56.5%) after 6 months of treatment (P < 0.05). FMT can effectively improve the clinical symptoms of FM. With the close relations between the changes of neurotransmitters and FM, certain neurotransmitters may serve as a diagnostic marker or potential target for FM patients. PERSPECTIVE: Fecal microbiota transplantation (FMT) is a novel therapy that aims to restore the gut microbial balance and modulate the gut-brain axis. It is valuable to further explore the therapeutic effect of FMT on FM. Furthermore, certain neurotransmitters may become a diagnostic marker or a new therapeutic target for FM patients.},
}

@article {pmid38663540,
year = {2024},
author = {Liang, L and Zhang, J and Chen, J and Tian, Y and Li, W and Shi, M and Cheng, S and Zheng, Y and Wang, C and Liu, H and Yang, X and Ye, W},
title = {Bazedoxifene attenuates dextran sodium sulfate-induced colitis in mice through gut microbiota modulation and inhibition of STAT3 and NF-κB pathways.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {176611},
doi = {10.1016/j.ejphar.2024.176611},
pmid = {38663540},
issn = {1879-0712},
abstract = {Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory disorder of the gastrointestinal tract for which treatment options remain limited. In this study, we used a dual-luciferase-based screening of an FDA-approved drug library, identifying Bazedoxifene (BZA) as an inhibitor of the NF-κB pathway. We further investigated its therapeutic effects in a dextran sodium sulfate (DSS)-induced colitis model and explored its impact on gut microbiota regulation and the underlying molecular mechanisms. Our results showed that BZA significantly reduced DSS-induced colitis symptoms in mice, evidenced by decreased colon length shortening, lower histological scores, and increased expression of intestinal mucosal barrier-associated proteins, such as Claudin 1, Occludin, Zo-1, Mucin 2 (Muc2), and E-cadherin. Used independently, BZA showed therapeutic effects comparable to those of infliximab (IFX). In addition, BZA modulated the abundance of gut microbiota especially Bifidobacterium pseudolongum, and influenced microbial metabolite production. Crucially, BZA's alleviation of DSS-induced colitis in mice was linked to change in gut microbiota composition, as evidenced by in vivo gut microbiota depletion and fecal microbiota transplantation (FMT) mice model. Molecularly, BZA inhibited STAT3 and NF-κB activation in DSS-induced colitis in mice. In general, BZA significantly reduced DSS-induced colitis in mice through modulating the gut microbiota and inhibiting STAT3 and NF-κB activation, and its independent use demonstrated a therapeutic potential comparable to IFX. This study highlights gut microbiota's role in IBD drug development, offering insights for BZA's future development and its clinical applications.},
}

@article {pmid38663526,
year = {2024},
author = {Zhang, S and Tang, S and Liu, Z and Lv, H and Cai, X and Zhong, R and Chen, L and Zhang, H},
title = {Baicalin restore intestinal damage after early-life antibiotic therapy: the role of the MAPK signaling pathway.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {107194},
doi = {10.1016/j.phrs.2024.107194},
pmid = {38663526},
issn = {1096-1186},
abstract = {Antibiotic related intestinal injury in early life affects subsequent health and susceptibility. Here, we employed weaned piglets as a model to investigate the protective effects of baicalin against early-life antibiotic exposure-induced microbial dysbiosis. Piglets exposed to lincomycin showed a marked reduction in body weight (p < 0.05) and deterioration of jejunum intestinal morphology, alongside an increase in antibiotic-resistant bacteria such as Staphylococcus, Dolosicoccus, Escherichia-Shigella, and Raoultella. In contrast, baicalin treatment resulted in body weights, intestinal morphology, and microbial profiles that closely resembled those of the control group (p > 0.05), with a significant increase in norank_f_Muribaculaceae and Prevotellaceae_NK3B31_group colonization compared with lincomycin group (p < 0.05). Further analysis through fecal microbial transplantation into mice revealed that lincomycin exposure led to significant alterations in intestinal morphology and microbial composition, notably increasing harmful microbes and decreasing beneficial ones such as norank_Muribaculaceae and Akkermansia (p < 0.05). This shift was associated with an increase in harmful metabolites and disruption of the calcium signaling pathway gene expression. Conversely, baicalin supplementation not only counteracted these effects but also enhanced beneficial metabolites and regulated genes within the MAPK signaling pathway (MAP3K11, MAP4K2, MAPK7, MAPK13) and calcium channel proteins (ORA13, CACNA1S, CACNA1F and CACNG8), suggesting a mechanism through which baicalin mitigates antibiotic-induced intestinal and microbial disturbances. These findings highlight baicalin's potential as a plant extract-based intervention for preventing antibiotic-related intestinal injury and offer new targets for therapeutic strategies.},
}

@article {pmid38663295,
year = {2024},
author = {Liu, A and Li, Y and Li, L and Chen, K and Tan, M and Zou, F and Zhang, X and Meng, X},
title = {Bile acid metabolism is altered in learning and memory impairment induced by chronic lead exposure.},
journal = {Journal of hazardous materials},
volume = {471},
number = {},
pages = {134360},
doi = {10.1016/j.jhazmat.2024.134360},
pmid = {38663295},
issn = {1873-3336},
abstract = {Lead is a neurotoxic contaminant that exists widely in the environment. Although lead neurotoxicity has been found to be tightly linked to gut microbiota disturbance, the effect of host metabolic disorders caused by gut microbiota disturbance on lead neurotoxicity has not been investigated. In this work, the results of new object recognition tests and Morris water maze tests showed that chronic low-dose lead exposure caused learning and memory dysfunction in mice. The results of 16 S rRNA sequencing of cecal contents and fecal microbiota transplantation showed that the neurotoxicity of lead could be transmitted through gut microbiota. The results of untargeted metabolomics and bile acid targeted metabolism analysis showed that the serum bile acid metabolism profile of lead-exposed mice was significantly changed. In addition, supplementation with TUDCA or INT-777 significantly alleviated chronic lead exposure-induced learning and memory impairment, primarily through inhibition of the NLRP3 inflammasome in the hippocampus to relieve neuroinflammation. In conclusion, our findings suggested that dysregulation of host bile acid metabolism may be one of the mechanisms of lead-induced neurotoxicity, and supplementation of specific bile acids may be a possible therapeutic strategy for lead-induced neurotoxicity.},
}

