@article {pmid40050761,
year = {2025},
author = {Salazar-Arenas, JA and Hurtado-Bermúdez, LJ and Salazar-Cardona, ED and Rojas-Rojas, NE and Cubides-Martinez, JF and Toro-Palma, JD and Zúñiga-Restrepo, V and Rojas-Rodríguez, CA},
title = {Clinical and microbiological profile of patients with diarrhea evaluated using the gastrointestinal panel in a high-complexity center.},
journal = {BMC gastroenterology},
volume = {25},
number = {1},
pages = {147},
pmid = {40050761},
issn = {1471-230X},
mesh = {Humans ; *Diarrhea/microbiology/epidemiology ; Male ; Female ; Cross-Sectional Studies ; Middle Aged ; Colombia/epidemiology ; *Immunocompromised Host ; Adult ; Aged ; Feces/microbiology/parasitology ; Young Adult ; },
abstract = {INTRODUCTION: Gastrointestinal infections represent a worldwide public health problem. In Colombia, the incidence reaches 21.4 cases per 1,000 inhabitants. Given the limitations of traditional diagnostic methods in terms of sensitivity and specificity, the gastrointestinal panel (GIP) has emerged as a promising tool, allowing rapid detection of 22 pathogens. This study aimed to describe the clinical and microbiological characteristics of immunosuppressed and immunocompetent adult patients with diarrhea and the influence of the gastrointestinal panel in their treatment in a high-complexity hospital in Colombia.

MATERIALS AND METHODS: A cross-sectional observational study was carried out including 350 adult patients treated at the Fundación Valle del Lili hospital between 2021 and 2022. Demographic and clinical variables, GIP findings and treatment were analyzed by univariate and bivariate analysis. We compare immunocompromised and immunocompetent adult patients using Chi-square tests, Fisher's F test for qualitative variables, Student's t-test, and the Mann-Whitney U test for quantitative variables. A significance level of 5% was applied to demonstrate the significance of the variables in all the tests used.

RESULTS: The results showed that 52% were men, with an average age of 52 years. 72.0% presented acute diarrhea, being inflammatory in 60.1%. 39.1% of the patients were immunosuppressed, mainly transplant recipients (31.3%). 53% of the GIPs were positive, with up to 5 pathogens per sample. Bacteria were detected in 80%, viruses in 14.4%, and parasites in 5.5%. The most frequent bacteria were enteropathogenic E. coli (43.0%), enteroaggregative E. coli (18.6%), and C. difficile (17.4%). Norovirus was the predominant virus (67.7%) and Cryptosporidium the most common parasite (41.7%). A higher frequency of Vibrio spp. was observed in non-immunosuppressed patients (p = 0.004) and of enterotoxigenic E. coli in immunosuppressed patients. 41.0% of patients received antibiotic/antiviral therapy, 83% empirically. GIP influenced the treatment of 56.7% of patients, with a 90.0% recovery rate.

CONCLUSION: This study confirms that GIP is a valuable diagnostic tool in the management of adult patients with diarrheal disease, particularly in immunocompromised patients. In our setting it is still a costly and difficult to access test, which makes it necessary to standardize the indications for its application. Future studies could evaluate its cost-effectiveness in our context.},
}

Humans
*Diarrhea/microbiology/epidemiology
Male
Female
Cross-Sectional Studies
Middle Aged
Colombia/epidemiology
*Immunocompromised Host
Adult
Aged
Feces/microbiology/parasitology
Young Adult

@article {pmid40049043,
year = {2025},
author = {Huang, JN and Gao, CC and Ren, HY and Wen, B and Wang, ZN and Gao, JZ and Chen, ZZ},
title = {Multi-omics association pattern between gut microbiota and host metabolism of a filter-feeding fish in situ exposed to microplastics.},
journal = {Environment international},
volume = {197},
number = {},
pages = {109360},
doi = {10.1016/j.envint.2025.109360},
pmid = {40049043},
issn = {1873-6750},
abstract = {Microplastics (MPs) are widespread in water environments and can affect gut microbiota and host metabolism of fish, but whether changes in host metabolism under MPs are mediated by gut microbiota remains unclear. Here, silver carp, a filter-feeding fish with important ecological functions, was in-situ exposure to environmentally relevant MPs. Multi-omics analysis and fecal microbiota transplantation were used to reveal the metabolic responses of carp along gut-liver-muscle axis. After three months of in situ exposure to MPs, community structure of gut microbiota of carp was reshaped, and five dominate phyla were significantly changed, including increased Cyanobacteria, Chloroflexi and Planctomycetota but decreased Firmicutes and Fusobacteriota. Weighted gene co-expression network analysis was further performed between these phyla and liver transcription spectrum, showing that the hub gene module contained up-regulated hppD, maiA and plg and activated ubiquinone and other terpenoid-quinone biosynthesis and phenylalanine metabolism. By fecal microbiota transplantation, the key gene module associated with core microbiota phyla of carp was verified in germ-free zebrafish. Interestingly, up-regulated hppD, maiA and plg and enriched phenylalanine metabolism were also observed in this module. Subsequently, metabolome performed in carp liver also shared activated phenylalanine metabolism, including increased trans-cinnamic acid and L-tyrosine. Furthermore, high-associated mapping showed that the differentially expressed metabolites (gamma-aminobutyric acid, ornithine and L-serine) related to amino acid metabolism in carp muscle were significantly accompanied with increased L-tyrosine in its liver. Overall, MPs exposure could change gut microbiome of silver carp and alter host metabolism especially amino acid metabolism along the gut-liver-muscle axis.},
}

@article {pmid40047909,
year = {2025},
author = {Heinze, T and Heimke, M and Stelzner, S and Wedel, T},
title = {[Surgical anatomy of the anorectum].},
journal = {Chirurgie (Heidelberg, Germany)},
volume = {},
number = {},
pages = {},
pmid = {40047909},
issn = {2731-698X},
abstract = {The anorectum corresponds to the last segment of the gastrointestinal tract and is responsible for mediating fecal continence and controlled defecation. An understanding of the complex topographic anatomy is an indispensable prerequisite for the surgical treatment of benign and malignant diseases in the anorectal region. The detailed description of perirectal fascia, anorectal blood supply and lymph vessel drainage, pelvic autonomic nerves and components of the anal canal and anal sphincter complex has significantly contributed to improvement of the oncological and functional surgical outcome. In this article the state of knowledge relating to the anorectal anatomy is outlined providing a practical basis for rectal and proctological surgical procedures.},
}

@article {pmid40046764,
year = {2025},
author = {Hou, PF and Yao, Y and Wu, Y and Yu, HT and Qin, Y and Yi, L and Mi, MT},
title = {Fecal microbiota transplantation improves hepatic steatosis induced by HFD in a mouse model associated with liver ILC1 regulation and indole-3-carbinol level.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1500293},
pmid = {40046764},
issn = {2296-861X},
abstract = {BACKGROUND: The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) has increased worldwide. In recent years, fecal microbiota transplantation (FMT) has become an important promising method for the treatment of MASLD. However, the mechanism remains unclear.

METHODS: The animal model with C57BL/6 male mice induced by high-fat diet (HFD) for 12 weeks has been introduced. Fecal microbiota and indole-3-carbinol (I3C) was given by oral gavage.

RESULTS: Our study demonstrated that a 6-week healthy gut microbiota transplantation tended to ameliorate hepatic steatosis and reverse the decreased liver ILC1 induced by HFD. Interestingly, there was also a negative correlation between liver ILC1 and liver TG, TC level. Furthermore, the protective effect was associated with the elevated levels of serum indole-3-carbinol (I3C). Also, a I3C administration for 6 weeks improved liver steatosis and increased the frequency of liver ILC1 induced by HFD through aryl hydrocarbon receptor (AhR) activation. Moreover, I3C binds to the residues of ALA349, PHE348, LEU309, TYR316, PHE318 on AhR through hydrogen bonds, Π bonds, hydrophobic bonds which was proved by molecular docking.

CONCLUSION: To conclude, our data demonstrated that FMT improved liver steatosis induced by HFD associated with liver ILC1 regulation and indole-3-carbinol level. The study highlighted the potential treatment value of FMT and microbiota-derived I3C in the MASLD treatment and regulation of liver ILC1 function.},
}

@article {pmid40046008,
year = {2024},
author = {Zeng, Z and Feng, M and He, F and Zhang, E and Li, X and Cao, Z},
title = {Gut microbiota mediates the pro-pyroptosis effect of xierezhuyubuxu decoction in hepatocellular carcinoma.},
journal = {Frontiers in microbiology},
volume = {15},
number = {},
pages = {1481111},
pmid = {40046008},
issn = {1664-302X},
abstract = {INTRODUCTION: Xierezhuyubuxu decoction (XRZYBXD) is prepared by adding and reducing the Dahuang Zhechong Pill, which is a traditional Chinese medicinal formula in "The Synopsis of Prescriptions of the Golden Chamber". XRZYBXD has previously been reported to have good efficacy in treating Hepatocellular carcinoma (HCC) in clinical and basic research. However, its underlying mechanism in treating HCC has not been fully elucidated. The aim of the study is to investigate the pro-pyroptosis effect of XRZYBXD in HCC and the role of gut microbiota in this process.

METHODS: Firstly, we executed comprehensive analyses of XRZYBXD on pyroptosis, intestinal flora, microbial metabolites and intestinal barrier function using TUNEL, IHC, ELISA, WB, Q-PCR, 16S rRNA sequencing, and untargeted metabolomics in a H22 tumor-bearing mice model. Further, through rescue experiment of antibiotics-induced microbiota depletion and fecal microbial transplantation (FMT) experiment, the mechanism of XRZYBXD promoting pyroptosis of HCC by improving intestinal flora was verified.

RESULTS: We found that XRZYBXD medium and high dose significantly inhibited the growth of tumor and induced pyroptosis of hepatoma cells. They also modified intestinal ecological disorders by expansion of the abundance of beneficial bacteria (such as Akkermansia muciniphila and Parabacteroides distasonis) and reduction of the abundance of harmful bacteria (such as Barnesiella intestinihominis). Accordingly, microbiota metabolites and intestinal barrier function were also significantly improved by XRZYBXD.

DISCUSSION: Further, elimination of gut microbiota by antibiotics weakened the efficacy of XRZYBXD, and FMT with feces from the XRZYBXD high dose group achieved similar therapeutic efficacy as XRZYBXD. In brief, XRZYBXD promote pyroptosis of hepatoma cells via adjusting intestinal dysbiosis.},
}

@article {pmid40045660,
year = {2025},
author = {Hu, J and Xu, F and Zhu, L and Cui, Y and Au, R and Li, Y and Tong, Y and Shen, H},
title = {Angelica dahurica Polysaccharides Ameliorate Colitis by Reducing the Restriction of Gut Microbiota-Derived Imidazole Propionate on PPAR-γ Signaling Activation.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.8466},
pmid = {40045660},
issn = {1099-1573},
support = {82205023//National Natural Science Foundation of China/ ; 82274483//National Natural Science Foundation of China/ ; },
abstract = {Angelica dahurica radix (ADR), the root of the botanical family Apiaceae (genus Angelica, species Angelica dahurica (Hoffm.)), has been used to treat colitis in clinical practice. The immunomodulatory effects of ADR are attributed to its polysaccharides (RP). However, its mechanism of action has not been elucidated. In this study, RP's structure was determined through nuclear magnetic resonance analysis. Dextran sulfate sodium-induced colitis in mice was utilized to assess the therapeutic efficacy of RP, while experiments involving fecal microbiota transplantation (FMT) and antibiotic treatment were performed to investigate the contribution of gut microbiota to RP's protective function. Non-targeted metabolomics was utilized to identify potential targets for elucidating the underlying mechanisms. RP is likely composed of (→4)-α-D-Glcp-(1→ and →4)-α-D-Galp-(1→). It effectively alleviated DSS-induced colitis by restoring the balance of the gut microbial community, a finding validated through FMT and antibiotic intervention experiments. Imidazole propionate (ImP) emerged as a potential target for RP's efficacy in treating colitis, which inhibits the activation of peroxisome proliferator-activated receptor gamma (PPAR-γ). Our findings suggest that RP may confer protection against colitis by activating the PPAR-γ signaling pathway through alleviating the constraint imposed by ImP.},
}

@article {pmid40044736,
year = {2025},
author = {Song, Y and Li, N and Jiang, S and Wang, K and Lv, G and Fan, Z and Du, X and Gao, W and Lei, L and Wang, Z and Liu, G and Li, X},
title = {Microbiota-derived H2S induces c-kit[+] cDC1 autophagic cell death and liver inflammation in metabolic dysfunction-associated steatohepatitis.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {2222},
pmid = {40044736},
issn = {2041-1723},
support = {U24A20454//National Natural Science Foundation of China (National Science Foundation of China)/ ; 32473104//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; Mice ; *Liver/pathology/metabolism ; Humans ; *Autophagy ; Male ; *Proto-Oncogene Proteins c-kit/metabolism/genetics ; *Hydrogen Sulfide/metabolism ; *Fatty Liver/metabolism/pathology/microbiology ; *Mice, Inbred C57BL ; Disease Models, Animal ; Dysbiosis/microbiology/metabolism ; Mice, Knockout ; Inflammation/metabolism/pathology ; Dendritic Cells/metabolism/immunology ; Diet, Western/adverse effects ; Female ; },
abstract = {Immune dysregulation-induced inflammation serves as a driving force in the progression of metabolic dysfunction-associated steatohepatitis (MASH), while the underlying cellular and molecular mechanisms remain largely uncharted. A Western diet (WD) is employed to construct mouse models of metabolic dysfunction associated steatotic liver disease (MASLD) or MASH. Mass cytometry identifies a c-kit[+] cDC1 subset whose frequency is reduced in the livers of mice and patients with MASH compared with healthy controls. Adoptive cell transfer of c-kit[+] cDC1 protects the progression of MASH. Moreover, analysis of gut microbe sequence shows that WD-fed mice and MASLD/MASH patients exhibit gut microbiota dysbiosis, with an elevated abundance of H2S-producing Desulfovibrio_sp. Transplanting of MASH-derived fecal flora, Desulfovibrio_sp., or injecting H2S intraperitoneally into MASLD mice decreases the c-kit[+]cDC1 population and exacerbates liver inflammation. Mechanistically, H2S induces autophagic cell death of cDC1 in a c-kit-dependent manner in cDC-specific c-kit[-/-] and Atg5[-/-] mice. We thus uncover that microbiota-derived H2S triggers the autophagic cell death of c-kit[+] cDC1 and ignites the liver inflammatory cascade in MASH.},
}

Animals
*Gastrointestinal Microbiome
Mice
*Liver/pathology/metabolism
Humans
*Autophagy
Male
*Proto-Oncogene Proteins c-kit/metabolism/genetics
*Hydrogen Sulfide/metabolism
*Fatty Liver/metabolism/pathology/microbiology
*Mice, Inbred C57BL
Disease Models, Animal
Dysbiosis/microbiology/metabolism
Mice, Knockout
Inflammation/metabolism/pathology
Dendritic Cells/metabolism/immunology
Diet, Western/adverse effects
Female

@article {pmid40042965,
year = {2025},
author = {Sun, W and Jia, J and Liu, G and Liang, S and Huang, Y and Xin, M and Chang, Z and Liu, X and Ma, C and Song, X and He, F and Song, Y and Wu, M},
title = {Polysaccharides Extracted from Old Stalks of Asparagus officinalis L. Improve Nonalcoholic Fatty Liver by Increasing the Gut Butyric Acid Content and Improving Gut Barrier Function.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c07078},
pmid = {40042965},
issn = {1520-5118},
abstract = {Nonalcoholic fatty liver disease (NAFLD) ranks among the most prevalent chronic liver diseases worldwide, yet effective treatments remain scarce. Old stalks of Asparagus officinalis L. are rich in polysaccharides. The anti-NAFLD mechanism of polysaccharides from old stalks of A. officinalis (AP) requires further study. Here, we studied the effects of AP on NAFLD mice and its impact on the gut microbiota. AP intervention reduces blood lipids and liver lipids and reduces liver injury and inflammation in mice with NAFLD. Moreover, AP intervention changed gut microbiota composition and increased the abundances of butyric acid-producing bacteria, thereby increasing plasma concentration of butyric acid. Furthermore, AP intervention regulated the AMPK/SREBPs signaling pathway, thereby affecting hepatic lipid synthesis. Additionally, AP intervention improved gut barrier function and reduced plasma LPS levels, which subsequently inhibited the LPS/TLR4/NF-κB signaling pathway, thereby alleviating inflammation in NAFLD model mice. Importantly, fecal microbiota transplant (FMT) outcomes demonstrated that AP-induced changes in the gut microbiota impact the AMPK/SREBPs and LPS/TLR4/NF-κB pathways. These data suggest that AP intervention ameliorates NAFLD by regulating the gut microbiota. These research provides a scientific foundation for the use of the stalks of A. officinalis in the treatment of NAFLD.},
}

@article {pmid40041456,
year = {2025},
author = {Farah, A and Paul, P and Khan, AS and Sarkar, A and Laws, S and Chaari, A},
title = {Targeting gut microbiota dysbiosis in inflammatory bowel disease: a systematic review of current evidence.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1435030},
pmid = {40041456},
issn = {2296-858X},
abstract = {INTRODUCTION: The dysbiosis of the gut microbiota has been identified as a central factor in the pathogenesis of inflammatory bowel disease (IBD), a chronic condition characterized by frequent recurrence and various adverse effects of traditional therapies. While treatments targeting the gut microbiota show promise, their efficacy in IBD management still requires extensive evaluation. Our systematic review analyzes recent studies to elucidate the advancements and challenges in treating IBD using microbial-based therapies.