@article {pmid38660489,
year = {2024},
author = {Zhang, J and Wang, H and Liu, Y and Shi, M and Zhang, M and Zhang, H and Chen, J},
title = {Advances in fecal microbiota transplantation for the treatment of diabetes mellitus.},
journal = {Frontiers in cellular and infection microbiology},
volume = {14},
number = {},
pages = {1370999},
pmid = {38660489},
issn = {2235-2988},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Gastrointestinal Microbiome ; *Diabetes Mellitus/therapy/microbiology ; Dysbiosis/therapy ; Animals ; Feces/microbiology ; },
abstract = {Diabetes mellitus (DM) refers to a group of chronic diseases with global prevalence, characterized by persistent hyperglycemia resulting from various etiologies. DM can harm various organ systems and lead to acute or chronic complications, which severely endanger human well-being. Traditional treatment mainly involves controlling blood sugar levels through replacement therapy with drugs and insulin; however, some patients still find a satisfactory curative effect difficult to achieve. Extensive research has demonstrated a close correlation between enteric dysbacteriosis and the pathogenesis of various types of DM, paving the way for novel therapeutic approaches targeting the gut microbiota to manage DM. Fecal microbiota transplantation (FMT), a method for re-establishing the intestinal microbiome balance, offers new possibilities for treating diabetes. This article provides a comprehensive review of the correlation between DM and the gut microbiota, as well as the current advancements in FMT treatment for DM, using FMT as an illustrative example. This study aims to offer novel perspectives and establish a theoretical foundation for the clinical diagnosis and management of DM.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Gastrointestinal Microbiome
*Diabetes Mellitus/therapy/microbiology
Dysbiosis/therapy
Animals
Feces/microbiology

@article {pmid38659636,
year = {2024},
author = {Herman, C and Barker, BM and Bartelli, TF and Chandra, V and Krajmalnik-Brown, R and Jewell, M and Li, L and Liao, C and McAllister, F and Nirmalkar, K and Xavier, JB and Caporaso, JG},
title = {Assessing Engraftment Following Fecal Microbiota Transplant.},
journal = {ArXiv},
volume = {},
number = {},
pages = {},
pmid = {38659636},
issn = {2331-8422},
abstract = {Fecal Microbiota Transplant (FMT) is an FDA approved treatment for recurrent Clostridium difficile infections, and is being explored for other clinical applications, from alleviating digestive and neurological disorders, to priming the microbiome for cancer treatment, and restoring microbiomes impacted by cancer treatment. Quantifying the extent of engraftment following an FMT is important in determining if a recipient didn't respond because the engrafted microbiome didn't produce the desired outcomes (a successful FMT, but negative treatment outcome), or the microbiome didn't engraft (an unsuccessful FMT and negative treatment outcome). The lack of a consistent methodology for quantifying FMT engraftment extent hinders the assessment of FMT success and its relation to clinical outcomes, and presents challenges for comparing FMT results and protocols across studies. Here we review 46 studies of FMT in humans and model organisms and group their approaches for assessing the extent to which an FMT engrafts into three criteria: 1) Chimeric Asymmetric Community Coalescence investigates microbiome shifts following FMT engraftment. 2) Donated Microbiome Indicator Features tracks donated microbiome features as a signal of engraftment with methods such as differential abundance testing based on the current sample collection, or tracking changes in feature abundances that have been previously identified. 3) Temporal Stability examines how resistant post-FMT recipient's microbiomes are to reverting back to their baseline microbiome. Investigated together, these criteria provide a clear assessment of microbiome engraftment. We discuss the pros and cons of each of these criteria, providing illustrative examples of their application. We also introduce key terminology and recommendations on how FMT studies can be analyzed for rigorous engraftment extent assessment.},
}

@article {pmid38659317,
year = {2024},
author = {Xiao, N and He, W and Chen, S and Yao, Y and Wu, N and Xu, M and Du, H and Zhao, Y and Tu, Y},
title = {Protective Effect of Egg Yolk Lipids against Dextran Sulfate Sodium-Induced Colitis: The Key Role of Gut Microbiota and Short-Chain Fatty Acids.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e2400048},
doi = {10.1002/mnfr.202400048},
pmid = {38659317},
issn = {1613-4133},
support = {82260642//National Natural Science Foundation of China/ ; 20224ACB205015//Key Program of Natural Science Foundation of Jiangxi Province, China/ ; 29202300002//Training Project of High-level and High-skilled Leading Talents of Jiangxi Province/ ; },
abstract = {Egg yolk lipids significantly alleviate dextran sulfate sodium (DSS)-induced colitis by inhibiting NLRP3 inflammasome, reversing gut microbiota dysbiosis, and increasing short chain fatty acids (SCFAs) concentrations. However, the role of gut microbiota and the relationship between SCFAs and NLRP3 inflammasome are still unknown. Here, this study confirms that antibiotic treatment abolishes the protective effect of egg yolk lipids on DSS-induced colonic inflammation, intestinal barrier damage, and lipopolysaccharide translocation. Fecal microbiota transplantation also supports that egg yolk lipids alleviate colitis in a gut microbiota-dependent manner. Then, the study investigates the relationship between SCFAs and NLRP3 inflammasome, and finds that SCFAs significantly suppress colitis via inhibiting colonic NLRP3 inflammasome activation and proinflammatory cytokines secretions (interleukin, IL)-1β and IL-18, and combined treatment of SCFAs and MCC950 (NLRP3 inhibitor) shows a better activity against colitis and NLRP3 inflammasome activation. Together, these findings provide positive evidence for gut microbiorta-SCFAs-NLRP3 axis as a novel target involving in the therapy of inflammatory bowel disease.},
}

@article {pmid38655401,
year = {2024},
author = {Shi, W and Li, Z and Wang, W and Liu, X and Wu, H and Chen, X and Zhou, X and Zhang, S},
title = {Dynamic gut microbiome-metabolome in cationic bovine serum albumin induced experimental immune-complex glomerulonephritis and effect of losartan and mycophenolate mofetil on microbiota modulation.},
journal = {Journal of pharmaceutical analysis},
volume = {14},
number = {4},
pages = {100931},
pmid = {38655401},
issn = {2214-0883},
abstract = {Dynamic changes in gut dysbiosis and metabolomic dysregulation are associated with immune-complex glomerulonephritis (ICGN). However, an in-depth study on this topic is currently lacking. Herein, we report an ICGN model to address this gap. ICGN was induced via the intravenous injection of cationized bovine serum albumin (c-BSA) into Sprague-Dawley (SD) rats for two weeks, after which mycophenolate mofetil (MMF) and losartan were administered orally. Two and six weeks after ICGN establishment, fecal samples were collected and 16S ribosomal DNA (rDNA) sequencing and untargeted metabolomic were conducted. Fecal microbiota transplantation (FMT) was conducted to determine whether gut normalization caused by MMF and losartan contributed to their renal protective effects. A gradual decline in microbial diversity and richness was accompanied by a loss of renal function. Approximately 18 genera were found to have significantly different relative abundances between the early and later stages, and Marvinbryantia and Allobaculum were markedly upregulated in both stages. Untargeted metabolomics indicated that the tryptophan metabolism was enhanced in ICGN, characterized by the overproduction of indole and kynurenic acid, while the serotonin pathway was reduced. Administration of losartan and MMF ameliorated microbial dysbiosis and reduced the accumulation of indoxyl conjugates in feces. FMT using feces from animals administered MMF and losartan improved gut dysbiosis by decreasing the Firmicutes/Bacteroidetes (F/B) ratio but did not improve renal function. These findings indicate that ICGN induces serous gut dysbiosis, wherein an altered tryptophan metabolism may contribute to its progression. MMF and losartan significantly reversed the gut microbial and metabolomic dysbiosis, which partially contributed to their renoprotective effects.},
}

@article {pmid38654015,
year = {2024},
author = {Lachance, G and Robitaille, K and Laaraj, J and Gevariya, N and Varin, TV and Feldiorean, A and Gaignier, F and Julien, IB and Xu, HW and Hallal, T and Pelletier, JF and Bouslama, S and Boufaied, N and Derome, N and Bergeron, A and Ellis, L and Piccirillo, CA and Raymond, F and Fradet, Y and Labbé, DP and Marette, A and Fradet, V},
title = {The gut microbiome-prostate cancer crosstalk is modulated by dietary polyunsaturated long-chain fatty acids.},
journal = {Nature communications},
volume = {15},
number = {1},
pages = {3431},
pmid = {38654015},
issn = {2041-1723},
support = {400345//Canadian Cancer Society Research Institute (Société Canadienne du Cancer)/ ; },
mesh = {Male ; *Gastrointestinal Microbiome ; *Prostatic Neoplasms/metabolism/diet therapy/microbiology ; Animals ; Humans ; Mice ; *Fecal Microbiota Transplantation ; *Feces/microbiology ; Fatty Acids, Omega-3/metabolism/administration & dosage ; Mice, Inbred C57BL ; Fatty Acids, Unsaturated/metabolism ; },
abstract = {The gut microbiota modulates response to hormonal treatments in prostate cancer (PCa) patients, but whether it influences PCa progression remains unknown. Here, we show a reduction in fecal microbiota alpha-diversity correlating with increase tumour burden in two distinct groups of hormonotherapy naïve PCa patients and three murine PCa models. Fecal microbiota transplantation (FMT) from patients with high PCa volume is sufficient to stimulate the growth of mouse PCa revealing the existence of a gut microbiome-cancer crosstalk. Analysis of gut microbial-related pathways in mice with aggressive PCa identifies three enzymes responsible for the metabolism of long-chain fatty acids (LCFA). Supplementation with LCFA omega-3 MAG-EPA is sufficient to reduce PCa growth in mice and cancer up-grading in pre-prostatectomy PCa patients correlating with a reduction of gut Ruminococcaceae in both and fecal butyrate levels in PCa patients. This suggests that the beneficial effect of omega-3 rich diet is mediated in part by modulating the crosstalk between gut microbes and their metabolites in men with PCa.},
}

Male
*Gastrointestinal Microbiome
*Prostatic Neoplasms/metabolism/diet therapy/microbiology
Animals
Humans
Mice
*Fecal Microbiota Transplantation
*Feces/microbiology
Fatty Acids, Omega-3/metabolism/administration & dosage
Mice, Inbred C57BL
Fatty Acids, Unsaturated/metabolism

@article {pmid38653643,
year = {2024},
author = {Taghaddos, D and Saqib, Z and Bai, X and Bercik, P and Collins, SM},
title = {Post-infectious ibs following Clostridioides difficile infection; role of microbiota and implications for treatment.},
journal = {Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.dld.2024.03.008},
pmid = {38653643},
issn = {1878-3562},
abstract = {Up to 25% of patients recovering from antibiotic-treated Clostridioides difficile infection (CDI) develop functional symptoms reminiscent of Post-Infectious Irritable Bowel Syndrome (PI-IBS). For patients with persistent symptoms following infection, a clinical dilemma arises as to whether to provide additional antibiotic treatment or to adopt a conservative symptom-based approach. Here, we review the literature on CDI-related PI-IBS and compare the findings with PI-IBS. We review proposed mechanisms, including the role of C. difficile toxins and the microbiota, and discuss implications for therapy. We suggest that gut dysfunction post-CDI may be initiated by toxin-induced damage to enteroglial cells and that a dysbiotic gut microbitota maintains the clinical phenotype over time, prompting consideration of microbiota-directed therapies. While Fecal Microbial Transplant (FMT) is currently reserved for recurrent CDI (rCDI), we propose that microbiota-directed therapies may have a role in primary CDI in order to avoid or mitigate futher antibiotic treatment that further disrupts the microbiota and thus prevent PI-IBS. We discuss novel microbial transfer therapies and as they emerge, we recommend clinical trials to determine whether microbial transfer therapy of the primary infection prevents both rCDI and CDI-related PI- IBS.},
}