METHODS: Through a comprehensive systematic review spanning key scientific databases-PubMed, Embase, Cochrane, Web of Science, Scopus, and Google Scholar-we scrutinized the impact of probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) on individuals with IBD. Our detailed analysis covered study and participant demographics, along with seven key outcome measures: disease activity index, inflammatory markers, serum cytokines, microbiome composition, adverse effects, and the rates of remission and relapse.

RESULTS: From 6,080 initial search hits, we included 71 studies that assessed various interventions compared to placebo or standard medical therapy. Although there was notable variation in clinical results while assessing different outcomes, overall, probiotics, prebiotics, and synbiotics enhanced the success rates in inducing remission among IBD patients. Furthermore, we noted significant reductions in levels of pro-inflammatory markers and cytokines. Additionally, the requirement for steroids, hospitalization, and poor outcomes in endoscopic and histological scores were significantly reduced in individuals undergoing FMT.

CONCLUSION: Our investigation highlights the potential of targeting gut microbiota dysbiosis with microbial-based therapies in patients with IBD. We recommend conducting larger, placebo-controlled randomized trials with extended follow-up periods to thoroughly assess these treatments' clinical efficacy and safety before widespread recommendations for clinical application.},
}

@article {pmid40040709,
year = {2025},
author = {Liu, X and Yang, K and Jia, Y and Yeertai, Y and Wu, C and Wang, X and Jia, Q and Gu, Z and Cong, J and Ling, J},
title = {Chaihushugan powder regulates the gut microbiota to alleviate mitochondrial oxidative stress in the gastric tissues of rats with functional dyspepsia.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1549554},
pmid = {40040709},
issn = {1664-3224},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Dyspepsia/drug therapy/metabolism/therapy ; *Oxidative Stress/drug effects ; Rats ; Male ; *Mitochondria/metabolism/drug effects ; Rats, Sprague-Dawley ; Disease Models, Animal ; Powders ; Gastric Mucosa/metabolism/microbiology/drug effects ; Fecal Microbiota Transplantation ; Drugs, Chinese Herbal/pharmacology/therapeutic use ; Gastrointestinal Motility/drug effects ; Antioxidants/pharmacology ; },
abstract = {INTRODUCTION: Functional dyspepsia (FD) is a prevalent functional gastrointestinal disorder associated with oxidative stress (OS) and dysbiosis. Chaihushugan powder (CHSGP) demonstrates efficacy in treating FD; however, the underlying therapeutic mechanism is not yet elucidated. This study aims to investigate the effects of CHSGP on OS and gut microbiota (GM) in FD rats, with a particular emphasis on the role of GM as a potential target for the antioxidant properties of CHSGP.

METHODS: The FD rat model was established with a modified tail-clamp stimulation and the administration of the CHSGP decoction at a dosage of 9.6 g/kg via gavage for a duration of 4 weeks. The GM was depleted by the administration of a cocktail of metronidazole (200 mg/kg), ampicillin (200 mg/kg), neomycin sulfate (200 mg/kg), and vancomycin (100 mg/kg). Fecal microbiota transplantation (FMT) was performed with CHSGP-treated fecal supernatant at a dosage of 10 mL/kg. The gastrointestinal motility was measured using the rates of gastric emptying and small intestine propulsion. Hematoxylin and eosin staining was employed to elucidate the pathological changes, while the transmission electron microscope was used to examine the microstructures of the interstitial cells of Cajal (ICC). Chemiluminescence, colorimetric assay, immunofluorescence co-staining, and western blot assay were employed to identify the OS-related markers (ROS, SOD, NOX4, PRDX1, and TRX2). Sequencing of fecal microbiota was performed utilizing 16S rDNA.

RESULTS: The CHSGP decoction promoted gastrointestinal motility, protected the microstructure of ICC, and reduced OS in FD rats. The GM composition was also regulated by CHSGP. However, these effects disappeared after microbiota depletion. Fortunately, the FMT therapy reinstated them.

CONCLUSION: Chaihushugan powder decoction might regulate the GM to alleviate mitochondrial OS in the gastric tissues of FD rats.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Dyspepsia/drug therapy/metabolism/therapy
*Oxidative Stress/drug effects
Rats
Male
*Mitochondria/metabolism/drug effects
Rats, Sprague-Dawley
Disease Models, Animal
Powders
Gastric Mucosa/metabolism/microbiology/drug effects
Fecal Microbiota Transplantation
Drugs, Chinese Herbal/pharmacology/therapeutic use
Gastrointestinal Motility/drug effects
Antioxidants/pharmacology

@article {pmid40040609,
year = {2025},
author = {Liu, FQ and An, ZY and Cui, LJ and Xiao, MY and Wu, YJ and Li, W and Zhang, BS and Yu, L and Feng, J and Liu, ZG and Feng, R and Jiang, ZX and Huang, RB and Jing, HM and Ren, JH and Zhu, XY and Cheng, YF and Li, YH and Zhou, HB and Gao, D and Liu, Y and Yu, F and Wang, X and Qiao, JL and Hu, DH and Wang, LL and Zang, MT and Chen, Q and Qu, QY and Zhou, JY and Li, ML and Chen, YX and Huang, QS and Fu, HX and Li, YY and Wang, QF and Huang, XJ and Zhang, XH and , },
title = {Correlation Between Fecal Microbiota and Corticosteroid Responsiveness in Primary Immune Thrombocytopenia: an Exploratory Study.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2410417},
doi = {10.1002/advs.202410417},
pmid = {40040609},
issn = {2198-3844},
support = {2023YFC2507803//Key Technologies Research and Development Program/ ; 82300149//National Natural Science Foundation of China/ ; 82130008//National Natural Science Foundation of China/ ; 82230004//National Natural Science Foundation of China/ ; 82350004//National Natural Science Foundation of China/ ; 82430006//National Natural Science Foundation of China/ ; 2024M761208//China Postdoctoral Science Foundation/ ; 2023ZB182//Department of Human Resources and Social Security of Jiangsu Province/ ; 2022-1-4082//Capital Health Research and Development of Special Fund/ ; 7242154//Natural Science Foundation of Beijing Municipality/ ; 7232188//Natural Science Foundation of Beijing Municipality/ ; 71003Y3035//Peking University Medicine/ ; },
abstract = {Corticosteroids (CSs) are the initial therapy for immune thrombocytopenia (ITP); however, their efficacy is not adequately predicted. As a novel biomarker, the composition of the gut microbiota is non-invasively tested and altered in patients with ITP. This study aims to develop a predictive model that leverages gut microbiome data to predict the CS response in patients with ITP within the initial four weeks of treatment. Metagenomic sequencing is performed on fecal samples from 212 patients with ITP, 152 of whom underwent CS treatment and follow-up. Predictive models are trained using six machine-learning algorithms, integrating clinical indices and gut microbiome data. The support vector machine (SVM) algorithm-based model has the highest accuracy (AUC = 0.80). This model utilized a comprehensive feature set that combined clinical data (including sex, age, duration, platelet count, and bleeding scales) with selected microbial species (including Bacteroides ovatus, Bacteroides xylanisolvens, and Parabacteroides gordonii), alpha diversities, KEGG pathways, and microbial modules. This study will provide new ideas for the prediction of clinical CS efficacy, enabling informed decision-making regarding the initiation of CS or personalized treatment in patients with ITP.},
}

@article {pmid40038211,
year = {2025},
author = {Malik, S and Naqvi, SAA and Shadali, AH and Khan, H and Christof, M and Niu, C and Schwartz, DA and Adler, DG},
title = {Fecal Microbiota Transplantation (FMT) and Clinical Outcomes Among Inflammatory Bowel Disease (IBD) Patients: An Umbrella Review.},
journal = {Digestive diseases and sciences},
volume = {},
number = {},
pages = {},
pmid = {40038211},
issn = {1573-2568},
abstract = {BACKGROUND AND AIMS: Recent systematic reviews and meta-analyses (SRMAs) have shown inconsistent effectiveness of FMT among patients with IBD. This study aimed to appraise the evidence for clinically relevant outcomes with FMT in patients with IBD using published SRMAs.

METHODS: We searched major databases from inception through Nov 2023 to identify SRMAs assessing the effectiveness of FMT in patients with IBD. Primary outcomes included clinical remission, clinical response, endoscopic remission/response, a composite endpoint, and adverse effects. We included SRMAs investigating FMT's effect in patients with IBD using RCTs and observational studies data. Methodological quality and evidence certainty were assessed using AMSTAR 2 and GRADE.

RESULTS: Out of 106 citations, 16 SRMAs were included with varying study sizes (2 to 60 primary studies) and participants (112 to 1169 per SRMA). Five SRMAs assessed FMT in IBD, while 11 focused on Ulcerative Colitis (UC). Seven SRMAs included RCTs only, and nine included both RCTs and observational studies. Methodological quality was critically low in 9 SRMAs (56%) and low in 7 studies (44%). FMT showed clinical remission benefit in all 16 SRMAs, with varying certainty: 3 high, 4 moderate, 4 low, and 5 very low. Endoscopic remission/response was reported in 5 meta-analyses on UC, with 1 high, 3 moderate, and 1 very low certainty. Combined clinical remission and endoscopic response were reported in 3 SRMAs on UC, with 1 low and 2 moderate certainty. Adverse events were reported in 6 SRMAs, with 1 high, 3 moderate, 1 low, and 1 very low certainty.

CONCLUSION: Current evidence shows potential benefits of FMT in IBD, particularly UC, supported by significant associations in 16 meta-analyses. However, poor methodological quality and variability in evidence certainty call for high-quality RCTs to strengthen the evidence.},
}

@article {pmid40037667,
year = {2025},
author = {Wei, Y and Qin, L and Wu, X and Li, D and Qian, D and Jiang, H and Geng, Q},
title = {Faecal microbiota transplantation combined with platinum-based doublet chemotherapy and tislelizumab as first-line treatment for driver-gene negative advanced non-small cell lung cancer (NSCLC): study protocol for a prospective, multicentre, single-arm exploratory trial.},
journal = {BMJ open},
volume = {15},
number = {3},
pages = {e094366},
pmid = {40037667},
issn = {2044-6055},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/therapy/drug therapy ; *Lung Neoplasms/therapy/drug therapy ; *Fecal Microbiota Transplantation/methods ; Prospective Studies ; *Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; Antibodies, Monoclonal, Humanized/therapeutic use ; Adult ; Female ; Multicenter Studies as Topic ; Male ; Middle Aged ; Combined Modality Therapy ; Aged ; },
abstract = {INTRODUCTION: The standard first-line treatment for driver-gene negative advanced non-small cell lung cancer (NSCLC) is chemotherapy combined with immunotherapy. However, owing to the immune microenvironment imbalance and immune status impairment caused by repeated chemotherapy, as well as the primary or secondary resistance to immune checkpoint inhibitors, the efficacy of immunotherapy combined with chemotherapy remains unsatisfactory. Recent studies have shown that faecal microbiota transplantation (FMT) can modulate the intestinal microflora, influence the tumour immune microenvironment and even enhance the efficacy of immunotherapy. Hence, we conduct such a prospective, exploratory study to evaluate the efficacy and safety of integrating FMT with standard first-line treatment in patients with driver-gene negative advanced NSCLC.

METHODS AND ANALYSIS: FMT-JSNO-02 (NCT06403111) is a prospective, multicentre, single-arm exploratory study. It is planned to include 62 cases of previously untreated driver-gene negative, Eastern Cooperative Oncology Group Performance Status 0-1, programmed death ligand 1<50% advanced NSCLC patients, who will be given FMT by orally ingested stool capsules on the basis of standard first-line treatment of chemotherapy combined with immunotherapy. The primary endpoint of this study is the 12-month progression-free survival rate.

ETHICS AND DISSEMINATION: The study was approved by the ethics committee of the Second People's Hospital of Changzhou (number [2024] YLJSA005) and is being conducted in accordance with the principles of the Declaration of Helsinki. The results of this study will be disseminated through publication in a peer-reviewed journal and presentation at scientific conferences.

TRIAL REGISTRATION NUMBER: NCT06403111. Date of registration: 7 May 2024, the first version protocol.},
}

Humans
*Carcinoma, Non-Small-Cell Lung/therapy/drug therapy
*Lung Neoplasms/therapy/drug therapy
*Fecal Microbiota Transplantation/methods
Prospective Studies
*Antineoplastic Combined Chemotherapy Protocols/therapeutic use
Antibodies, Monoclonal, Humanized/therapeutic use
Adult
Female
Multicenter Studies as Topic
Male
Middle Aged
Combined Modality Therapy
Aged

@article {pmid40037430,
year = {2025},
author = {Gao, J and He, Y and Shi, F and Hou, F and Wu, X and Yi, Y and Zhang, Y and Gong, Q},
title = {Activation of Sirt6 by icariside Ⅱ alleviates depressive behaviors in mice with poststroke depression by modulating microbiota-gut-brain axis.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2025.03.002},
pmid = {40037430},
issn = {2090-1224},
abstract = {BACKGROUND: Sirt6-mediated gut microbiota plays a vital role in poststroke depression (PSD). Icariside Ⅱ (ICS Ⅱ) is a naturally-occurring neuroprotectant with Sirt6 induction potency. However, it is unknown whether ICS Ⅱ protects against PSD through modulation of gut microbiota.

OBJECTIVE: This study aimed to reveal the effect and potential mechanisms of ICS Ⅱ on PSD, and the role of the microbiota-gut-brain axis was investigated.

METHODS: Using middle cerebral artery occlusion (MCAO) and chronic unpredictable mild stress (CUMS) to establish post-stroke depression (PSD) mice, we assessed anti-depressant effects of ICS Ⅱ via behavioral tests, immunohistochemistry, and western blot. Transcriptome profiling, molecular docking, and surface plasmon resonance were used to identify key targets. 16S rDNA genomic-derived taxonomic profiling and fecal microbiota transplantation (FMT) were conducted to figure out the mechanistic role of the gut microbiota and short-chain fatty acids (SCFAs).

RESULTS: ICS Ⅱ ameliorated depressive-like behaviors in PSD mice as evidenced by sucrose preference test, forced swimming test and tail suspension test. ICS Ⅱ restored mitochondrial function, reduced oxidative damage and pro-inflammatory cytokines both in brain and intestine through regulation of Sirt6/NF-κB pathway. ICS Ⅱ significantly increased the abundance of gut microbiota (such asAkkermansia and Ligilactobacillus), enhanced SCFAs concentrations, repaired intestinal barrier integrity and upreglated the tight junction protein expression. FMT from ICS II-treated mice replicated these benefits, confirming gut microbiota's role. Mechanistically, ICS Ⅱ directly bound to Sirt6 and enhanced its activity. However, ICS Ⅱ-mediated neuroprotection was neutralized in PSD mice or hydrogen peroxide-induced enteric glial cells when Sirt6 was absent.