@article {pmid38648368,
year = {2024},
author = {Muchhala, KH and Kallurkar, PS and Kang, M and Koseli, E and Poklis, JL and Xu, Q and Dewey, WL and Fettweis, JM and Jimenez, NR and Akbarali, HI},
title = {The role of morphine- and fentanyl-induced impairment of intestinal epithelial antibacterial activity in dysbiosis and its impact on the microbiota-gut-brain axis.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {38},
number = {8},
pages = {e23603},
doi = {10.1096/fj.202301590RR},
pmid = {38648368},
issn = {1530-6860},
support = {P30DA033934//HHS | National Institutes of Health (NIH)/ ; R01DA024009//HHS | National Institutes of Health (NIH)/ ; T32DA007027//HHS | National Institutes of Health (NIH)/ ; 2214-A//TUBITAK/ ; },
abstract = {Recent evidence suggests that chronic exposure to opioid analgesics such as morphine disrupts the intestinal epithelial layer and causes intestinal dysbiosis. Depleting gut bacteria can preclude the development of tolerance to opioid-induced antinociception, suggesting an important role of the gut-brain axis in mediating opioid effects. The mechanism underlying opioid-induced dysbiosis, however, remains unclear. Host-produced antimicrobial peptides (AMPs) are critical for the integrity of the intestinal epithelial barrier as they prevent the pathogenesis of the enteric microbiota. Here, we report that chronic morphine or fentanyl exposure reduces the antimicrobial activity in the ileum, resulting in changes in the composition of bacteria. Fecal samples from morphine-treated mice had increased levels of Akkermansia muciniphila with a shift in the abundance ratio of Firmicutes and Bacteroidetes. Fecal microbial transplant (FMT) from morphine-naïve mice or oral supplementation with butyrate restored (a) the antimicrobial activity, (b) the expression of the antimicrobial peptide, Reg3γ, (c) prevented the increase in intestinal permeability and (d) prevented the development of antinociceptive tolerance in morphine-dependent mice. Improved epithelial barrier function with FMT or butyrate prevented the enrichment of the mucin-degrading A. muciniphila in morphine-dependent mice. These data implicate impairment of the antimicrobial activity of the intestinal epithelium as a mechanism by which opioids disrupt the microbiota-gut-brain axis.},
}

@article {pmid38647627,
year = {2023},
author = {Zhuang, X and Zhao, M and Ji, X and Yang, S and Yin, H and Zhao, L},
title = {Chitobiose exhibited a lipid-lowering effect in ob/ob[-/-] mice via butyric acid enrolled liver-gut crosstalk.},
journal = {Bioresources and bioprocessing},
volume = {10},
number = {1},
pages = {79},
pmid = {38647627},
issn = {2197-4365},
support = {23ZR1417300//Shanghai Natural Science Foundation General program/ ; 2022153//Shanghai post-doctoral Excellence Program/ ; 2019YFD090180302//National key R&D Program of China/ ; B18022//111 Project/ ; },
abstract = {Chitobiose (COS2) efficiently lowers lipids in vivo and facilitates butyric acid enrichment during human fecal fermentation. However, whether COS2 can interact with butyric acid to generate a hypolipidemic effect remains unclear. This study examined the hypolipidemic mechanism of COS2 involving butyric acid, which could alleviate non-alcoholic fatty liver disease (NAFLD). The results revealed that COS2 administration modulated the β-oxidation pathway in the liver and restructured the short chain fatty acids in the fecal of ob/ob[-/-] mice. Moreover, the hypolipidemic effect of COS2 and its specific accumulated metabolite butyric acid was verified in sodium oleate-induced HepG2 cells. Butyric acid was more effective to reverse lipid accumulation and up-regulate β-oxidation pathway at lower concentrations. Furthermore, structural analysis suggested that butyric acid formed hydrogen bonds with key residues in hydrophilic ligand binding domains (LBDs) of PPARα and activated the transcriptional activity of the receptor. Therefore, the potential mechanism behind the lipid-lowering effect of COS2 in vivo involved restoring hepatic lipid disorders via butyric acid accumulation and liver-gut axis signaling.},
}

@article {pmid38647957,
year = {2024},
author = {Singh, V and Mahra, K and Jung, D and Shin, JH},
title = {Gut Microbes in Polycystic Ovary Syndrome and Associated Comorbidities; Type 2 Diabetes, Non-Alcoholic Fatty Liver Disease (NAFLD), Cardiovascular Disease (CVD), and the Potential of Microbial Therapeutics.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {38647957},
issn = {1867-1314},
support = {2021R1A6C101A416//Korea Basic Science Institute/ ; },
abstract = {Polycystic ovary syndrome (PCOS) is one of the most common endocrine anomalies among females of reproductive age, highlighted by hyperandrogenism. PCOS is multifactorial as it can be associated with obesity, insulin resistance, low-grade chronic inflammation, and dyslipidemia. PCOS also leads to dysbiosis by lowering microbial diversity and beneficial microbes, such as Faecalibacterium, Roseburia, Akkermenisa, and Bifidobacterium, and by causing a higher load of opportunistic pathogens, such as Escherichia/Shigella, Fusobacterium, Bilophila, and Sutterella. Wherein, butyrate producers and Akkermansia participate in the glucose uptake by inducing glucagon-like peptide-1 (GLP-1) and glucose metabolism, respectively. The abovementioned gut microbes also maintain the gut barrier function and glucose homeostasis by releasing metabolites such as short-chain fatty acids (SCFAs) and Amuc_1100 protein. In addition, PCOS-associated gut is found to be higher in gut-microbial enzyme β-glucuronidase, causing the de-glucuronidation of conjugated androgen, making it susceptible to reabsorption by entero-hepatic circulation, leading to a higher level of androgen in the circulatory system. Overall, in PCOS, such dysbiosis increases the gut permeability and LPS in the systemic circulation, trimethylamine N-oxide (TMAO) in the circulatory system, chronic inflammation in the adipose tissue and liver, and oxidative stress and lipid accumulation in the liver. Thus, in women with PCOS, dysbiosis can promote the progression and severity of type 2 diabetes, non-alcoholic fatty liver disease (NAFLD), and cardiovascular diseases (CVD). To alleviate such PCOS-associated complications, microbial therapeutics (probiotics and fecal microbiome transplantation) can be used without any side effects, unlike in the case of hormonal therapy. Therefore, this study sought to understand the mechanistic significance of gut microbes in PCOS and associated comorbidities, along with the role of microbial therapeutics that can ease the life of PCOS-affected women.},
}

@article {pmid38647087,
year = {2024},
author = {Zhou, F and Zhang, Q and Zheng, X and Shi, F and Ma, K and Ji, F and Meng, N and Li, R and Lv, J and Li, Q},
title = {Antiaging Effects of Human Fecal Transplants with Different Combinations of Bifidobacterium bifidum LTBB21J1 and Lactobacillus casei LTL1361 in d-Galactose-Induced Mice.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.3c09815},
pmid = {38647087},
issn = {1520-5118},
abstract = {The feces of healthy middle-aged and old people were first transplanted into d-galactose-induced aging mice to construct humanized aging mice with gut microbiota (FMTC) to confirm the antiaging effect of probiotics produced from centenarians. The mouse model was then treated with centenarian-derived Bifidobacterium bifidum (FMTL), Lactobacillus casei (FMTB), and their mixtures (FMTM), and young mice were used as the control. Compared with the FMTC group, the results demonstrated that the probiotics and their combinations alleviated neuronal damage, increased antioxidant capacity, decreased inflammation, and enhanced cognitive and memory functions in aging mice. In the gut microbiota, the relative abundance of Lactobacillus, Ligilactobacillus, and Akkermansia increased and that of Desulfovibrio and Colidextribacter decreased in the FMTM group compared with that in the FMTC group. The three probiotic groups displayed significant changes in 15 metabolites compared with the FMTC group, with 4 metabolites showing increased expression and 11 metabolites showing decreased expression. The groups were graded as Control > FMTM > FMTB > FMTL > FMTC using a newly developed comprehensive quantitative scoring system that thoroughly analyzed the various indicators of this study. The beneficial antiaging effects of probiotics derived from centenarians were quantitatively described using a novel perspective in this study; it is confirmed that both probiotics and their combinations exert antiaging effects, with the probiotic complex group exhibiting a larger effect.},
}

@article {pmid38646653,
year = {2024},
author = {Liu, Q and Yang, Y and Pan, M and Yang, F and Yu, Y and Qian, Z},
title = {Role of the gut microbiota in tumorigenesis and treatment.},
journal = {Theranostics},
volume = {14},
number = {6},
pages = {2304-2328},
pmid = {38646653},
issn = {1838-7640},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Carcinogenesis ; *Neoplasms/microbiology/therapy ; *Dysbiosis/microbiology ; Animals ; },
abstract = {The gut microbiota is a crucial component of the intricate microecosystem within the human body that engages in interactions with the host and influences various physiological processes and pathological conditions. In recent years, the association between dysbiosis of the gut microbiota and tumorigenesis has garnered increasing attention, as it is recognized as a hallmark of cancer within the scientific community. However, only a few microorganisms have been identified as potential drivers of tumorigenesis, and enhancing the molecular understanding of this process has substantial scientific importance and clinical relevance for cancer treatment. In this review, we delineate the impact of the gut microbiota on tumorigenesis and treatment in multiple types of cancer while also analyzing the associated molecular mechanisms. Moreover, we discuss the utility of gut microbiota data in cancer diagnosis and patient stratification. We further outline current research on harnessing microorganisms for cancer treatment while also analyzing the prospects and challenges associated with this approach.},
}

Humans
*Gastrointestinal Microbiome
*Carcinogenesis
*Neoplasms/microbiology/therapy
*Dysbiosis/microbiology
Animals

@article {pmid38644237,
year = {2024},
author = {, and , and , },
title = {[Chinese expert consensus on the clinical diagnosis and treatment of gut microecology in chronic constipation (2024 edition)].},
journal = {Zhonghua wei chang wai ke za zhi = Chinese journal of gastrointestinal surgery},
volume = {27},
number = {4},
pages = {326-337},
doi = {10.3760/cma.j.cn441530-20240313-00096},
pmid = {38644237},
issn = {1671-0274},
support = {2022YFC2010101//"Thirteenth Five-Year Plan" National Key Research and Development Program "Proactive Health and Aging Science and Technology Response" Key Project/ ; 82100698//National Natural Science Foundation of China/ ; 21Y11908300, 22DZ2203700//Shanghai Municipal Science and Technology Innovation Action Plan/ ; },
mesh = {Humans ; *Constipation/therapy/diagnosis ; *Gastrointestinal Microbiome ; Chronic Disease ; *Fecal Microbiota Transplantation ; China ; *Consensus ; Dysbiosis/therapy/diagnosis ; Quality of Life ; },
abstract = {Chronic constipation is one of the common gastrointestinal disorders, with an incidence rate that is gradually increasing yearly and becoming an important chronic disease that affects people's health and quality of life. In recent years, significant progress has been made in the basic and clinical research of chronic constipation, especially the gut microbiota therapy methods have received increasing attention. Therefore, under the initiative of the Parenteral and Enteral Nutrition Branch of the Chinese Medical Association, Chinese Society for the Promotion of Human Health Science and Technology, and Committee on Gut Microecology and Fecal Microbiota Transplantation, experts from relevant fields in China have been organized to establish the "Chinese Expert Consensus on the Clinical Diagnosis and Treatment of Gut Microecology in Chronic Constipation (2024 Edition)" committee. Focusing on the dysbiosis of gut microbiota, the indications for gut microbiota therapy, and the protocols for fecal microbiota transplantation, 16 consensus opinions were proposed based on the review of domestic and international literature and the clinical experience of experts, aiming to standardize the clinical application of gut microbiota in chronic constipation.},
}

Humans
*Constipation/therapy/diagnosis
*Gastrointestinal Microbiome
Chronic Disease
*Fecal Microbiota Transplantation
China
*Consensus
Dysbiosis/therapy/diagnosis
Quality of Life

@article {pmid38642272,
year = {2024},
author = {Chen, LA and Boyle, K},
title = {The Role of the Gut Microbiome in Health and Disease in the Elderly.},
journal = {Current gastroenterology reports},
volume = {},
number = {},
pages = {},
pmid = {38642272},
issn = {1534-312X},
abstract = {PURPOSE OF REVIEW: Growing evidence supports the contribution of age in the composition and function of the gut microbiome, with specific findings associated with health in old age and longevity.