CONCLUSION: Our findings expand the pharmacological properties of ICS II by demonstrating its ability to ameliorate PSD through modulation of the microbiota-gut-brain axis. ICS Ⅱ, as a novel Sirt6 activator, could be translated into an alternative microbiota-targeted avenue for coping with PSD.},
}

@article {pmid40037353,
year = {2025},
author = {Tian, S and Kim, MS and Zhao, J and Heber, K and Hao, F and Koslicki, D and Tian, S and Singh, V and Patterson, AD and Bisanz, JE},
title = {A designed synthetic microbiota provides insight to community function in Clostridioides difficile resistance.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2025.02.007},
pmid = {40037353},
issn = {1934-6069},
abstract = {Clostridioides difficile, a major cause of antibiotic-associated diarrhea, is suppressed by the gut microbiome, but the precise mechanisms are not fully described. Through a meta-analysis of 12 human studies, we designed a synthetic fecal microbiota transplant (sFMT1) by reconstructing microbial networks negatively associated with C. difficile colonization. This lab-built 37-strain consortium formed a functional community suppressing C. difficile in vitro and in animal models. Using sFMT1 as a tractable model system, we find that bile acid 7α-dehydroxylation is not a determinant of sFMT1 efficacy while one strain performing Stickland fermentation-a pathway of competitive nutrient utilization-is both necessary and sufficient for the suppression of C. difficile, replicating the efficacy of a human fecal transplant in a gnotobiotic mouse model. Our data illustrate the significance of nutrient competition in suppression of C. difficile and a generalizable approach to interrogating complex community function through robust methods to leverage publicly available sequencing data.},
}

@article {pmid40036939,
year = {2025},
author = {Mallick, K and Khodve, G and Ruwatia, R and Banerjee, S},
title = {Gut microbes: Therapeutic Target for neuropsychiatric disorders.},
journal = {Journal of psychiatric research},
volume = {184},
number = {},
pages = {27-38},
doi = {10.1016/j.jpsychires.2025.02.031},
pmid = {40036939},
issn = {1879-1379},
abstract = {Neuropsychiatric diseases encompass a range of mental and neurological disorders that have a significant and far-reaching effect on an individual's quality of life. These conditions affect not only the mental status but also the physical well-being of individuals, which leads to weakened immune systems and other diseases. Emerging research underscores a significant connection between the gut microbiome and neuropsychiatric diseases, suggesting that microbial communities within the gastrointestinal tract may influence brain function and mental health. Gut dysbiosis is caused by various factors, including stress, diet, inappropriate usage of antibiotics, infections, and so on, all of which can disrupt numerous pathways, resulting in abnormal neurotransmitter signaling, inflammation, and impaired brain function. Similarly, various neuropsychiatric diseases can disrupt the specific microbiome in the gut, leading to gut dysbiosis, often impairing memory and cognitive function. The growing evidence supporting the role of gut dysbiosis in neuropsychiatric disorders has opened up new avenues for therapeutic interventions. Modulating the gut microbiome through strategies such as probiotics, prebiotics, or fecal microbiota transplantation has shown promising results in various studies of neuropsychiatric disorders. However, further research is needed to fully elucidate the mechanisms involved in gut dysbiosis-associated brain changes to develop effective and personalized treatment strategies for neuropsychiatric diseases.},
}

@article {pmid40035163,
year = {2025},
author = {Longhitano, A and Roder, C and Blackmore, T and Campbell, A and May, M and Athan, E},
title = {Australasian Society of Infectious Diseases updated guidelines for the management of Clostridioides difficile infection in adults and children in Australia and New Zealand.},
journal = {Internal medicine journal},
volume = {},
number = {},
pages = {},
doi = {10.1111/imj.16638},
pmid = {40035163},
issn = {1445-5994},
abstract = {Clostridioides difficile infection (CDI) is associated with significant morbidity and mortality within the Australian population. Treatment recommendations for CDI pose challenges at both community and hospital-based levels due to the recurrent, refractory and potentially severe nature of the disease. Since the last published Australasian guidelines in 2016, new therapeutic options are available, prompting a necessary update to management recommendations. On behalf of the Australasian Society of Infectious Diseases, we present the updated guidelines for the management of CDI in adults and children exploring the changes to treatment recommendations - including the replacement of oral metronidazole with vancomycin for initial CDI and the emerging role for fidaxomicin and faecal-microbiota transplant.},
}

@article {pmid40033229,
year = {2025},
author = {Sóti, Á and Nagy, G and Győri, Z and Vass, T and Hetzman, L and Fenyves, BG and Varga, C},
title = {Tension pneumothorax from large bowel herniation and perforation as a late presentation of traumatic diaphragmatic hernia during pregnancy: a case report.},
journal = {International journal of emergency medicine},
volume = {18},
number = {1},
pages = {40},
pmid = {40033229},
issn = {1865-1372},
abstract = {BACKGROUND: Diaphragmatic hernias can be congenital or acquired, with trauma being the primary cause of the latter. Both types may have delayed presentations, with abdominal organs protruding into the thoracic cavity, causing symptoms of varying severity. Pregnancy can sometimes precipitate the condition. Tension pneumothorax resulting from bowel perforation into the thorax is exceptionally rare, with only a few cases reported. To the best of the authors knowledge, this is the third documented case of a late-presenting trauma-related diaphragmatic hernia during pregnancy, complicated by tension pneumothorax.

CASE PRESENTATION: A 30-year-old woman, 29 weeks pregnant, was referred to Semmelweis University emergency department with moderate dyspnea. Initial investigation revealed tension pneumothorax. Chest tube placement released air, pus, and feces. Computer tomography identified a diaphragmatic hernia with bowel incarceration and perforation as the underlying cause. The patient underwent a delayed cesarean section and surgical repair, with a good outcome. A history of thoracic trauma eight years prior was later revealed.

CONCLUSION: Evaluating pregnant patients with shortness of breath in the emergency department is challenging. Identifying a history of thoracic or abdominal trauma is crucial, as this can raise the suspicion of diaphragmatic hernia, which can present with a wide range of symptoms. Spontaneous tension pneumothorax in pregnant women is extremely rare and requires cautious management. A multidisciplinary approach is crucial for the successful treatment of maternal diaphragmatic hernia.},
}

@article {pmid40027572,
year = {2025},
author = {Zhang, JG and Wang, YW and Wang, QY and Wen, B},
title = {Clinical features and risk factors for combined Klebsiella pneumoniae infection in patients with liver cirrhosis.},
journal = {World journal of hepatology},
volume = {17},
number = {2},
pages = {103648},
pmid = {40027572},
issn = {1948-5182},
abstract = {This article discusses the findings presented by Zhang et al. They analyzed the risk factors and clinical characteristics associated with Klebsiella pneumoniae infection in patients with liver cirrhosis treated at a hospital in Beijing. In this article, we focus on the connection between chronic kidney disease and the intestinal microbiota, and propose microbiota transplantation as a potential treatment for this patient group. We also examine an intriguing phenomenon related to hepatic encephalopathy, and provide insights into the future research.},
}

@article {pmid40027490,
year = {2025},
author = {Xie, C and Cheng, J and Chen, P and Yan, X and Luo, C and Qu, H and Shu, D and Ji, J},
title = {Integrating gut and IgA-coated microbiota to identify Blautia as a probiotic for enhancing feed efficiency in chickens.},
journal = {iMeta},
volume = {4},
number = {1},
pages = {e264},
pmid = {40027490},
issn = {2770-596X},
abstract = {This study explores the role of IgA-coated bacteria in improving feed efficiency in chickens, offering a novel perspective for probiotic screening. Chickens with high feed efficiency were found to have a greater abundance of Gram-positive bacteria, while low feed efficiency chickens exhibited higher levels of Gram-negative bacteria and potential pathogens. Through fecal microbiota transplantation (FMT) and integrating analysis of cecal and IgA-coated microbiota, we precisely identified Blautia as a key genus linked to improved feed efficiency. Further validation demonstrated that Blautia coccoides, a representative species of this genus, enhances feed efficiency and activates B cells to produce Immunoglobulin A (IgA), both in vivo and in vitro. Our findings provide new insights into the potential of IgA-coated bacteria as functional probiotics, offering a promising strategy for enhancing feed efficiency in animal production.},
}

@article {pmid40027485,
year = {2025},
author = {Liu, Y and Li, H and Sun, T and Sun, G and Jiang, B and Liu, M and Wang, Q and Li, T and Cao, J and Zhao, L and Xiao, F and Zhao, F and Cui, H},
title = {Gut microbiome and metabolome characteristics of patients with cholesterol gallstones suggest the preventive potential of prebiotics.},
journal = {iMeta},
volume = {4},
number = {1},
pages = {e70000},
pmid = {40027485},
issn = {2770-596X},
abstract = {Cholesterol gallstones (CGS) still lack effective noninvasive treatment. The etiology of experimentally proven cholesterol stones remains underexplored. This cross-sectional study aims to comprehensively evaluate potential biomarkers in patients with gallstones and assess the effects of microbiome-targeted interventions in mice. Microbiome taxonomic profiling was conducted on 191 samples via V3-V4 16S rRNA sequencing. Next, 60 samples (30 age- and sex-matched CGS patients and 30 controls) were selected for metagenomic sequencing and fecal metabolite profiling via liquid chromatography-mass spectrometry. Microbiome and metabolite characterizations were performed to identify potential biomarkers for CGS. Eight-week-old male C57BL/6J mice were given a lithogenic diet for 8 weeks to promote gallstone development. The causal relationship was examined through monocolonization in antibiotics-treated mice. The effects of short-chain fatty acids such as sodium butyrate, sodium acetate (NaA), sodium propionate, and fructooligosaccharides (FOS) on lithogenic diet-induced gallstones were investigated in mice. Gut microbiota and metabolites exhibited distinct characteristics, and selected biomarkers demonstrated good diagnostic performance in distinguishing CGS patients from healthy controls. Multi-omics data indicated associations between CGS and pathways involving butanoate and propanoate metabolism, fatty acid biosynthesis and degradation pathways, taurine and hypotaurine metabolism, and glyoxylate and dicarboxylate metabolism. The incidence of gallstones was significantly higher in the Clostridium glycyrrhizinilyticum group compared to the control group in mice. The grade of experimental gallstones in control mice was significantly higher than in mice treated with NaA and FOS. FOS could completely inhibit the formation of gallstones in mice. This study characterized gut microbiome and metabolome alterations in CGS. C. glycyrrhizinilyticum contributed to gallstone formation in mice. Supplementing with FOS could serve as a potential approach for managing CGS by altering the composition and functionality of gut microbiota.},
}

@article {pmid40027479,
year = {2025},
author = {Shi, Y and Chen, Z and Fang, T and Chen, X and Deng, Y and Qin, H and Lian, M and Shen, J and Zong, Y and Chu, H and Hoebinger, C and Guo, H and Yuan, Z and Zheng, J and Zhou, Y and Pan, Y and Mendes, BG and Lang, S and Hendrikx, T and Zeng, S and Cao, H and Yang, L and Chen, L and Chen, P and Dai, L and Wang, H and Yin, S and Zhu, S and Ma, X and Schnabl, B and Chen, H and Duan, Y},
title = {Gut microbiota in treating inflammatory digestive diseases: Current challenges and therapeutic opportunities.},
journal = {iMeta},
volume = {4},
number = {1},
pages = {e265},
pmid = {40027479},
issn = {2770-596X},
support = {P30 DK120515/DK/NIDDK NIH HHS/United States ; P50 AA011999/AA/NIAAA NIH HHS/United States ; },
abstract = {Accumulating evidence indicates that the gut microbiota is intricately involved in the initiation and progression of human diseases, forming a multidirectional regulatory axis centered on intestinal microbiota. This article illustrates the challenges in exploring the role of the gut microbiota in inflammatory digestive diseases, such as metabolic dysfunction-associated steatotic liver disease (MASLD) and inflammatory bowel disease (IBD), and summarizes the existing microbiome-focused treatment strategies (probiotics, prebiotics, symbiotics, fecal microbiota transplantation, and bacteriophages therapy), emerging technologies (gut microbiome-on-a-chip and artificial intelligence), as well as possible future research directions. Taken together, these therapeutic strategies and technologies present both opportunities and challenges, which require researchers and clinicians to test the rationality and feasibility of various therapeutic modalities in continuous practice.},
}

@article {pmid39805029,
year = {2025},
author = {Xiong, Y and Lu, X and Li, B and Xu, S and Fu, B and Sha, Z and Tian, R and Yao, R and Li, Q and Yan, J and Guo, D and Cong, Z and Du, Y and Lin, X and Wu, H},
title = {Bacteroides Fragilis Transplantation Reverses Reproductive Senescence by Transporting Extracellular Vesicles Through the Gut-Ovary Axis.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {12},
number = {9},
pages = {e2409740},
pmid = {39805029},
issn = {2198-3844},
support = {92369115,92469110,82422048//National Natural Science Foundation of China/ ; 2024CDJXY-016//Fundamental Research Funds for the Central Universities/ ; CSTB2023NSCQMSX0402//Natural Science Foundation of Chongqing, China/ ; cstc2021ycjh-bgzxm0099//Chongqing Talents: Exceptional Young Talents Project/ ; },
mesh = {*Extracellular Vesicles/metabolism ; Female ; *Bacteroides fragilis/metabolism ; Animals ; *Gastrointestinal Microbiome/physiology ; Mice ; *Ovary/metabolism/microbiology ; Reproduction/physiology ; Fecal Microbiota Transplantation/methods ; Models, Animal ; Aging/metabolism/physiology ; },
abstract = {The diverse and dynamic population of microorganisms present in the gut microbiota may affect host health. There are evidences to support the role of gut microbiota as a key player in reproductive development. Unfortunately, the relationship between reproductive disorders caused by aging and gut microbiota remains largely unknown. Here, it is shown for the first time that gut microorganism Bacteroides fragilis (BF) transplantation ameliorates ovarian aging by transporting extracellular vesicles (EVs) through the gut-ovary axis. Mechanistically, miR-1246 is enriched in EVs derived from BF-treated intestinal cells, and these miR-1246-enriched EVs are transferred to ovaries, thereby effectively improving reproductive senescence by reducing oxidative stress in the ovaries. Specifically, miR-1246 reduces the ubiquitination of p62 and stabilizes the protein level of p62 by targeting E3 ligase SKP2. Then Keap1-Nrf2 complex is dissociated and Keap1 is recruited to form the p62-Keap1 complex. With the dissociation of Keap1-Nrf2 complex, Nrf2 is released and activated, thus promoting the transcription of antioxidant enzymes and relieving reproductive senescence. Collectively, the data indicates that intestinal cell-derived EVs serve as natural information carriers in the crosstalk between the gut and the ovary, and intestinal microorganism transplantation is a promising approach for the treatment of ovarian dysfunction diseases.},
}

*Extracellular Vesicles/metabolism
Female
*Bacteroides fragilis/metabolism
Animals
*Gastrointestinal Microbiome/physiology
Mice
*Ovary/metabolism/microbiology
Reproduction/physiology
Fecal Microbiota Transplantation/methods
Models, Animal
Aging/metabolism/physiology

@article {pmid38579985,
year = {2025},
author = {Tao, W and Zhang, Y and Wang, B and Nie, S and Fang, L and Xiao, J and Wu, Y},
title = {Advances in molecular mechanisms and therapeutic strategies for central nervous system diseases based on gut microbiota imbalance.},
journal = {Journal of advanced research},
volume = {69},
number = {},
pages = {261-278},
doi = {10.1016/j.jare.2024.03.023},
pmid = {38579985},
issn = {2090-1224},
mesh = {*Gastrointestinal Microbiome ; Humans ; Animals ; *Central Nervous System Diseases/microbiology/therapy/metabolism ; *Probiotics/therapeutic use ; *Prebiotics/administration & dosage ; Fecal Microbiota Transplantation/methods ; Mice ; Dysbiosis/microbiology/therapy ; },
abstract = {BACKGROUD: Central nervous system (CNS) diseases pose a serious threat to human health, but the regulatory mechanisms and therapeutic strategies of CNS diseases need to be further explored. It has been demonstrated that the gut microbiota (GM) is closely related to CNS disease. GM structure disorders, abnormal microbial metabolites, intestinal barrier destruction and elevated inflammation exist in patients with CNS diseases and promote the development of CNS diseases. More importantly, GM remodeling alleviates CNS pathology to some extent.

AIM OF REVIEW: Here, we have summarized the regulatory mechanism of the GM in CNS diseases and the potential treatment strategies for CNS repair based on GM regulation, aiming to provide safer and more effective strategies for CNS repair from the perspective of GM regulation.

The abundance and composition of GM is closely associated with the CNS diseases. On the basis of in-depth analysis of GM changes in mice with CNS disease, as well as the changes in its metabolites, therapeutic strategies, such as probiotics, prebiotics, and FMT, may be used to regulate GM balance and affect its microbial metabolites, thereby promoting the recovery of CNS diseases.},
}

*Gastrointestinal Microbiome
Humans
Animals
*Central Nervous System Diseases/microbiology/therapy/metabolism
*Probiotics/therapeutic use
*Prebiotics/administration & dosage
Fecal Microbiota Transplantation/methods
Mice
Dysbiosis/microbiology/therapy

@article {pmid40026419,
year = {2025},
author = {Marizzoni, M and Tournier, BB and Chevalier, C and Saleri, S and Lathuilière, A and Ceyzériat, K and Paquis, A and Park, R and Troesch, E and Cattaneo, A and Millet, P and Frisoni, GB},
title = {Stools from a human APOEe2 donor reduces amyloid and tau pathology and increases neuroinflammation in a 3xTg AD mouse model.},
journal = {Frontiers in aging neuroscience},
volume = {17},
number = {},
pages = {1539067},
pmid = {40026419},
issn = {1663-4365},
abstract = {BACKGROUND: The mechanisms underlying the protective effect of the e2 variant of the APOE gene (APOEe2) against Alzheimer's disease (AD) have not been elucidated. We altered the microbiota of 3xTgAD mice by fecal microbiota transplantation from a human APOEe2 donor (e2-FMT) and tested the effect of microbiota perturbations on brain AD pathology.

METHODS: FMT of bacteria isolated from stools of untreated 3xTgAD mice (M-FMT) or e2-FMT were transplanted in 15-month-old 3xTgAD mice. FMT was done alone or in combination with antibiotic and proton-pump inhibitor following the Microbiota Transfer Therapy protocol (MTT). The effect of donor (M or e2) and transplantation protocol (FMT or MTT) on hippocampal amyloid, tau pathology and neuroinflammation were assessed at the end of the treatment.