RECENT FINDINGS: Current studies have associated certain microbiota, such as Butyricimonas, Akkermansia, and Odoribacter, with healthy aging and the ability to survive into extreme old age. Furthermore, emerging clinical and pre-clinical research have shown promising mechanisms for restoring a healthy microbiome in elderly populations through various interventions such as fecal microbiota transplant (FMT), dietary interventions, and exercise programs. Despite several conceptually exciting interventional studies, the field of microbiome research in the elderly remains limited. Specifically, large longitudinal studies are needed to better understand causative relationships between the microbiome and healthy aging. Additionally, individualized approaches to microbiome interventions based on patients' co-morbidities and the underlying functional capacity of their microbiomes are needed to achieve optimal results.},
}

@article {pmid38639049,
year = {2024},
author = {Peng, Z and Zhang, J and Zhang, M and Yin, L and Zhou, Z and Lv, C and Wang, Z and Tang, J},
title = {Tryptophan metabolites relieve intestinal Candida albicans infection by altering the gut microbiota to reduce IL-22 release from group 3 innate lymphoid cells of the colon lamina propria.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d4fo00432a},
pmid = {38639049},
issn = {2042-650X},
abstract = {Invasive candidiasis may be caused by Candida albicans (C. albicans) colonization of the intestinal tract. Preventing intestinal damage caused by Candida albicans infection and protecting intestinal barrier function have become a critical issue. Integrated analyses of the microbiome with metabolome revealed a remarkable shift of the gut microbiota and tryptophan metabolites, kynurenic acid (KynA), and indolacrylic acid (IA) in mice infected with C. albicans. The transcriptome sequencing indicated that differentially expressed genes were significantly associated with innate immune responses and inflammatory responses. The results of this study suggest that KynA and IA (KI) can alleviate intestinal damage caused by Candida albicans infection in mice by reducing intestinal permeability, increasing intestinal firmness, alleviating intestinal inflammation, and reducing the secretion of interleukin-22 (IL-22) in the 3 groups of colon innate lymphoid cells (ILC3). We performed a fecal microbiota transplantation (FMT) experiment and found that the intestinal barrier function, inflammation, and IL-22 secretion of ILC3 in the colon lamina propria of the recipient mice subjected to C. albicans infection and KI treatment were consistent with the trends of the donor mice. Our results suggest that tryptophan metabolites may directly regulate colon lamina ILC3 to promote intestinal resistance to C. albicans invasion, or indirectly regulate the ILC3 secretion of IL-22 to play a protective role in the intestinal barrier by affecting intestinal microorganisms, which may become a potential target for alleviating intestine borne C. albicans infection.},
}

@article {pmid38638595,
year = {2024},
author = {Srikrishnaraj, A and Lanting, BA and Burton, JP and Teeter, MG},
title = {The Microbial Revolution in the World of Joint Replacement Surgery.},
journal = {JB & JS open access},
volume = {9},
number = {2},
pages = {},
pmid = {38638595},
issn = {2472-7245},
abstract = {BACKGROUND: The prevalence of revision surgery due to aseptic loosening and periprosthetic joint infection (PJI) following total hip and knee arthroplasty is growing. Strategies to prevent the need for revision surgery and its associated health-care costs and patient morbidity are needed. Therapies that modulate the gut microbiota to influence bone health and systemic inflammation are a novel area of research.

METHODS: A literature review of preclinical and clinical peer-reviewed articles relating to the role of the gut microbiota in bone health and PJI was performed.

RESULTS: There is evidence that the gut microbiota plays a role in maintaining bone mineral density, which can contribute to osseointegration, osteolysis, aseptic loosening, and periprosthetic fractures. Similarly, the gut microbiota influences gut permeability and the potential for bacterial translocation to the bloodstream, increasing susceptibility to PJI.

CONCLUSIONS: Emerging evidence supports the role of the gut microbiota in the development of complications such as aseptic loosening and PJI after total hip or knee arthroplasty. There is a potential for microbial therapies such as probiotics or fecal microbial transplantation to moderate the risk of developing these complications. However, further investigation is required.

CLINICAL RELEVANCE: Modulation of the gut microbiota may influence patient outcomes following total joint arthroplasty.},
}

@article {pmid38637862,
year = {2024},
author = {Zhao, H and Zhou, Y and Xu, J and Zhang, Y and Wang, H and Zhao, C and Huang, H and Yang, J and Huang, C and Li, Y and Wang, L and Nie, Y},
title = {Short-chain fatty acid-producing bacterial strains attenuate experimental ulcerative colitis by promoting M2 macrophage polarization via JAK/STAT3/FOXO3 axis inactivation.},
journal = {Journal of translational medicine},
volume = {22},
number = {1},
pages = {369},
pmid = {38637862},
issn = {1479-5876},
support = {82270577//National Natural Science Foundation of China/ ; 202201020297//Guangzhou Planned Project of Science and Technology/ ; 202201020248,202002020012//Guangzhou Planned Project of Science and Technology/ ; 202102080044//Guangzhou Planned Project of Science and Technology/ ; KY17010003//Guangzhou Key Laboratory of Digestive Diseases (2022-2023)/ ; 2020A1515011000//Natural Science Foundation of Guangdong Province/ ; 2020ZYGXZR024//Fundamental Research Funds for the Central Universities/ ; },
mesh = {Humans ; Mice ; Animals ; *Colitis, Ulcerative/therapy ; RNA, Ribosomal, 16S/genetics/metabolism ; *Gastrointestinal Microbiome ; *Colitis ; *Inflammatory Bowel Diseases ; Fatty Acids, Volatile/adverse effects/metabolism ; Bacteria/metabolism ; Disease Models, Animal ; Inflammation ; Dextran Sulfate/adverse effects ; Mice, Inbred C57BL ; Colon ; Forkhead Box Protein O3/metabolism ; *STAT3 Transcription Factor ; },
abstract = {BACKGROUND: Patients with inflammatory bowel disease (IBD), dysbiosis, and immunosuppression who receive fecal microbiota transplantation (FMT) from healthy donors are at an increased risk of developing bacteremia. This study investigates the efficacy of a mixture of seven short-chain fatty acid (SCFA)-producing bacterial strains (7-mix), the resulting culture supernatant mixture (mix-sup), and FMT for treating experimental ulcerative colitis (UC) and evaluates underlying mechanisms.