RESULTS: e2-FMT reduced amyloid, and tau pathology as well as increased neuroinflammation as compared with M-FMT. MTT was associated with reduced number of Aβ40+ plaques and tau pathology. Low levels of amyloid were associated with high levels of pro-inflammatory molecules in e2-FMT mice. These associations were partially attenuated by MTT.

CONCLUSION: Bacteria from a human APOEe2 donor reduced AD pathology and increased neuroinflammation in mice suggesting that the gut microbiota may be a mediator of the protective effect of APOEe2.},
}

@article {pmid40025650,
year = {2025},
author = {Qi, C and Li, Z and Tu, H and Sun, F and Guo, W and Di, C and He, R and Ze, X and Zhang, L and Gao, R and Hu, P and Yang, W and Li, K and Liu, J and Pan, X and Jin, Z and Sun, J},
title = {2'-FL and cross-feeding bifidobacteria reshaped the gut microbiota of infants with atopic dermatitis ex vivo and prevented dermatitis in mice post-microbiota transplantation through retinol metabolism activation.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2474148},
doi = {10.1080/19490976.2025.2474148},
pmid = {40025650},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome ; Mice ; Humans ; *Dermatitis, Atopic/microbiology/therapy/metabolism ; *Bifidobacterium/metabolism ; Infant ; *Trisaccharides/metabolism ; *Vitamin A/metabolism ; *Fatty Acids, Volatile/metabolism ; Milk, Human/metabolism ; Fecal Microbiota Transplantation ; Probiotics/administration & dosage ; Female ; Male ; Bifidobacterium bifidum/physiology/metabolism ; Mice, Inbred BALB C ; },
abstract = {2'-Fucosyllactose (2'-FL), a predominant human milk oligosaccharide, plays a crucial role in the development of the infant gut microbiota and immune system. However, the microbiota of infants with atopic dermatitis (AD) often has difficulty utilizing 2'-FL. Here, we found that strains from human milk, Bifidobacterium bifidum FN120 and Bifidobacterium longum subsp. longum FN103, utilized 2'-FL for growth by cross-feeding. Through an ex vivo continuous fermentation system, we found that 2'-FL and cross-feeding bifidobacteria synergistically enhanced the production of short-chain fatty acids (SCFAs), particularly acetate and propionate, while reshaping the gut microbiota in infants with AD. The reshaped microbiota was then transplanted into oxazolone-induced mice. We observed that AD symptoms in mice were effectively prevented, with significant changes in the ileum microbiota and increased intestinal SCFA levels. RNA sequencing analysis of Peyer's patches in the small intestine revealed activation of the retinol metabolic pathway. Nontargeted metabolomics analysis revealed a significant increase in plasma retinoate levels, which correlated markedly with AD-related markers. Collectively, our study demonstrated that supplementation with cross-feeding bifidobacteria and 2'-FL reshaped the gut microbiota, activated retinol metabolic pathways, promoted immune tolerance, and thereby prevented AD. Our findings provide novel insights into the therapeutic potential of combining prebiotics and probiotics to modulate the gut - skin axis and support immune tolerance in early life, offering a promising strategy for infantile AD management and prevention.},
}

Animals
*Gastrointestinal Microbiome
Mice
Humans
*Dermatitis, Atopic/microbiology/therapy/metabolism
*Bifidobacterium/metabolism
Infant
*Trisaccharides/metabolism
*Vitamin A/metabolism
*Fatty Acids, Volatile/metabolism
Milk, Human/metabolism
Fecal Microbiota Transplantation
Probiotics/administration & dosage
Female
Male
Bifidobacterium bifidum/physiology/metabolism
Mice, Inbred BALB C

@article {pmid40025585,
year = {2025},
author = {Guo, H and Jiang, H and Liu, H},
title = {Case report of clostridium difficile infection after rectal resection with ileostomy.},
journal = {World journal of surgical oncology},
volume = {23},
number = {1},
pages = {70},
pmid = {40025585},
issn = {1477-7819},
mesh = {Humans ; *Ileostomy/adverse effects ; *Clostridioides difficile/isolation & purification ; *Rectal Neoplasms/surgery/pathology ; *Clostridium Infections/etiology/diagnosis/microbiology/therapy ; *Postoperative Complications/microbiology/diagnosis/etiology ; Male ; Prognosis ; Fecal Microbiota Transplantation/adverse effects ; Proctectomy/adverse effects ; Aged ; Middle Aged ; },
abstract = {Colorectal cancer is the third most common cancer worldwide, with high incidence and mortality rates. Surgical resection is the primary treatment for rectal cancer. To reduce the occurrence and severity of postoperative complications such as anastomotic leakage, prophylactic ileostomy is often performed concurrently. However, following ileostomy creation, there is a disruption in intestinal ecology, making patients susceptible to clostridium difficile infection. clostridium difficile is a Gram-positive anaerobic spore-forming bacterium that is resistant to most antibiotics due to spore formation, leading to high recurrence rates and treatment failure. Additionally, in the early stages of clostridium difficile infection, increased ileostomy output can be challenging to differentiate from normal postoperative conditions, potentially resulting in missed diagnosis, delayed treatment, and increased healthcare burden.This case report describes a case of high out-put ileostomy caused by clostridium difficile infection following rectal resection with ileostomy, which was successfully treated by fecal microbiota transplantation, providing evidence-based medicine for clinical practice.},
}

Humans
*Ileostomy/adverse effects
*Clostridioides difficile/isolation & purification
*Rectal Neoplasms/surgery/pathology
*Clostridium Infections/etiology/diagnosis/microbiology/therapy
*Postoperative Complications/microbiology/diagnosis/etiology
Male
Prognosis
Fecal Microbiota Transplantation/adverse effects
Proctectomy/adverse effects
Aged
Middle Aged

@article {pmid40024791,
year = {2025},
author = {Kushima, H and Ishii, H},
title = {Cryptococcosis.},
journal = {Medical mycology journal},
volume = {66},
number = {1},
pages = {27-31},
doi = {10.3314/mmj.25.001},
pmid = {40024791},
issn = {2186-165X},
mesh = {Humans ; *Cryptococcosis/immunology/drug therapy/diagnosis ; *Cryptococcus neoformans/isolation & purification/immunology/pathogenicity ; *Immunocompromised Host ; Animals ; Antifungal Agents/therapeutic use ; Organ Transplantation/adverse effects ; },
abstract = {Approximately one million new cases of cryptococcosis develop each year worldwide, resulting in approximately 600,000 deaths. Most cases occurred in HIV patients from African countries south of the Sahara Desert. In light of this situation, in 2022, the World Health Organization presented a list of priority fungal pathogens to guide research, development, and public health action, with Cryptococcus neoformans as the most important critical fungus. In contrast, a recent retrospective study in developed countries showed that 90% of cases with cryptococcosis were non-HIV patients, including immunocompetent individuals. Underlying diseases of non-HIV immunocompromised patients include cancer and solid organ transplantation. High serum titers cryptococcal antigens independently predicted the risk of central nervous system involvement. Even if the patient is asymptomatic, high antigen levels are considered a possibility of cryptococcal meningitis, and a spinal fluid examination may be recommended. The absence of a history of contact with pigeons should not be used as a basis for denying cryptococcosis because C. neoformans is often detected in old and dried feces of chickens other than pigeons. Donor-derived cryptococcosis is a unique feature of cryptococcosis in solid organ transplant recipients. Pre-transplant screening tests for cryptococcosis, pre-transplant treatment for the donor, and prophylactic antifungal therapy for the recipient may be useful. Defense against cryptococcal infection is regulated by various mechanisms, including Th1, Th2, and Th17 immune responses. Molecularly targeted medicines that target specific cytokines or surface antigen molecules have been widely used with excellent clinical efficacy for the treatment of various diseases. Since cryptococcosis has been recently reported to develop during the use of certain medicines, such as ibrutinib and eculizumab, clinicians need to be mindful that the number of similar cases may increase in the future.},
}

Humans
*Cryptococcosis/immunology/drug therapy/diagnosis
*Cryptococcus neoformans/isolation & purification/immunology/pathogenicity
*Immunocompromised Host
Animals
Antifungal Agents/therapeutic use
Organ Transplantation/adverse effects

@article {pmid40024538,
year = {2025},
author = {Sliti, A and Kim, RH and Lee, D and Shin, JH},
title = {Whole Genome Sequencing and In Silico Analysis of the Safety and Probiotic Features of Lacticaseibacillus paracasei FMT2 Isolated from Fecal Microbiota Transplantation (FMT) Capsules.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {107405},
doi = {10.1016/j.micpath.2025.107405},
pmid = {40024538},
issn = {1096-1208},
abstract = {Lacticaseibacillus paracasei is widely used as a probiotic supplement and food additive in the medicinal and food industries. However, its application requires careful evaluation of safety traits associated with probiotic pathogenesis, including the transfer of antibiotic-resistance genes, the presence of virulence and pathogenicity factors, and the potential disruptions of the gut microbiome and immune system. In this study, we conducted whole genome sequencing (WGS) of L. paracasei FMT2 isolated from fecal microbiota transplantation (FMT) capsules and performed genome annotation to assess its probiotic and safety attributes. Our comparative genomic analysis assessed this novel strain's genetic attributes and functional diversity and unraveled its evolutionary relationships with other L. paracasei strains. The assembly yielded three contigs: one corresponding to the chromosome and two corresponding to plasmids. Genome annotation revealed the presence of 2,838 DNA-coding sequences (CDS), 78 ribosomal RNAs (rRNAs), 60 transfer RNAs (tRNAs), three non-coding RNAs (ncRNAs), and 126 pseudogenes. The strain lacked antibiotic resistance genes and pathogenicity factors. Two intact prophages, one Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR) region, and three antimicrobial peptide gene clusters were identified, highlighting the genomic stability and antimicrobial potential of the strain. Furthermore, genes linked to probiotic functions, such as mucosal colonization, stress resistance, and biofilm formation, were characterized. The pan-genome analysis identified 3,358 orthologous clusters, including 1,775 single-copy clusters, across all L. paracasei strains. Notably, L. paracasei FMT2 contained many unique singleton genes, potentially contributing to its distinctive probiotic properties. Our findings confirm the potential of L. paracasei FMT2 for food and therapeutic applications based on its probiotic profile and safety.},
}

@article {pmid40024260,
year = {2025},
author = {Karmisholt Grosen, A and Mikkelsen, S and Aas Hindhede, L and Ellegaard Paaske, S and Dahl Baunwall, SM and Mejlby Hansen, M and Frederik Dahlerup, J and Steen Mortensen, M and Rask Licht, T and Kjærgaard Boldsen, J and Tornvig Erikstrup, L and Lodberg Hvas, C and Erikstrup, C},
title = {Effects of clinical donor characteristics on the success of faecal microbiota transplantation for patients in Denmark with Clostridioides difficile infection: a single-centre, prospective cohort study.},
journal = {The Lancet. Microbe},
volume = {},
number = {},
pages = {101034},
doi = {10.1016/j.lanmic.2024.101034},
pmid = {40024260},
issn = {2666-5247},
abstract = {BACKGROUND: Faecal microbiota transplantation (FMT) is an effective treatment for patients with recurrent Clostridioides difficile infection, but donor selection can influence its clinical success. We aimed to investigate the effect of clinical donor characteristics on FMT outcomes in patients with C difficile infection.

METHODS: In this single-centre, prospective cohort study, we included all donors who fulfilled the national criteria for faeces donation and delivered donations to the Centre for Faecal Microbiota Transplantation, Aarhus University Hospital, Denmark, between May 2, 2016, and Oct 31, 2023, and corresponding recipients treated with one-dose FMT for primary or recurrent C difficile infection. In mixed-effects models, we evaluated the effect of donor sex, age, BMI, smoking status, donation stool consistency, total donation weight, antibiotic use, Helicobacter pylori carriage, birth mode, donor-recipient sex concordance, and the alpha diversity of faeces donations on FMT outcomes in recipients. The primary outcome was the resolution of diarrhoea associated with C difficile infection in patients 8 weeks after FMT.

FINDINGS: Among 145 blood donors who also donated faeces, 115 (79·3%) were men and 30 (20·7%) were women. 90 (62·1%) provided faeces for 1351 evaluable FMTs in 952 patients with C difficile infection. 1037 (76·8%) FMTs were administered through oral capsules, 151 (11·2%) via colonoscopy, and 163 FMTs (12·1%) via nasojejunal tube. Antibiotic use 3-12 months before donation decreased the effectiveness of FMT (odds ratio 0·55 [95% CI 0·33-0·91]; p=0·019). Compared with donations with a Bristol Stool Form Scale (BSFS) score of 3, donations with a score of 4 (odds ratio 1·38 [95% CI 1·04-1·83]; p=0·024) and 5 or above (2·89 [1·33-6·26]; p=0·0072) showed improved FMT effectiveness. Donor sex, BMI, smoking status, H pylori carriage, birth mode, total donation weight, and donor-recipient sex concordance did not affect FMT outcomes.

INTERPRETATION: Expanding current donor selection criteria to avoid antibiotic use in the 12 months preceding donation and including donations with a BSFS score of 5 might improve FMT outcomes for patients with C difficile infection. Our findings call for the revision of current clinical donor screening practices, and future studies could further optimise the criteria for selecting optimal faeces donors.

FUNDING: Innovation Fund Denmark.},
}

@article {pmid40023843,
year = {2025},
author = {Golomb, SM and Guldner, IH and Aleksandrovic, E and Fross, SR and Liu, X and Diao, L and Liang, K and Wu, J and Wang, Q and Lopez, JA and Zhang, S},
title = {Temporal dynamics of immune cell transcriptomics in brain metastasis progression influenced by gut microbiome dysbiosis.},
journal = {Cell reports},
volume = {44},
number = {3},
pages = {115356},
doi = {10.1016/j.celrep.2025.115356},
pmid = {40023843},
issn = {2211-1247},
abstract = {Interactions between metastatic cancer cells and the brain microenvironment regulate brain metastasis (BrMet) progression. Central nervous system (CNS)-native and peripheral immune cells influence the BrMet immune landscape, but the dynamics and factors modulating this microenvironment remain unclear. As the gut microbiome impacts CNS and peripheral immune activity, we investigated its role in regulating immune response dynamics throughout BrMet stages. Antibiotic-induced (ABX) gut dysbiosis significantly increased BrMet burden versus controls but was equalized with fecal matter transplantation, highlighting microbiome diversity as a regulator of BrMet. Single-cell sequencing revealed a highly dynamic immune landscape during BrMet progression in both conditions. However, the timing of the monocyte inflammatory response was altered. Microglia displayed an elevated activation signature in late-stage metastasis in ABX-treated mice. T cell and microglia perturbation revealed involvement of these cell types in modulating BrMet under gut dysbiosis. These data indicate profound effects on immune response dynamics imposed by gut dysbiosis across BrMet progression.},
}

@article {pmid40023320,
year = {2025},
author = {Petracco, G and Faimann, I and Reichmann, F},
title = {Inflammatory bowel disease and neuropsychiatric disorders: Mechanisms and emerging therapeutics targeting the microbiota-gut-brain axis.},
journal = {Pharmacology & therapeutics},
volume = {},
number = {},
pages = {108831},
doi = {10.1016/j.pharmthera.2025.108831},
pmid = {40023320},
issn = {1879-016X},
abstract = {Crohn's disease (CD) and ulcerative colitis (UC) are the two major entities of inflammatory bowel disease (IBD). These disorders are known for their relapsing disease course and severe gastrointestinal symptoms including pain, diarrhoea and bloody stool. Accumulating evidence suggests that IBD is not only restricted to the gastrointestinal tract and that disease processes are able to reach distant organs including the brain. In fact, up to 35 % of IBD patients also suffer from neuropsychiatric disorders such as generalized anxiety disorder and major depressive disorder. Emerging research in this area indicates that in many cases these neuropsychiatric disorders are a secondary condition as a consequence of the disturbed communication between the gut and the brain via the microbiota-gut-brain axis. In this review, we summarise the current knowledge on IBD-associated neuropsychiatric disorders. We examine the role of different pathways of the microbiota-gut-brain axis in the development of CNS disorders highlighting altered neural, immunological, humoral and microbial communication. Finally, we discuss emerging therapies targeting the microbiota-gut-brain axis to alleviate IBD and neuropsychiatric symptoms including faecal microbiota transplantation, psychobiotics, microbial metabolites and vagus nerve stimulation.},
}

@article {pmid40022204,
year = {2025},
author = {Debray, R and Dickson, CC and Webb, SE and Archie, EA and Tung, J},
title = {Shared environments complicate the use of strain-resolved metagenomics to infer microbiome transmission.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {59},
pmid = {40022204},
issn = {2049-2618},
support = {R01AG071684/NH/NIH HHS/United States ; R01AG071684/NH/NIH HHS/United States ; R61AG078470//National Science Foundation/ ; R61AG078470//National Science Foundation/ ; },
mesh = {Animals ; *Metagenomics/methods ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation ; Humans ; Papio/microbiology ; Feces/microbiology ; Bacteria/classification/genetics/isolation & purification ; Metagenome ; },
abstract = {BACKGROUND: In humans and other social animals, social partners have more similar microbiomes than expected by chance, suggesting that social contact transfers microorganisms. Yet, social microbiome transmission can be difficult to identify based on compositional data alone. To overcome this challenge, recent studies have used information about microbial strain sharing (i.e., the shared presence of highly similar microbial sequences) to infer transmission. However, the degree to which strain sharing is influenced by shared traits and environments among social partners, rather than transmission per se, is not well understood.

RESULTS: Here, we first use a fecal microbiota transplant dataset to show that strain sharing can recapitulate true transmission networks under ideal settings when donor-recipient pairs are unambiguous and recipients are sampled shortly after transmission. In contrast, in gut metagenomes from a wild baboon population, we find that demographic and environmental factors can override signals of strain sharing among social partners.

CONCLUSIONS: We conclude that strain-level analyses provide useful information about microbiome similarity, but other facets of study design, especially longitudinal sampling and careful consideration of host characteristics, are essential for inferring the underlying mechanisms of strain sharing and resolving true social transmission network. Video Abstract.},
}

Animals
*Metagenomics/methods
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation
Humans
Papio/microbiology
Feces/microbiology
Bacteria/classification/genetics/isolation & purification
Metagenome

@article {pmid40020386,
year = {2025},
author = {Zhang, W and Qi, X and Han, M and Jia, Q and Li, X and Yin, W and Wang, Y and Wu, H and Shao, H and Peng, C and Su, C and Sai, L},
title = {Activation of Sirt1 by acetate alleviates silicofibrosis: Contribution of the gut microbiota.},
journal = {Ecotoxicology and environmental safety},
volume = {292},
number = {},
pages = {117969},
doi = {10.1016/j.ecoenv.2025.117969},
pmid = {40020386},
issn = {1090-2414},
abstract = {Silicosis is a prevalent occupational disease marked by progressive pulmonary fibrosis. Despite its significant health burden, the pathogenesis of silicosis remains unclear, and no specific therapeutic drugs are available. In this study, we developed a novel intervention strategy targeting gut microbiota and investigated its underlying mechanisms. Using 16S rRNA gene sequencing, we observed significant gut microbiota dysbiosis in silicosis rats at different times (1-8 weeks), notably characterized by altered relative abundance of Ruminococcus and Lactobacillus. Fecal microbiota transplantation altered the gut microbiota structure of silicosis rats, alleviated silica-induced lung histopathological injury, with LEfSe analysis identifying Bifidobacterium as a potential biomarker. Treatment with Bifidobacterium reduced the level of pro-inflammatory cytokines (IL-1β, IL-6 and TNF-α) and fibrosis markers (collagen III, α-SMA and vimentin) in the lungs of silicosis rats, accompanied with increased serum acetic acid levels. Acetate, a major metabolite of Bifidobacterium, demonstrated similar protective effects against silicosis in this study, suggesting its role as a key mediator of Bifidobacterium action in the lungs. Both Bifidobacterium and acetate significantly upregulated Sirt1 in intestinal and lung tissues, while Sirt1 inhibition diminished their benefits to silicosis. As a widely studied histone deacetylase, Sirt1 was proven to be markedly reduced in the lungs of silicosis rats in this study. EX-527, a potent Sirt1 inhibitor, could worsen silicosis damage by upregulating the level of TGF-β1 and the degree of Smad2/3 acetylation. Our study highlights the efficacy of postbiotics, such as Bifidobacterium and acetate, and identifies Sirt1 as a promising target for silicosis treatment.},
}

@article {pmid40019272,
year = {2025},
author = {Peng, C and Lei, P and Qi, H and Zhu, Q and Huang, C and Fu, J and Zhao, C},
title = {Effect of fecal microbiota transplantation on diabetic wound healing through the IL-17A-mTOR-HIF1α signaling axis.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0201924},
doi = {10.1128/aem.02019-24},
pmid = {40019272},
issn = {1098-5336},
abstract = {UNLABELLED: Diabetes is the third most common chronic disorder worldwide. Diabetic wounds are a severe complication that is costly and often results in non-traumatic lower limb amputation. Recent investigations have demonstrated that the gut microbiota as a "virtual organ" can regulate metabolic diseases like diabetes. Fecal microbiota transplantation (FMT) is an innovative therapeutic approach for promoting wound healing, but its function remains incompletely defined. A diabetes model was established by supplying mice with a high-fat diet and performing an intraperitoneal injection of streptozotocin. Diabetic wounds were then created, followed by bacterial transplantation. The relevant indexes of wound healing were evaluated to verify the promoting effect of FMT on the diabetic wounds. Human skin keratinocytes were also cultured, and cell scratch experiments were conducted to further investigate the underlying mechanism. The FMT regulated the levels of specific bacteria in the diabetic mice and helped restore the balance of intestinal microbes. This transplantation also enhanced wound healing in the diabetic mice by augmenting the closure rate, accelerating re-epithelialization, and boosting collagen deposition in skin wounds. Furthermore, FMT promoted the production of IL-17A, which significantly enhanced the growth and movement of human keratinocytes. Inhibiting molecules related to the IL-17A-mTOR-HIF1α signaling axis were shown to hinder wound re-epithelialization.This study clarifies the function of the IL-17A-mTOR-HIF1α signaling axis in the utilization of FMT in diabetic wound healing, providing a new therapeutic method and target for promoting the healing of diabetic wounds.

IMPORTANCE: The Intestinal microbiota, as the organ with the largest number of microorganisms in the body, plays a crucial role in the physiological functions of the human body. Normal microbiota can be involved in various functions such as energy absorption, metabolism, and immunity of the body, and microbiota imbalance is related to many diseases such as obesity and diabetes. Diabetes, as one of the world's three major chronic diseases, is a significant health issue that troubles more than a billion people globally. Diabetic wounds are a problem that all diabetic patients must confront when undergoing surgery, and it is an important cause of non-traumatic amputations. Exploring the role of intestinal microorganisms in the wound-healing process of diabetic mice can offer the possibility of using microorganisms as a therapeutic means to intervene in clinically related diseases.},
}

@article {pmid40015179,
year = {2025},
author = {Patra, D and Dev, G and Hand, TW and Overacre-Delgoffe, A},
title = {Friends close, enemies closer: the complex role of the microbiome in antitumor immunity.},
journal = {Current opinion in immunology},
volume = {93},
number = {},
pages = {102537},
doi = {10.1016/j.coi.2025.102537},
pmid = {40015179},
issn = {1879-0372},
abstract = {Immunotherapy has achieved remarkable advances in cancer treatment by harnessing the immune system to combat tumors, yet its effectiveness remains inconsistent across patients and tumor types. The microbiota, a diverse assemblage of microorganisms residing at host barrier surfaces, is pivotal in shaping immune responses. This review explores the direct and indirect mechanisms via which the microbiota modulates antitumor immune responses both locally within the tumor microenvironment and systemically by affecting distant tumors. We discuss recent findings linking microbiota-derived metabolites and microbiota-derived antigens with antitumor immunity and immunotherapy response. Additionally, we discuss recent advances in microbiome-based therapies, including fecal microbiota transplantation. We propose the use and development of new analytical techniques to further characterize the complex functions and interactions between the microbiome and immune system. To conclude, we outline recommendations for future research and therapeutic approaches to leverage the microbiome to improve current immunotherapies.},
}

@article {pmid40015156,
year = {2025},
author = {Tang, L and Li, J and Luan, M and Qin, M and Zhong, C and Zhang, Y and Xie, Y and Shi, M and Qiu, L and Yu, J},
title = {Edgeworthia gardneri (Wall.) Meisn protects against HFD-induced murine atherosclerosis through improving gut microbiota-mediated intestinal barrier integrity.},
journal = {Atherosclerosis},
volume = {403},
number = {},
pages = {119132},
doi = {10.1016/j.atherosclerosis.2025.119132},
pmid = {40015156},
issn = {1879-1484},
abstract = {BACKGROUND: Gut microbiota plays a crucial role in the development and progression of atherosclerosis. Edgeworthia gardneri (Wall.) Meisn, a member of the Thymelaeaceae family and the Edgeworthia genus, has been previously shown in our studies to attenuate atherogenesis when administered orally as an ethanolic extract (EEEG). However, the interaction between EEEG and gut microbiota, and the mechanism by which gut microbiota exerts anti-atherosclerotic effects, remains unclear.

AIMS: This study aims to determine whether the anti-atherosclerotic properties of EEEG are associated with gut microbiota remodeling.

METHOD: Atherosclerosis was induced in ApoE[-/-] mice using a high-fat diet (HFD). The mice were treated with EEEG or Lactobacillus plantarum for 16 weeks. The composition of gut microbiota was analyzed through 16S rDNA sequencing. To assess whether the anti-atherosclerotic effects of EEEG depend on the gut microbiota, HFD-fed mice were treated with a cocktail of antibiotics or underwent fecal microbiota transplantation (FMT). Simultaneously, plaque areas in the aortic roots and whole aortas of apolipoprotein E deficient (ApoE[-/-]) mice were evaluated using oil red O staining and hematoxylin-eosin staining. Serum levels of LPS, fluorescein isothiocyanate-dextran, and expression levels of tight junction proteins were measured to identify the effects of EEEG on gut barrier dysfunction in HFD-fed ApoE[-/-] mice.

RESULTS: The results revealed that EEEG treatment significantly reduced atherosclerotic lesions by ameliorating lipid accumulation and preserving gut barrier integrity. The protective effects were abrogated by antibiotics administration, concomitant with an increase in gut barrier permeability by decreasing expression of tight junction proteins. The microbial analysis indicated an augmented abundance of Lactobacillus, Turicibacter, Faecalibacterium, Akkermansia, and Desulfovibrio following EEEG treatment. Meanwhile, transplantation of fecal microbiota from EEEG-treated mice exerted the anti-atherosclerotic effect in the high-fat diet (HFD)-fed ApoE[-/-] recipient mice, accompanied by improvement of gut barrier integrity through upregulation of tight junction protein expression. Furthermore, exogenous supplementation of Lactobacillus plantarum mitigated AS in ApoE[-/-] mice and improved the gut epithelial barrier function by increasing the expression level of Zo-1.

CONCLUSION: These results suggest that the anti-atherosclerotic efficacy of EEEG is attributed to the preservation of gut barrier integrity mediated by gut microbiota. EEEG and its enriched Lactobacillus plantarum may be promising adjuncts for AS management.

IMPORTANCE: Atherosclerosis (AS) is the primary pathological basis of cardiovascular disease (CVD). The gut microbiota is known to play an important role in the development and progression of atherosclerosis. In the clinical management of AS, pharmacological classes such as antioxidants, lipid-lowering drugs, and antiplatelet agents are commonly utilized. Despite their ability to decelerate the progression of AS, complications and adverse reactions still limit their application. Edgeworthia gardneri (Wall.) Meisn, a member of the Thymelaeaceae family and Edgeworthia Meisn genus, has been shown in previous studies to attenuate atherogenesis when orally administered as an ethanolic extract (EEEG). However, the interaction between EEEG and the gut microbiota, as well as the mechanism by which the gut microbiota exerts its anti-atherosclerotic effects, remain unclear. The significance of our research lies in identifying the mechanism behind the anti-atherosclerotic effect of Edgeworthia gardneri. The expected results will provide an important scientific basis for the clinical development and application of Edgeworthia gardneri in the prevention and treatment of AS.},
}

@article {pmid40013938,
year = {2025},
author = {Hou, S and Yu, J and Li, Y and Zhao, D and Zhang, Z},
title = {Advances in Fecal Microbiota Transplantation for Gut Dysbiosis-Related Diseases.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2413197},
doi = {10.1002/advs.202413197},
pmid = {40013938},
issn = {2198-3844},
abstract = {This article provides an overview of the advancements in the application of fecal microbiota transplantation (FMT) in treating diseases related to intestinal dysbiosis. FMT involves the transfer of healthy donor fecal microbiota into the patient's body, aiming to restore the balance of intestinal microbiota and thereby treat a variety of intestinal diseases such as recurrent Clostridioides difficile infection (rCDI), inflammatory bowel disease (IBD), constipation, short bowel syndrome (SBS), and irritable bowel syndrome (IBS). While FMT has shown high efficacy in the treatment of rCDI, further research is needed for its application in other chronic conditions. This article elaborates on the application of FMT in intestinal diseases and the mechanisms of intestinal dysbiosis, as well as discusses key factors influencing the effectiveness of FMT, including donor selection, recipient characteristics, treatment protocols, and methods for assessing microbiota. Additionally, it emphasizes the key to successful FMT. Future research should focus on optimizing the FMT process to ensure long-term safety and explore the potential application of FMT in a broader range of medical conditions.},
}

@article {pmid40012737,
year = {2025},
author = {Yassin, LK and Nakhal, MM and Alderei, A and Almehairbi, A and Mydeen, AB and Akour, A and Hamad, MIK},
title = {Exploring the microbiota-gut-brain axis: impact on brain structure and function.},
journal = {Frontiers in neuroanatomy},
volume = {19},
number = {},
pages = {1504065},
pmid = {40012737},
issn = {1662-5129},
abstract = {The microbiota-gut-brain axis (MGBA) plays a significant role in the maintenance of brain structure and function. The MGBA serves as a conduit between the CNS and the ENS, facilitating communication between the emotional and cognitive centers of the brain via diverse pathways. In the initial stages of this review, we will examine the way how MGBA affects neurogenesis, neuronal dendritic morphology, axonal myelination, microglia structure, brain blood barrier (BBB) structure and permeability, and synaptic structure. Furthermore, we will review the potential mechanistic pathways of neuroplasticity through MGBA influence. The short-chain fatty acids (SCFAs) play a pivotal role in the MGBA, where they can modify the BBB. We will therefore discuss how SCFAs can influence microglia, neuronal, and astrocyte function, as well as their role in brain disorders such as Alzheimer's disease (AD), and Parkinson's disease (PD). Subsequently, we will examine the technical strategies employed to study MGBA interactions, including using germ-free (GF) animals, probiotics, fecal microbiota transplantation (FMT), and antibiotics-induced dysbiosis. Finally, we will examine how particular bacterial strains can affect brain structure and function. By gaining a deeper understanding of the MGBA, it may be possible to facilitate research into microbial-based pharmacological interventions and therapeutic strategies for neurological diseases.},
}

@article {pmid40011318,
year = {2025},
author = {Sedeek, SA and Farowski, F and Youssafi, S and Tsakmaklis, A and Brodesser, S and El-Attar, MM and Abdelmalek, MO and Vehreschild, MJGT},
title = {In vitro validation concept for lyophilized fecal microbiota products with a focus on bacterial viability.},
journal = {World journal of microbiology & biotechnology},
volume = {41},
number = {3},
pages = {83},
pmid = {40011318},
issn = {1573-0972},
mesh = {Humans ; *Feces/microbiology ; *Freeze Drying ; *RNA, Ribosomal, 16S/genetics ; *Microbial Viability ; *Fecal Microbiota Transplantation/methods ; *Bile Acids and Salts ; Clostridium Infections/microbiology ; Bacteria/classification/genetics/isolation & purification/growth & development ; Gastrointestinal Microbiome ; Clostridioides difficile ; Germany ; },
abstract = {Fecal microbiota transplantation (FMT) effectively treats recurrent Clostridioides difficile infection (rCDI), typically administered as a fresh or frozen stool suspension through colonoscopy, nasojejunal tube, or oral capsules. Lyophilized fecal microbiota (LFM) are an alternative to frozen FM products. We aimed to assess whether lyophilization affects bacterial viability and metabolite levels and to develop LFM capsules for clinical use in Germany. Fecal donations from pre-screened volunteers were aliquoted and analyzed through microbial cell counting, bacterial culture, 16S rRNA gene amplicon sequencing, and bile acid assays. Results showed higher counts of viable bacterial cells and cultured anaerobes in unprocessed stool compared to freshly processed stool (p = 0.012 and p < 0.001, respectively). No significant difference in viable bacterial counts was found between freshly processed (day 0), lyophilized (day 3) and frozen FM (day 3) (p = 0.15), nor between freshly processed (day 0), lyophilized (days 30 and 90) and frozen FM (day 30) (p = 0.07). lyophilization did not significantly impact bile acid and 16S rRNA profiling. Encapsulation of lyophilized powder required fewer capsules (10-14) than frozen capsules (30). LFM products are a practical, viable alternative to frozen and fresh FM products, potentially improving storage and patient acceptance.},
}

Humans
*Feces/microbiology
*Freeze Drying
*RNA, Ribosomal, 16S/genetics
*Microbial Viability
*Fecal Microbiota Transplantation/methods
*Bile Acids and Salts
Clostridium Infections/microbiology
Bacteria/classification/genetics/isolation & purification/growth & development
Gastrointestinal Microbiome
Clostridioides difficile
Germany