METHODS: Utilizing culturomics, we isolated and cultured SCFA-producing bacteria from the stool of healthy donors. We used a mouse model of acute UC induced by dextran sulfate sodium (DSS) to assess the effects of 7-mix, mix-sup, and FMT on intestinal inflammation and barrier function, microbial abundance and diversity, and gut macrophage polarization by flow cytometry, immunohistochemistry, 16S rRNA gene sequencing, and transwell assays.

RESULTS: The abundance of several SCFA-producing bacterial taxa decreased in patients with UC. Seven-mix and mix-sup suppressed the inflammatory response and enhanced intestinal mucosal barrier function in the mouse model of UC to an extent similar to or superior to that of FMT. Moreover, 7-mix and mix-sup increased the abundance of SCFA-producing bacteria and SCFA concentrations in colitic mice. The effects of these interventions on the inflammatory response and gut barrier function were mediated by JAK/STAT3/FOXO3 axis inactivation in macrophages by inducing M2 macrophage polarization in vivo and in vitro.

CONCLUSIONS: Our approach provides new opportunities to rationally harness live gut probiotic strains and metabolites to reduce intestinal inflammation, restore gut microbial composition, and expedite the development of safe and effective treatments for IBD.},
}

Humans
Mice
Animals
*Colitis, Ulcerative/therapy
RNA, Ribosomal, 16S/genetics/metabolism
*Gastrointestinal Microbiome
*Colitis
*Inflammatory Bowel Diseases
Fatty Acids, Volatile/adverse effects/metabolism
Bacteria/metabolism
Disease Models, Animal
Inflammation
Dextran Sulfate/adverse effects
Mice, Inbred C57BL
Colon
Forkhead Box Protein O3/metabolism
*STAT3 Transcription Factor

@article {pmid38635481,
year = {2024},
author = {Zambrano, LD and Newhams, MM and Simeone, RM and Payne, AB and Wu, M and Orzel-Lockwood, AO and Halasa, NB and Calixte, JM and Pannaraj, PS and Mongkolrattanothai, K and Boom, JA and Sahni, LC and Kamidani, S and Chiotos, K and Cameron, MA and Maddux, AB and Irby, K and Schuster, JE and Mack, EH and Biggs, A and Coates, BM and Michelson, KN and Bline, KE and Nofziger, RA and Crandall, H and Hobbs, CV and Gertz, SJ and Heidemann, SM and Bradford, TT and Walker, TC and Schwartz, SP and Staat, MA and Bhumbra, SS and Hume, JR and Kong, M and Stockwell, MS and Connors, TJ and Cullimore, ML and Flori, HR and Levy, ER and Cvijanovich, NZ and Zinter, MS and Maamari, M and Bowens, C and Zerr, DM and Guzman-Cottrill, JA and Gonzalez, I and Campbell, AP and Randolph, AG and , },
title = {Durability of Original Monovalent mRNA Vaccine Effectiveness Against COVID-19 Omicron-Associated Hospitalization in Children and Adolescents - United States, 2021-2023.},
journal = {MMWR. Morbidity and mortality weekly report},
volume = {73},
number = {15},
pages = {330-338},
doi = {10.15585/mmwr.mm7315a2},
pmid = {38635481},
issn = {1545-861X},
mesh = {Humans ; Adolescent ; Child ; United States/epidemiology ; *COVID-19 Vaccines ; *COVID-19/epidemiology/prevention & control ; mRNA Vaccines ; Vaccine Efficacy ; SARS-CoV-2 ; Hospitalization ; RNA, Messenger ; },
abstract = {Pediatric COVID-19 vaccination is effective in preventing COVID-19-related hospitalization, but duration of protection of the original monovalent vaccine during SARS-CoV-2 Omicron predominance merits evaluation, particularly given low coverage with updated COVID-19 vaccines. During December 19, 2021-October 29, 2023, the Overcoming COVID-19 Network evaluated vaccine effectiveness (VE) of ≥2 original monovalent COVID-19 mRNA vaccine doses against COVID-19-related hospitalization and critical illness among U.S. children and adolescents aged 5-18 years, using a case-control design. Too few children and adolescents received bivalent or updated monovalent vaccines to separately evaluate their effectiveness. Most case-patients (persons with a positive SARS-CoV-2 test result) were unvaccinated, despite the high frequency of reported underlying conditions associated with severe COVID-19. VE of the original monovalent vaccine against COVID-19-related hospitalizations was 52% (95% CI = 33%-66%) when the most recent dose was administered <120 days before hospitalization and 19% (95% CI = 2%-32%) if the interval was 120-364 days. VE of the original monovalent vaccine against COVID-19-related hospitalization was 31% (95% CI = 18%-43%) if the last dose was received any time within the previous year. VE against critical COVID-19-related illness, defined as receipt of noninvasive or invasive mechanical ventilation, vasoactive infusions, extracorporeal membrane oxygenation, and illness resulting in death, was 57% (95% CI = 21%-76%) when the most recent dose was received <120 days before hospitalization, 25% (95% CI = -9% to 49%) if it was received 120-364 days before hospitalization, and 38% (95% CI = 15%-55%) if the last dose was received any time within the previous year. VE was similar after excluding children and adolescents with documented immunocompromising conditions. Because of the low frequency of children who received updated COVID-19 vaccines and waning effectiveness of original monovalent doses, these data support CDC recommendations that all children and adolescents receive updated COVID-19 vaccines to protect against severe COVID-19.},
}

Humans
Adolescent
Child
United States/epidemiology
*COVID-19 Vaccines
*COVID-19/epidemiology/prevention & control
mRNA Vaccines
Vaccine Efficacy
SARS-CoV-2
Hospitalization
RNA, Messenger