@article {pmid40011195,
year = {2025},
author = {Li, T and Chen, J and Xu, Y and Ji, W and Yang, S and Wang, X},
title = {Hawthorn Pectin Alleviates DSS-Induced Colitis in Mice by Ameliorating Intestinal Barrier Function and Modulating Gut Microbiota.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c07965},
pmid = {40011195},
issn = {1520-5118},
abstract = {Pectin, as a kind of soluble dietary fiber in hawthorns, exhibits a wide range of biological activities. Nevertheless, its role and mechanism in ulcerative colitis (UC) remain unclear. In this study, the effect of hawthorn pectin (HP) against dextran sulfate sodium (DSS)-induced UC in mice and its underlying mechanism were evaluated. HP dramatically alleviated the pathological symptoms related to colitis in mice, displaying an increase in body weight and colon length and inhibition in colon damage. Importantly, HP inhibited the serum levels of inflammation-related factors including tumor necrosis factor-α, IL-1β, and IL-6 as well as decreased the number of F4/80-positive macrophages in the colon. Moreover, the expression levels of ZO-1 and occludin proteins related to intestinal permeability were increased. A significant decrease in a dose-dependent manner at the gut bacterial genus level (such as Alistipes, Colidextribacter, and Blautia) was observed after HP treatment. HP improved the metabolic pathways of gut microbiota and increased the concentrations of short-chain fatty acids in cecal contents of UC mice. Intriguingly, fecal microbiota transplantation intervention with an HP-derived microbiome notably increased the length and relieved histopathological changes of colon in UC mice. Conclusively, our study provided valuable insights into the potential of HP as a prebiotic for maintaining intestinal health and confirmed that HP could ameliorate UC in a gut microbiota-dependent manner.},
}

@article {pmid40010549,
year = {2025},
author = {Wei, J and Chen, A and Huang, D and Teng, C and Cai, D and Wu, X and Wang, T and Hu, W and Huang, Z and Wang, P and Guan, X and Zheng, X and Chen, X},
title = {Gut microbiome-derived lipopolysaccharides aggravate cognitive impairment via TLR4-mediated inflammatory signaling in neonatal rats following hypoxic-ischemic brain damage.},
journal = {Brain, behavior, and immunity},
volume = {127},
number = {},
pages = {4-24},
doi = {10.1016/j.bbi.2025.02.029},
pmid = {40010549},
issn = {1090-2139},
abstract = {Hypoxic-ischemic brain damage (HIBD) is a leading cause of infant mortality and neurological disabilities in children. Recent evidence indicates that gut microbiota significantly contributes to the development of inflammation and cognitive impairments following brain injury. However, the mechanisms by which gut microbiota influence inflammation and cognitive function in the neonates after HIBD are not well understood. This study established a neonatal rat model of HIBD by the classic Rice-Vannucci technique to investigate gut dysbiosis following hypoxic-ischemic (HI) insult and to elucidate the causal relationship between gut dysbiosis and cognitive impairments. Our results demonstrated that HI insult resulted in significant gut microbial dysbiosis, characterized by an expansion of Enterobacteriaceae. This dysbiosis was associated with intestinal barrier damage, lipopolysaccharides (LPS) leakage, and systemic inflammation. Conversely, administration of aminoguanidine (AG) to inhibit Enterobacteriaceae overgrowth restored intestinal barrier integrity and reduced systemic inflammation. Importantly, AG treatment effectively suppressed microglial activation, neuronal damage, and cognitive impairments in the neonatal rats subjected to HI insult. Additionally, RNA sequencing analysis revealed that differentially expressed genes in both colonic and hippocampal tissues were primarily associated with inflammation and neuronal apoptosis after HI insult. Further mechanistic exploration revealed that AG treatment mitigated intestinal LPS leakage, thereby reducing the activation of the TLR4/MyD88/NF-κB signaling pathway and production of the downstream inflammatory cytokines in both the colon and hippocampus. Notably, fecal microbiota transplantation (FMT) from the HIBD rats to the antibiotic cocktail-treated recipient rats resulted in microglial activation, neuronal damage, and cognitive impairments in the recipients. However, these adverse effects were effectively mitigated in the recipient rats that received FMT from the AG-treated donors, as well as in those undergoing hippocampal TLR4 knockdown. In conclusion, our findings indicate that LPS derived from gut Enterobacteriaceae overgrowth plays a critical role in the TLR4-mediated inflammatory signaling, providing a novel microbiota-based therapeutic approach for cognitive impairments following neonatal HIBD.},
}

@article {pmid40009694,
year = {2025},
author = {Wang, LL and Shen, X and Xie, Y and Ge, A and Lu, H and Gu, S and Kong, L and Narayana, JK and Mattner, J and Chotirmall, SH and Xu, JF},
title = {A gut Eggerthella lenta-derived metabolite impairs neutrophil function to aggravate bacterial lung infection.},
journal = {Science translational medicine},
volume = {17},
number = {787},
pages = {eadq4409},
doi = {10.1126/scitranslmed.adq4409},
pmid = {40009694},
issn = {1946-6242},
mesh = {Animals ; *Neutrophils/metabolism ; Humans ; *Gastrointestinal Microbiome/drug effects ; *Pseudomonas aeruginosa ; Lung/microbiology/pathology ; Mice ; Pseudomonas Infections/drug therapy/microbiology/metabolism ; AMP-Activated Protein Kinases/metabolism ; Mice, Inbred C57BL ; Bronchiectasis/microbiology/drug therapy ; Female ; Male ; Disease Models, Animal ; Metformin/pharmacology/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {The composition of the gut microbiota in patients with bronchiectasis has been proven to be distinct from that of healthy individuals, and this disrupted gut microbiota can exacerbate lung infections. However, the responsible microbes and mechanisms in the "gut-lung" axis in bronchiectasis remain unknown. Here, we report that Eggerthella lenta was enriched in the gut, and taurine ursodeoxycholic acid (TUDCA) was enriched in both the guts and sera of patients with bronchiectasis, with both being associated with disease severity. Fecal microbiota transfer from patients with bronchiectasis as well as administration of E. lenta independently exacerbated pulmonary Pseudomonas aeruginosa infections in murine models. E. lenta-associated TUDCA bound adenosine monophosphate-activated protein kinase (AMPK) within neutrophils and interfered with the interaction between liver kinase B1 and AMPK, with a consequential decrease in AMPK phosphorylation. This ultimately reduced ATP production in neutrophils, inhibited their function, and compromised P. aeruginosa elimination from the lung, aggravating tissue injury. Metformin treatment improved disease severity and outcome in the mouse models. In sum, the gut bacterium E. lenta raises the stakes of bacterial lung infection because it causes dysfunction of neutrophils circulated from serum to lung via the metabolite TUDCA. Interventions targeting E. lenta or AMPK phosphorylation may serve as adjunctive strategies to complement existing approaches for managing chronic pulmonary infection in bronchiectasis and other chronic respiratory disease states.},
}

Animals
*Neutrophils/metabolism
Humans
*Gastrointestinal Microbiome/drug effects
*Pseudomonas aeruginosa
Lung/microbiology/pathology
Mice
Pseudomonas Infections/drug therapy/microbiology/metabolism
AMP-Activated Protein Kinases/metabolism
Mice, Inbred C57BL
Bronchiectasis/microbiology/drug therapy
Female
Male
Disease Models, Animal
Metformin/pharmacology/therapeutic use
Fecal Microbiota Transplantation

@article {pmid39675817,
year = {2025},
author = {Ang, TL and Koo, SH and Ang, D and Tan, CK and Wang, LM and Wong, SH and Chow, PKH},
title = {Postcholecystectomy Gut Microbiome Changes and the Clinical Impact: A Systematic Review With Narrative Synthesis.},
journal = {Journal of gastroenterology and hepatology},
volume = {40},
number = {3},
pages = {574-583},
doi = {10.1111/jgh.16846},
pmid = {39675817},
issn = {1440-1746},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Cholecystectomy/adverse effects ; *Dysbiosis ; Diarrhea/microbiology/etiology ; Feces/microbiology ; Bile Acids and Salts/metabolism ; Female ; Prevotella/isolation & purification ; Male ; Bacteroides/isolation & purification ; Firmicutes/isolation & purification ; },
abstract = {BACKGROUND: Cholecystectomy (CCE) can affect the enterohepatic circulation of bile acids and result in gut microbiome changes. This systematic review aimed to clarify the effect of CCE on gut microbiome composition and its clinical impact.

METHOD: A systematic search was conducted in PubMed, Web of Science, and Scopus, combining keywords such as "cholecystectomy" or "post-cholecystectomy" with "gut microbiome," "stool microbiome," or "gut dysbiosis." Data were extracted and synthesized using narrative review. Study quality was assessed using the Newcastle-Ottawa scale.

RESULTS: A total of 1373 articles were screened and 14 studies were selected. Significant but inconsistent microbiome changes were reported. Changes were observed in alpha and beta diversity. At phylum level, an increase in Bacteroides and Ascomycota, decrease in Firmicutes, Actinomycetes, and Basidiomycota, and both increase and decrease in Fusobacteria were reported. At genus level, an increase in Prevotella and a decrease in Faecalibacterium were reported. In post-CCE diarrhea, decreased beta diversity, a decreased F/B ratio, an increase in Prevotella, an increase in Phocaeicola vulgatus, and a decrease in Prevotella copri were noted. For post-CCE syndrome, a higher abundance of Proteobacteria and decreased Firmicutes/Bacteroides (F/B) ratio were reported. A decreased relative abundance of Bifidobacterium longum subsp. longum from controls to CCE without colonic neoplasia to CCE with colonic neoplasia, and an increased abundance of Candida glabrata from controls, to CCE without colonic neoplasia and CCE with colonic neoplasia, were reported.

CONCLUSION: Patients who underwent CCE had significant gut dysbiosis. However, current studies could not clarify the detailed gut microbial structural and functional changes associated with CCE.},
}

*Gastrointestinal Microbiome
Humans
*Cholecystectomy/adverse effects
*Dysbiosis
Diarrhea/microbiology/etiology
Feces/microbiology
Bile Acids and Salts/metabolism
Female
Prevotella/isolation & purification
Male
Bacteroides/isolation & purification
Firmicutes/isolation & purification

@article {pmid38535607,
year = {2024},
author = {George, UE and Faleye, TOC and De Coninck, L and Agbaje, ST and Ifeorah, IM and Onoja, BA and Oni, EI and Olayinka, AO and Ajileye, TG and Oragwa, AO and Akinleye, TE and Popoola, BO and Osasona, OG and Olayinka, OT and George, OA and Muhammad, AI and Komolafe, I and Adeniji, AJ and Matthijnssens, J and Adewumi, MO},
title = {Metagenomic Detection and Genetic Characterization of Human Sapoviruses among Children with Acute Flaccid Paralysis in Nigeria.},
journal = {Pathogens (Basel, Switzerland)},
volume = {13},
number = {3},
pages = {},
pmid = {38535607},
issn = {2076-0817},
mesh = {Humans ; Nigeria/epidemiology ; *Sapovirus/genetics/isolation & purification ; *Phylogeny ; *Genotype ; *Genome, Viral/genetics ; *Caliciviridae Infections/virology/epidemiology/diagnosis ; *Metagenomics ; Child ; Child, Preschool ; *Feces/virology ; Gastroenteritis/virology/epidemiology ; Genetic Variation/genetics ; Infant ; Male ; Female ; Paralysis/virology/epidemiology ; },
abstract = {Using a metagenomic sequencing approach on stool samples from children with Acute Flaccid Paralysis (AFP), we describe the genetic diversity of Sapoviruses (SaVs) in children in Nigeria. We identified six complete genome sequences and two partial genome sequences. Several SaV genogroups and genotypes were detected, including GII (GII.4 and GII.8), GIV (GIV.1), and GI (GI.2 and GI.7). To our knowledge, this is the first description of SaV infections and complete genomes from Nigeria. Pairwise identity and phylogenetic analysis showed that the Nigerian SaVs were related to previously documented gastroenteritis outbreaks with associated strains from China and Japan. Minor variations in the functional motifs of the nonstructural proteins NS3 and NS5 were seen in the Nigerian strains. To adequately understand the effect of such amino acid changes, a better understanding of the biological function of these proteins is vital. The identification of distinct SaVs reinforces the need for robust surveillance in acute gastroenteritis (AGE) and non-AGE cohorts to better understand SaVs genotype diversity, evolution, and its role in disease burden in Nigeria. Future studies in different populations are, therefore, recommended.},
}

Humans
Nigeria/epidemiology
*Sapovirus/genetics/isolation & purification
*Phylogeny
*Genotype
*Genome, Viral/genetics
*Caliciviridae Infections/virology/epidemiology/diagnosis
*Metagenomics
Child
Child, Preschool
*Feces/virology
Gastroenteritis/virology/epidemiology
Genetic Variation/genetics
Infant
Male
Female
Paralysis/virology/epidemiology

@article {pmid40008452,
year = {2025},
author = {Chen, A and Teng, C and Wei, J and Wu, X and Zhang, H and Chen, P and Cai, D and Qian, H and Zhu, H and Zheng, X and Chen, X},
title = {Gut microbial dysbiosis exacerbates long-term cognitive impairments by promoting intestinal dysfunction and neuroinflammation following neonatal hypoxia-ischemia.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2471015},
pmid = {40008452},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Dysbiosis/microbiology ; *Cognitive Dysfunction/etiology/physiopathology ; Rats ; *Animals, Newborn ; *Hypoxia-Ischemia, Brain/microbiology ; *Rats, Sprague-Dawley ; *Toll-Like Receptor 4/metabolism/genetics ; Male ; Neuroinflammatory Diseases ; Fecal Microbiota Transplantation ; Intestines/microbiology/pathology ; Lipopolysaccharides ; Hippocampus/metabolism ; Dexamethasone/pharmacology ; Brain-Gut Axis/physiology ; Bacteria/classification/isolation & purification ; Disease Models, Animal ; },
abstract = {Neonatal hypoxic-ischemic brain damage (HIBD) is considered as a major cause of long-term cognitive impairments in newborns. It has been demonstrated that gut microbiota is closely associated with the prognosis of various neurological disorders. However, the role of microbiota-gut-brain axis on cognitive function following neonatal HIBD remains elusive. In this experiment, the correlation analysis supported the involvement of gut microbial changes following hypoxic-ischemic (HI) insult in the development of long-term cognitive impairments. Subsequent experiment revealed the involvement of the intestinal dysfunction in the hippocampal neuroinflammation and synaptic injury. In causal relationship validation experiments, fecal microbiota transplantation (FMT) from cognitively normal rats could restore gut microbial composition, improve intestinal dysfunction, reduce the serum levels of lipopolysaccharides (LPS) and inflammatory mediators, and alleviate neuroinflammation, synaptic damage and cognitive impairments in neonatal HIBD recipient rats. Conversely, the FMT from neonatal HIBD rats could induce above adverse pathological changes in the normal recipient rats. Moreover, oral administration of anti-inflammatory agent dexamethasone (DEX) exhibited the potential to alleviate these detrimental effects in neonatal HIBD rats, with the efficacy being partly reliant on gut microbiota. Further experiment on the potential molecular mechanisms using RNA sequencing indicated a significant increase in the toll-like receptor 4 (TLR4) gene in the intestinal tissues of neonatal HIBD rats. Additionally, the interventions such as TLR4 inhibitor TLR4-IN-C34 administration, FMT, and oral DEX were demonstrated to modulate intestinal function by inhibiting the LPS/TLR4 signaling pathway, thereby exerting neuroprotective effects. Collectively, these findings underscore the contribution of gut microbial dysbiosis post HI insult in activating the LPS/TLR4 signaling pathway, triggering intestinal inflammation and dysfunction, exacerbating systemic inflammation, and consequently worsening synaptic and cognitive impairments in neonatal HIBD rats. Hence, rectifying gut microbial dysbiosis or regulating intestinal function may represent a promising strategy for alleviating long-term cognitive impairments in neonates affected by HIBD.},
}

Animals
*Gastrointestinal Microbiome
*Dysbiosis/microbiology
*Cognitive Dysfunction/etiology/physiopathology
Rats
*Animals, Newborn
*Hypoxia-Ischemia, Brain/microbiology
*Rats, Sprague-Dawley
*Toll-Like Receptor 4/metabolism/genetics
Male
Neuroinflammatory Diseases
Fecal Microbiota Transplantation
Intestines/microbiology/pathology
Lipopolysaccharides
Hippocampus/metabolism
Dexamethasone/pharmacology
Brain-Gut Axis/physiology
Bacteria/classification/isolation & purification
Disease Models, Animal

@article {pmid40008084,
year = {2025},
author = {Zheng, J and Huang, Y and Zhang, L and Liu, T and Zou, Y and He, L and Guo, S},
title = {Role of the Gut-Lung Microbiome Axis in Airway Inflammation in OVA-Challenged Mice and the Effect of Azithromycin.},
journal = {Journal of inflammation research},
volume = {18},
number = {},
pages = {2661-2676},
pmid = {40008084},
issn = {1178-7031},
abstract = {OBJECTIVE: This study aimed to investigate the role of the gut-lung microbiome axis in airway inflammation in asthma and to evaluate the effect of azithromycin on this axis, with a focus on the potential mechanism by which azithromycin reduces allergic airway inflammation.

METHODS: Haematoxylin and eosin (H&E) and periodic acid-Schiff (PAS) staining were used to assess pathological changes in the lung tissues of asthmatic mice. Leukocyte cell types in bronchoalveolar lavage fluid (BALF) samples were quantified following Wright-Giemsa staining. Total IgE, OVA-specific IgE, IL-4, IL-6, and IL-17A levels in BALF and total IgE in serum were measured by ELISA. The respiratory and gut microbiota were analysed using 16S rRNA gene sequencing and subsequent taxonomic analysis.

RESULTS: OVA-challenged asthmatic mice with gut microbiota dysbiosis exhibited alterations in the respiratory microbiota, resulting in further aggravation of airway inflammation. Following faecal microbiota transplantation (FMT) to restore gut microbiota, respiratory microbiota dysbiosis was partially improved, and airway inflammation was significantly alleviated. Furthermore, azithromycin reduced airway inflammation in asthmatic mice, particularly non-eosinophilic inflammation, for which low-dose azithromycin combined with budesonide proved more effective. Azithromycin significantly enhanced the diversity and microbial composition of the gut microbiota and also affected the respiratory microbiota. At the phylum level, azithromycin decreased the abundance of Proteobacteria in the gut microbiota. At the genus level, azithromycin reduced the abundance of Pseudomonas in the respiratory microbiota.

CONCLUSION: The gut-lung microbiome axis plays a crucial role in airway inflammation in asthma. Azithromycin may reduce airway inflammation in asthma through modulation of the gut-lung microbiome axis.},
}

@article {pmid40007342,
year = {2025},
author = {Wang, L and Zhang, Z and Chen, X and Wang, Z and Song, X and Geng, Z and Zhang, X and Wang, Y and Li, J and Hu, J and Zuo, L},
title = {Sakuranetin ameliorates experimental colitis in a gut microbiota-dependent manner.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {139},
number = {},
pages = {156540},
doi = {10.1016/j.phymed.2025.156540},
pmid = {40007342},
issn = {1618-095X},
abstract = {BACKGROUND: The progression of inflammatory bowel disease (IBD) is closely connected with intestinal flora dysbiosis. Sakuranetin (SAK) is a natural compound with anti-inflammatory and antibiosis activities. We investigated the properties and mechanisms of SAK on IBD-like colitis.

METHODS: Mice with dextran sulfate sodium (DSS)-induced colitis were accomplished to assess the effects of SAK on colitis, as well as intestinal mucosal immune imbalance and intestinal barrier dysfunction. 16S rDNA was used to characterize the intestinal flora, and the short-chain fatty acid (SCFA) content in faeces was calculated using GS‒MS. Faecal microbiota transplantation (FMT) and a pseudosterile model (antibiotic cocktail, ABX) were used to evaluate whether the effects of SAK on colitis were dependent on the gut flora. Pathohistological and biochemical tests were used to estimate the safety of SAK.

RESULTS: SAK significantly ameliorated DSS-induced colitis in mice, verified by decreased weight loss, less colon shortening, and lower disease activity, histology and colonoscopy scores. Moreover, SAK alleviated gut dysbiosis and elevated the abundance of SCFA-producing bacteria in DSS-treated mice. Meanwhile, SAK increased faecal SCFA levels and activated GPR41/43 signalling. SAK also improved Treg/Th17 homeostasis and intestinal barrier function. In addition, ABX and FMT experiments confirmed that the ability of SAK to alleviate colitis was mediated through the gut flora. Finally, a safety experiment revealed that SAK had no significant adverse effects on major organ or liver/kidney function.

CONCLUSIONS: SAK may improve the intestinal immune balance and barrier function by regulating intestinal flora dysbiosis and increasing SCFA production, thereby protecting against colitis.},
}

@article {pmid40007058,
year = {2025},
author = {Ge, P and Guo, Y and Che, B and Jin, H and Chen, L and Chen, Z and Tang, K},
title = {Modulation of NLRP3 Inflammasome Activation by QYHT Decoction: Implications for the Treatment of Erectile Dysfunction in Hyperuricemia.},
journal = {American journal of men's health},
volume = {19},
number = {1},
pages = {15579883251318307},
pmid = {40007058},
issn = {1557-9891},
mesh = {Male ; *Erectile Dysfunction/drug therapy ; Animals ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Rats ; *Hyperuricemia/drug therapy ; *Inflammasomes/metabolism ; *Drugs, Chinese Herbal/pharmacology ; Humans ; Disease Models, Animal ; Oxidative Stress/drug effects ; Rats, Sprague-Dawley ; Gastrointestinal Microbiome/drug effects ; Fecal Microbiota Transplantation ; Middle Aged ; },
abstract = {Hyperuricemia (HUA) causes vascular endothelial dysfunction and oxidative stress, and simultaneously activates the NLRP3 inflammasome, leading to inflammatory reactions and erectile dysfunction (ED). This study aimed to investigate the effects of QYHT (Quyuhuatanerxian decoction) decoction on the NLRP3 inflammasome and explore its potential in treating HUA-induced ED. This study employed four treatment methods: (a) treating HUA-induced ED patients with QYHT and analyzing changes in gut microbiota abundance and fecal metabolites through 16S sequencing; (b) establishing an HUA-induced ED rat model, treating with different doses of QYHT, and examining changes in serum metabolites; (c) conducting fecal microbiota transplantation (FMT) therapy; evaluating erectile function, oxidative stress, inflammatory response, and NLRP3 inflammasome activation levels; and (d) exploring key monomeric compounds and potential targets in QYHT through network pharmacology and molecular docking. The treatment with QYHT and FMT increased testosterone levels, reduced oxidative stress and inflammatory marker levels, and inhibited the expressions of NLRP3-related factors. QYHT affected the gut microbiota structure and metabolite levels. The key components were linoleoyl acetate and mandanol, and the target was JAK2. QYHT decoction regulates the distribution of gut microbiota, improves amino acid metabolism, and effectively inhibits the activation of NLRP3 inflammasomes. This, in turn, enhances erectile function and reduces oxidative stress and inflammatory response levels, leading to successful treatment of HUA-induced ED.},
}

Male
*Erectile Dysfunction/drug therapy
Animals
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
Rats
*Hyperuricemia/drug therapy
*Inflammasomes/metabolism
*Drugs, Chinese Herbal/pharmacology
Humans
Disease Models, Animal
Oxidative Stress/drug effects
Rats, Sprague-Dawley
Gastrointestinal Microbiome/drug effects
Fecal Microbiota Transplantation
Middle Aged

@article {pmid40005809,
year = {2025},
author = {Parodi, E and Novi, M and Bottino, P and La Porta, E and Merlotti, G and Castello, LM and Gotta, F and Rocchetti, A and Quaglia, M},
title = {The Complex Role of Gut Microbiota in Systemic Lupus Erythematosus and Lupus Nephritis: From Pathogenetic Factor to Therapeutic Target.},
journal = {Microorganisms},
volume = {13},
number = {2},
pages = {},
pmid = {40005809},
issn = {2076-2607},
abstract = {The role of gut microbiota (GM) and intestinal dysbiosis in triggering the onset and/or modulating the severity and progression of lupus nephritis (LN) has been the object of intense research over the last few years. Some alterations at the phyla level, such as the abundance of Proteobacteria and reduction in Firmicutes/Bacteroidetes (F/B) ratio and in α-diversity have been consistently reported in systemic lupus erythematosus (SLE), whereas a more specific role has been ascribed to some species (Bacteroides thetaiotaomicron and Ruminococcus gnavus) in LN. Underlying mechanisms include microbial translocation through a "leaky gut" and subsequent molecular mimicry, immune dysregulation (alteration of IFNγ levels and of balance between Treg and Th17 subsets), and epigenetic interactions. Levels of bacterial metabolites, such as butyrate and other short-chain fatty acids (SCFAs), appear to play a key role in modulating LN. Beyond bacterial components of GM, virome and mycobiome are also increasingly recognized as important players in the modulation of an immune response. On the other hand, microbiota-based therapy appears promising and includes diet, prebiotics, probiotics, symbiotics, and fecal microbiota transplantation (FMT). The modulation of microbiota could correct critical alterations, such as F/B ratio and Treg/Th17 imbalance, and blunt production of autoantibodies and renal damage. Despite current limits, GM is emerging as a powerful environmental factor that could be harnessed to interfere with key mechanisms leading to SLE, preventing flares and organ damage, including LN. The aim of this review is to provide a state-of-the-art analysis of the role of GM in triggering and modulating SLE and LN on the one hand, while exploring possible therapeutic manipulation of GM to control the disease on the other hand.},
}

@article {pmid40005733,
year = {2025},
author = {Romano, FS and Lallo, MA and Romano, RS and Isidoro, LPS and Cardoso, MR and Sodré, LC and Melchert, A and Guimarães-Okamoto, PTC and Pappalardo, MCF and Amaral, AR and Vendramini, THA},
title = {Fecal Microbiota Transplantation as a Treatment for Granulomatous Colitis in a French Bulldog: A Case Report.},
journal = {Microorganisms},
volume = {13},
number = {2},
pages = {},
pmid = {40005733},
issn = {2076-2607},
abstract = {Granulomatous colitis, or ulcerative colitis, is an infectious and inflammatory disease that primarily affects the colon and occasionally extends to the ileum, particularly in young Boxer and French Bulldogs. Unlike typical chronic colitis in small animals, the early onset of the disease suggests a genetic predisposition. The condition is characterized by the overgrowth of Escherichia coli, specifically the enteroinvasive variant, which displaces beneficial gut bacteria, contributing to its infectious nature. Secondary dysbiosis and chronic-active inflammation involving histiocytes and other leukocytic infiltrates are prominent features. Clinical manifestations include chronic diarrhea with blood and mucus, frequent tenesmus, and pain, with variable degrees of weight loss depending on disease severity. The final diagnosis is based on clinical history (chronic diarrhea with hematochezia), macroscopic findings from colonoscopy (edema, ulcers, and wall hyperplasia), histopathology (presence of histiocytes), and Escherichia coli growth in culture from a colon fragment. Treatment is guided by colon antibiograms, which often require prolonged antibiotic therapy. Fecal microbiota transplantation (FMT) has emerged as a potential treatment, either as a primary intervention or adjunctive therapy, for conditions such as acute enteritis (e.g., canine parvovirus), dysbiosis, and chronic enteropathies. However, its application to modulate the microbiota and reduce inflammation in granulomatous colitis, potentially leading to longer intervals between relapses, remains an area of ongoing investigation. This is a case report of a French Bulldog diagnosed with ulcerative colitis accompanied by dysbiosis and refractory to standard treatments but sensitive and partially responsive to amikacin. The patient achieved control and sustained improvement in fecal scoring following fecal transplantation. This approach prevented the need for additional antibiotic therapy, ensuring clinical amelioration alongside microbiome restoration.},
}

@article {pmid40005617,
year = {2025},
author = {Kaltsas, A and Giannakodimos, I and Markou, E and Adamos, K and Stavropoulos, M and Kratiras, Z and Zachariou, A and Dimitriadis, F and Sofikitis, N and Chrisofos, M},
title = {The Role of Gut Microbiota Dysbiosis in Erectile Dysfunction: From Pathophysiology to Treatment Strategies.},
journal = {Microorganisms},
volume = {13},
number = {2},
pages = {},
pmid = {40005617},
issn = {2076-2607},
abstract = {Erectile dysfunction (ED) is a prevalent male sexual disorder characterized by the persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance. While its etiology is multifactorial, encompassing vascular, neurological, hormonal, and psychological components, emerging evidence suggests a significant role for gut microbiota dysbiosis in its development. The gut microbiota influences various metabolic, inflammatory, and neuropsychological processes critical to erectile function. Dysbiosis can lead to systemic inflammation, endothelial dysfunction, hormonal imbalances, and altered neurotransmitter production, all of which are key factors in ED pathogenesis. This narrative review synthesizes current research on the association between gut microbiota alterations and ED, highlighting specific bacterial taxa implicated in ED through mechanisms involving inflammation, metabolic disturbances, and hormonal regulation. This review explores potential mechanisms linking gut microbiota and ED, including pro-inflammatory cytokines, gut barrier integrity disruption, metabolic disorders, psychological factors via the gut-brain axis, and hormonal regulation. Furthermore, the gut microbiota offers promising avenues for developing non-invasive biomarkers and therapeutic interventions such as probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation. Future research should focus on longitudinal studies, mechanistic explorations, and clinical trials to validate these findings and translate them into clinical practice. Understanding the interplay between the gut microbiota and erectile function could unveil novel diagnostic biomarkers and pave the way for innovative treatments targeting the microbiota, ultimately improving men's sexual and overall health.},
}

@article {pmid40005608,
year = {2025},
author = {Pasta, A and Formisano, E and Calabrese, F and Marabotto, E and Furnari, M and Bodini, G and Torres, MCP and Pisciotta, L and Giannini, EG and Zentilin, P},
title = {From Dysbiosis to Hepatic Inflammation: A Narrative Review on the Diet-Microbiota-Liver Axis in Steatotic Liver Disease.},
journal = {Microorganisms},
volume = {13},
number = {2},
pages = {},
pmid = {40005608},
issn = {2076-2607},
abstract = {The gut microbiota has emerged as a critical player in metabolic and liver health, with its influence extending to the pathogenesis and progression of steatotic liver diseases. This review delves into the gut-liver axis, a dynamic communication network linking the gut microbiome and liver through metabolic, immunological, and inflammatory pathways. Dysbiosis, characterized by altered microbial composition, contributes significantly to the development of hepatic steatosis, inflammation, and fibrosis via mechanisms such as gut barrier dysfunction, microbial metabolite production, and systemic inflammation. Dietary patterns, including the Mediterranean diet, are highlighted for their role in modulating the gut microbiota, improving gut-liver axis integrity, and attenuating liver injury. Additionally, emerging microbiota-based interventions, such as fecal microbiota transplantation and bacteriophage therapy, show promise as therapeutic strategies for steatotic liver disease. However, challenges such as population heterogeneity, methodological variability, and knowledge gaps hinder the translational application of current findings. Addressing these barriers through standardized approaches and integrative research will pave the way for microbiota-targeted therapies to mitigate the global burden of steatotic liver disease.},
}

@article {pmid40005065,
year = {2025},
author = {Noureldein, MH and Rumora, AE and Teener, SJ and Rigan, DM and Hayes, JM and Mendelson, FE and Carter, AD and Rubin, WG and Savelieff, MG and Feldman, EL},
title = {Dietary Fatty Acid Composition Alters Gut Microbiome in Mice with Obesity-Induced Peripheral Neuropathy.},
journal = {Nutrients},
volume = {17},
number = {4},
pages = {},
pmid = {40005065},
issn = {2072-6643},
support = {1R01DK076169-00A1/NH/NIH HHS/United States ; 1R01DK115255-00A1/NH/NIH HHS/United States ; 1K99AG081390-00A1/NH/NIH HHS/United States ; 1R00DK119366-00A1/NH/NIH HHS/United States ; 1P30DK063608-00A20/NH/NIH HHS/United States ; 1R01DK130913-00A1/NH/NIH HHS/United States ; P30DK020572//Michigan Diabetes Research Center/ ; not applicable//Dr. John H. Doran Neuropathy Research Initiative/ ; not applicable//Richard and Jane Manoogian Foundation/ ; not applicable//Nathan and Rose Milstein Research Fund/ ; not applicable//Sinai Medical Staff Foundation/ ; not applicable//Taubman Foundation/ ; not applicable//NeuroNetwork for Emerging Therapies/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Obesity/microbiology ; Mice ; *Peripheral Nervous System Diseases/etiology ; *Mice, Inbred C57BL ; *Fatty Acids/metabolism ; *Diet, High-Fat/adverse effects ; Male ; Fecal Microbiota Transplantation ; Dietary Fats ; Disease Models, Animal ; Fatty Acids, Monounsaturated/metabolism ; },
abstract = {BACKGROUND: Peripheral neuropathy (PN), a complication of diabetes and obesity, progresses through a complex pathophysiology. Lifestyle interventions to manage systemic metabolism are recommended to prevent or slow PN, given the multifactorial risks of diabetes and obesity. A high-fat diet rich in saturated fatty acids (SFAs) induces PN, which a diet rich in monounsaturated fatty acids (MUFAs) rescues, independent of weight loss, suggesting factors beyond systemic metabolism impact nerve health. Interest has grown in gut microbiome mechanisms in PN, which is characterized by a distinct microbiota signature that correlates with sciatic nerve lipidome.