@article {pmid38635321,
year = {2024},
author = {Wang, M and Lkhagva, E and Kim, S and Zhai, C and Islam, MM and Kim, HJ and Hong, ST},
title = {The gut microbe pair of Oribacterium sp. GMB0313 and Ruminococcus sp. GMB0270 confers complete protection against SARS-CoV-2 infection by activating CD8+ T cell-mediated immunity.},
journal = {Gut microbes},
volume = {16},
number = {1},
pages = {2342497},
pmid = {38635321},
issn = {1949-0984},
mesh = {Animals ; Cricetinae ; Ruminococcus ; *Gastrointestinal Microbiome ; *COVID-19 ; SARS-CoV-2 ; Clostridiales ; CD8-Positive T-Lymphocytes ; Immunity, Cellular ; },
abstract = {Despite the potential protective role of the gut microbiome against COVID-19, specific microbes conferring resistance to COVID-19 have not yet been identified. In this work, we aimed to identify and validate gut microbes at the species level that provide protection against SARS-CoV-2 infection. To identify gut microbes conferring protection against COVID-19, we conducted a fecal microbiota transplantation (FMT) from an individual with no history of COVID-19 infection or immunization into a lethal COVID-19 hamster model. FMT from this COVID-19-resistant donor resulted in significant phenotypic changes related to COVID-19 sensitivity in the hamsters. Metagenomic analysis revealed distinct differences in the gut microbiome composition among the hamster groups, leading to the identification of two previously unknown bacterial species: Oribacterium sp. GMB0313 and Ruminococcus sp. GMB0270, both associated with COVID-19 resistance. Subsequently, we conducted a proof-of-concept confirmation animal experiment adhering to Koch's postulates. Oral administration of this gut microbe pair, Oribacterium sp. GMB0313 and Ruminococcus sp. GMB0270, to the hamsters provided complete protection against SARS-CoV-2 infection through the activation of CD8+ T cell mediated immunity. The prophylactic efficacy of the gut microbe pair against SARS-CoV-2 infection was comparable to, or even superior to, current mRNA vaccines. This strong prophylactic efficacy suggests that the gut microbe pair could be developed as a host-directed universal vaccine for all betacoronaviruses, including potential future emerging viruses.},
}

Animals
Cricetinae
Ruminococcus
*Gastrointestinal Microbiome
*COVID-19
SARS-CoV-2
Clostridiales
CD8-Positive T-Lymphocytes
Immunity, Cellular

@article {pmid38635003,
year = {2024},
author = {Lee, SH and Lee, JH and Lee, SW},
title = {Application of Microbiome-Based Therapies in Chronic Respiratory Diseases.},
journal = {Journal of microbiology (Seoul, Korea)},
volume = {},
number = {},
pages = {},
pmid = {38635003},
issn = {1976-3794},
support = {2020R1A2C1008431//National Research Foundation of Korea/ ; 2023R1A2C2006688//National Research Foundation of Korea/ ; RS-2023-00222687//National Research Foundation of Korea/ ; 2022M3A9G8017220//National Research Foundation of Korea/ ; },
abstract = {The application of microbiome-based therapies in various areas of human disease has recently increased. In chronic respiratory disease, microbiome-based clinical applications are considered compelling options due to the limitations of current treatments. The lung microbiome is ecologically dynamic and affected by various conditions, and dysbiosis is associated with disease severity, exacerbation, and phenotype as well as with chronic respiratory disease endotype. However, it is not easy to directly modulate the lung microbiome. Additionally, studies have shown that chronic respiratory diseases can be improved by modulating gut microbiome and administrating metabolites. Although the composition, diversity, and abundance of the microbiome between the gut and lung are considerably different, modulation of the gut microbiome could improve lung dysbiosis. The gut microbiome influences that of the lung via bacterial-derived components and metabolic degradation products, including short-chain fatty acids. This phenomenon might be associated with the cross-talk between the gut microbiome and lung, called gut-lung axis. There are multiple alternatives to modulate the gut microbiome, such as prebiotics, probiotics, and postbiotics ingestion and fecal material transplantation. Several studies have shown that high-fiber diets, for example, present beneficial effects through the production of short-chain fatty acids. Additionally, genetically modified probiotics to secrete some beneficial molecules might also be utilized to treat chronic respiratory diseases. Further studies on microbial modulation to regulate immunity and potentiate conventional pharmacotherapy will improve microbiome modulation techniques, which will develop as a new therapeutic area in chronic respiratory diseases.},
}

@article {pmid38631415,
year = {2024},
author = {Lee, CYQ and Margolis, KG},
title = {Unlocking the potential of fecal virome transplants (FVT): modulating the gut-brain axis in stress-related disorders.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2024.04.006},
pmid = {38631415},
issn = {1528-0012},
}

@article {pmid38631285,
year = {2024},
author = {Kang, X and Lau, HC and Yu, J},
title = {Modulating gut microbiome in cancer immunotherapy: Harnessing microbes to enhance treatment efficacy.},
journal = {Cell reports. Medicine},
volume = {5},
number = {4},
pages = {101478},
pmid = {38631285},
issn = {2666-3791},
mesh = {Humans ; *Gastrointestinal Microbiome ; Immunotherapy ; Treatment Outcome ; *Microbiota ; Fecal Microbiota Transplantation ; *Neoplasms ; },
abstract = {Immunotherapy has emerged as a robust approach against cancer, yet its efficacy has varied among individuals, accompanied by the occurrence of immune-related adverse events. As a result, the efficacy of immunotherapy is far from satisfactory, and enormous efforts have been invested to develop strategies to improve patient outcomes. The gut microbiome is now well acknowledged for its critical role in immunotherapy, with better understanding on host-microbes interaction in the context of cancer treatment. Also, an increasing number of trials have been conducted to evaluate the potential and feasibility of microbiome-targeting approaches to enhance efficacy of cancer treatment in patients. Here, the role of the gut microbiome and metabolites (e.g., short-chain fatty acids, tryptophan metabolites) in immunotherapy and the underlying mechanisms are explored. The application of microbiome-targeting approaches that aim to improve immunotherapy efficacy (e.g., fecal microbiota transplantation, probiotics, dietary intervention) is also elaborated, with further discussion on current challenges and suggestions for future research.},
}

Humans
*Gastrointestinal Microbiome
Immunotherapy
Treatment Outcome
*Microbiota
Fecal Microbiota Transplantation
*Neoplasms