METHODS: Herein, we postulated that SFA- versus MUFA-rich diet would impact gut microbiome composition and correlate with PN development. To assess causality, we performed fecal microbiota transplantation (FMT) from donor mice fed SFA- versus MUFA-rich diet to lean recipient mice and assessed metabolic and PN phenotypes.

RESULTS: We found that the SFA-rich diet altered the microbiome community structure, which the MUFA-rich diet partially reversed. PN metrics correlated with several microbial families, some containing genera with feasible mechanisms of action for microbiome-mediated effects on PN. SFA and MUFA FMT did not impact metabolic phenotypes in recipient mice although SFA FMT marginally induced motor PN.

CONCLUSIONS: The involvement of diet-mediated changes in the microbiome on PN and gut-nerve axis may warrant further study.},
}

Animals
*Gastrointestinal Microbiome
*Obesity/microbiology
Mice
*Peripheral Nervous System Diseases/etiology
*Mice, Inbred C57BL
*Fatty Acids/metabolism
*Diet, High-Fat/adverse effects
Male
Fecal Microbiota Transplantation
Dietary Fats
Disease Models, Animal
Fatty Acids, Monounsaturated/metabolism

@article {pmid40004205,
year = {2025},
author = {Blanquet, L and Serra, D and Marrinhas, C and Almeida, A},
title = {Exploring Gut Microbiota-Targeted Therapies for Canine Idiopathic Epilepsy.},
journal = {International journal of molecular sciences},
volume = {26},
number = {4},
pages = {},
pmid = {40004205},
issn = {1422-0067},
mesh = {Dogs ; Animals ; *Gastrointestinal Microbiome ; *Epilepsy/microbiology/therapy ; *Dog Diseases/microbiology/therapy ; *Dysbiosis/microbiology ; Brain-Gut Axis ; },
abstract = {Epilepsy stands out as one of the most prevalent chronic neurological conditions affecting companion animals. Recent research has increasingly focused on exploring the role of gut microbiota in influencing neurological conditions, like epilepsy. This influence stems from the bidirectional communication pathways between gut bacteria and the brain, which involve metabolic, neural, immunological, and endocrine mechanisms. In fact, a balanced and stable gut microbiota is essential to maintaining normal gut physiology and ensuring appropriate signaling along the gut-brain axis. Conversely, dysbiosis can have detrimental effects on gut physiology and may contribute to the development or exacerbation of neurological conditions, including epilepsy. Considering these findings, this review article aims to deepen the understanding of the mechanisms underlying the microbiota-gut-brain connection in the context of canine idiopathic epilepsy. Moreover, this review presents recent data on innovative gut-related therapeutic strategies for canine idiopathic epilepsy treatment.},
}

Dogs
Animals
*Gastrointestinal Microbiome
*Epilepsy/microbiology/therapy
*Dog Diseases/microbiology/therapy
*Dysbiosis/microbiology
Brain-Gut Axis

@article {pmid40004161,
year = {2025},
author = {Wang, Z and Ma, X and Shi, W and Zhu, W and Feng, X and Xin, H and Zhang, Y and Cong, B and Li, Y},
title = {The Gut Microbiota Metabolite Butyrate Modulates Acute Stress-Induced Ferroptosis in the Prefrontal Cortex via the Gut-Brain Axis.},
journal = {International journal of molecular sciences},
volume = {26},
number = {4},
pages = {},
pmid = {40004161},
issn = {1422-0067},
support = {82072109//National Natural Science Foundation of China/ ; 82130055//National Natural Science Foundation of China/ ; 82293651//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Prefrontal Cortex/metabolism ; *Ferroptosis/drug effects ; Mice ; Male ; *Stress, Psychological/microbiology/metabolism ; *Brain-Gut Axis/drug effects ; Butyrates/metabolism/pharmacology ; Depression/metabolism/drug therapy/microbiology ; Neurons/metabolism/drug effects ; Mice, Inbred C57BL ; Disease Models, Animal ; Fecal Microbiota Transplantation ; },
abstract = {Stress has been implicated in the onset of mental disorders such as depression, with the prefrontal cortex (PFC) playing a crucial role. However, the underlying mechanisms remain to be fully elucidated. Metabolites secreted by intestinal flora can enter the bloodstream and exert regulatory effects on the body. Consequently, this study aims to investigate the molecular mechanisms by which gut flora influences ferroptosis in PFC neurons, thereby affecting depression-like behavioral changes in mice subjected to acute stress. Initially, we established a mouse model of acute restraint stress (3-day duration) and verified that stress-induced ferroptosis of PFC neurons contributed to depression-like behavioral alterations in mice, as evidenced by morphological, behavioral, and molecular biology assessments. Subsequently, through fecal microbiota transplantation (FMT) experiments, we established a significant correlation between gut microbiota and ferroptosis of PFC neurons in acute stress-exposed mice. 16S rDNA sequencing identified butyric acid-producing bacteria, specifically g_Butyricimonas and its primary metabolite, butyric acid, as critical regulators of ferroptosis in PFC neurons in acutely stressed mice. Furthermore, the intervention of butyrate demonstrated its potential to ameliorate damage to the intestinal and blood-brain barriers in these mice. This intervention also mitigated depression-like behaviors induced by ferroptosis of PFC neurons by alleviating systemic inflammatory responses. The findings of this study indicate that acute stress-induced ferroptosis of PFC neurons plays a critical role in depression-like behavioral changes in mice. Additionally, the gut microbiota metabolite butyrate can modulate ferroptosis and depression-like behavioral changes through the gut-brain axis.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Prefrontal Cortex/metabolism
*Ferroptosis/drug effects
Mice
Male
*Stress, Psychological/microbiology/metabolism
*Brain-Gut Axis/drug effects
Butyrates/metabolism/pharmacology
Depression/metabolism/drug therapy/microbiology
Neurons/metabolism/drug effects
Mice, Inbred C57BL
Disease Models, Animal
Fecal Microbiota Transplantation

@article {pmid40004115,
year = {2025},
author = {Zhang, J and Wei, J and Lai, W and Sun, J and Bai, Y and Cao, H and Guo, J and Su, Z},
title = {Focus on Glucagon-like Peptide-1 Target: Drugs Approved or Designed to Treat Obesity.},
journal = {International journal of molecular sciences},
volume = {26},
number = {4},
pages = {},
pmid = {40004115},
issn = {1422-0067},
mesh = {Humans ; *Obesity/drug therapy/metabolism ; *Glucagon-Like Peptide 1/metabolism ; Animals ; Anti-Obesity Agents/therapeutic use/pharmacology ; Glucagon-Like Peptide-1 Receptor/metabolism ; Gastrointestinal Microbiome/drug effects ; },
abstract = {Obesity is closely related to metabolic diseases, which brings a heavy burden to the health care system. It is urgent to formulate and implement effective treatment strategies. Glucagon-like peptide-1 (GLP-1) is a protein with seven transmembrane domains connected by type B and G proteins, which is widely distributed and expressed in many organs and tissues. GLP-1 analogues can reduce weight, lower blood pressure, and improve blood lipids. Obesity, diabetes, cardiovascular diseases, and other diseases have caused scientists' research and development boom. Among them, GLP-1R agonist drugs have developed rapidly in weight-loss drugs. In this paper, based on the target of GLP-1, the mechanism of action of GLP-1 in obesity treatment was deeply studied, and the drugs approved and designed for obesity treatment based on GLP-1 target were elaborated in detail. Innovatively put forward and summarized the double and triple GLP-1 targeted drugs in the treatment of obesity with better effects and less toxic and side effects, and this can make full use of multi-target methods to treat other diseases in the future. Finally, it is pointed out that intestinal flora and microorganisms have many benefits in the treatment of obesity, and fecal bacteria transplantation may be a potential treatment for obesity with less harm to the body. This article provides some promising methods to treat obesity, which have strong practical value.},
}

Humans
*Obesity/drug therapy/metabolism
*Glucagon-Like Peptide 1/metabolism
Animals
Anti-Obesity Agents/therapeutic use/pharmacology
Glucagon-Like Peptide-1 Receptor/metabolism
Gastrointestinal Microbiome/drug effects

@article {pmid40003979,
year = {2025},
author = {Flynn, CK and Adams, JB and Krajmalnik-Brown, R and Khoruts, A and Sadowsky, MJ and Nirmalkar, K and Takyi, E and Whiteley, P},
title = {Review of Elevated Para-Cresol in Autism and Possible Impact on Symptoms.},
journal = {International journal of molecular sciences},
volume = {26},
number = {4},
pages = {},
pmid = {40003979},
issn = {1422-0067},
support = {N/A//Zoowalk for Autism Research/ ; },
mesh = {*Cresols/metabolism/urine ; Humans ; Animals ; *Gastrointestinal Microbiome ; Autism Spectrum Disorder/metabolism/microbiology ; Autistic Disorder/metabolism ; Mice ; Sulfuric Acid Esters/metabolism/urine ; Child ; },
abstract = {Para-cresol (p-cresol), and its primary human metabolite p-cresol sulfate (pCS), are among the most studied gut-derived metabolites relevant to autism spectrum disorder (ASD). P-cresol is produced by bacterial modification of phenylalanine or tyrosine and is one of many potentially deleterious metabolites produced by the gut microbiota. Seventeen studies have observed p-cresol and/or p-cresol sulfate as being higher in the urine of children with autism spectrum disorder (ASD) vs. controls. P-cresol has harmful effects on the body, including within the gut, brain, kidneys, liver, immune system, and mitochondria. Some of these effects may contribute to autism and comorbid symptoms. In the gut, p-cresol acts as an antibiotic, altering the gut microbiome to favor the bacteria that produce it. In the mitochondria, p-cresol disrupts ATP production and increases oxidative stress, which is also common in autism. In the brain, p-cresol impairs neuronal development. P-cresol inactivates dopamine beta-hydroxylase, which converts dopamine to noradrenaline. P-cresol sulfate impairs kidney function and is linked to chronic kidney disease (CKD), which is more common in ASD adults. P-cresol also interferes with immune function. Three animal studies have demonstrated that p-cresol causes autism-related symptoms in mice, and that mice can be recovered by the administration of fecal microbiota transplant from healthy mice. Similarly, it was found that microbiota transplant therapy treatment in children with ASD significantly reduced p-cresol sulfate levels to normal and led to significant improvements in gastrointestinal (GI) and ASD symptoms. In summary, p-cresol and pCS likely contribute to ASD core symptoms in a substantial subset of children with ASD.},
}

*Cresols/metabolism/urine
Humans
Animals
*Gastrointestinal Microbiome
Autism Spectrum Disorder/metabolism/microbiology
Autistic Disorder/metabolism
Mice
Sulfuric Acid Esters/metabolism/urine
Child

@article {pmid40003971,
year = {2025},
author = {Yu, F and Zhu, C and Wu, W},
title = {Senile Osteoarthritis Regulated by the Gut Microbiota: From Mechanisms to Treatments.},
journal = {International journal of molecular sciences},
volume = {26},
number = {4},
pages = {},
pmid = {40003971},
issn = {1422-0067},
support = {11DZ2261100//Shanghai Key Laboratory of Human Performance/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Osteoarthritis/microbiology/therapy ; *Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; Animals ; Aging ; Medicine, Chinese Traditional/methods ; },
abstract = {Osteoarthritis (OA) is a chronic, progressive degenerative joint disease that affects the entire synovial joint, leading to the progressive degeneration of articular cartilage. It seriously affects the quality of life and global disability of patients. OA is affected by a variety of factors; the most significant risk factor for OA is age. As individuals age, the risk and severity of OA increase due to the exacerbation of cartilage degeneration and wear and tear. In recent years, research has indicated that the gut microbiota may play a significant role in the aging and OA processes. It is anticipated that regulating the gut microbiota may offer novel approaches to the treatment of OA. The objective of this paper is to examine the relationship between the gut microbiota and senile OA, to investigate the potential mechanisms involved. This review also summarizes the therapeutic strategies related to gut flora in OA management, such as prebiotics and probiotics, diet, exercise, traditional Chinese medicine (TCM) modification, and fecal microbiota transplantation (FMT), highlighting the potential clinical value of gut flora and elucidating the current challenges. The foundation for future research directions is established through the summarization of current research progress.},
}

Humans
*Gastrointestinal Microbiome
*Osteoarthritis/microbiology/therapy
*Fecal Microbiota Transplantation
Probiotics/therapeutic use
Prebiotics/administration & dosage
Animals
Aging
Medicine, Chinese Traditional/methods

@article {pmid40003268,
year = {2025},
author = {Todor, SB and Ichim, C},
title = {Microbiome Modulation in Pediatric Leukemia: Impact on Graft-Versus-Host Disease and Treatment Outcomes: A Narrative Review.},
journal = {Children (Basel, Switzerland)},
volume = {12},
number = {2},
pages = {},
doi = {10.3390/children12020166},
pmid = {40003268},
issn = {2227-9067},
abstract = {The gut microbiome significantly influences the outcomes of pediatric leukemia, particularly in patients undergoing hematopoietic stem cell transplantation (HSCT). Dysbiosis, caused by chemotherapy, antibiotics, and immune system changes, contributes to complications such as graft-versus-host disease (GVHD), gastrointestinal issues, and infections. Various microbiome-related interventions, including prebiotics, probiotics, postbiotics, and fecal microbiota transplantation (FMT), have shown potential in mitigating these complications. Specific microbial signatures have been linked to GVHD risk, and interventions like inulin, Lactobacillus, and SCFAs (short-chain fatty acids), particularly butyrate, may help modulate the immune system and improve outcomes. FMT, while showing promising results in restoring microbial balance and alleviating GVHD, still requires careful monitoring due to potential risks in immunocompromised patients. Despite positive findings, more research is needed to optimize microbiome-based therapies and ensure their safety and efficacy in pediatric leukemia care.},
}

@article {pmid40002939,
year = {2025},
author = {Vučinić, D and Redžović, A and Hauser, G and Mikolašević, I},
title = {Microbiota and Radiotherapy: Unlocking the Potential for Improved Gastrointestinal Cancer Treatment.},
journal = {Biomedicines},
volume = {13},
number = {2},
pages = {},
doi = {10.3390/biomedicines13020526},
pmid = {40002939},
issn = {2227-9059},
abstract = {Radiotherapy (RT) is one of the major cornerstones in managing gastrointestinal (GI) cancers. However, several side effects, such as intestinal inflammation, mucosal injury, and dysbiosis, often compromise this. The gut microbiota increasingly attracts much interest as an essential modulator of RT effects influencing immune responses and tissue repair. Through short-chain fatty acids such as butyrate, representatives of certain bacterial species play a crucial role under normal conditions, keeping the mucosal integrity intact and reducing oxidative stress-mediated damage. Dysbiosis, a state where diminished microbial diversity and increased pathogenic species in the microbiota are seen, amplifies RT-induced toxicity in patients. Clinical investigations highlight that microbiota-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, hold the means to augment RT efficacy and lessen toxicity. Increased microflora diversity and specific microbial profiles have yielded serious patient improvements. Advanced RT methods use stereotactic body radiotherapy combined with microbiota modulation as a promising technique to shield healthy tissue and maximize immune-mediated antitumor effects. Additionally, there is an implication in tumor behavior regulated by the intratumoral microbiota regarding the response to radiotherapy. Notably, the modulation of gut and tumor microbiota provides an avenue to optimize RT benefits in GI cancers, underscoring the importance of personalized therapy.},
}

@article {pmid40002835,
year = {2025},
author = {Mafe, AN and Büsselberg, D},
title = {Microbiome Integrity Enhances the Efficacy and Safety of Anticancer Drug.},
journal = {Biomedicines},
volume = {13},
number = {2},
pages = {},
doi = {10.3390/biomedicines13020422},
pmid = {40002835},
issn = {2227-9059},
support = {NPRP 14S0311-210033//QNRF/ ; },
abstract = {The intricate relationship between anticancer drugs and the gut microbiome influences cancer treatment outcomes. This review paper focuses on the role of microbiome integrity in enhancing the efficacy and safety of anticancer drug therapy, emphasizing the pharmacokinetic interactions between anticancer drugs and the gut microbiota. It explores how disruptions to microbiome composition, or dysbiosis, can alter drug metabolism, immune responses, and treatment side effects. By examining the mechanisms of microbiome disruption caused by anticancer drugs, this paper highlights specific case studies of drugs like cyclophosphamide, 5-fluorouracil, and irinotecan, and their impact on microbial diversity and clinical outcomes. The review also discusses microbiome-targeted strategies, including prebiotics, probiotics, postbiotics, and fecal microbiota transplantation (FMT), as promising interventions to enhance cancer treatment. Furthermore, the potential of microbiome profiling in personalizing therapy and integrating these interventions into clinical practice is explored. Finally, this paper proposes future research directions, including developing novel biomarkers and a deeper comprehension of drug-microbiome interactions, to respond to current gaps in knowledge and improve patient outcomes in cancer care.},
}

@article {pmid40002529,
year = {2025},
author = {Kalaga, P and Ray, SK},
title = {Mental Health Disorders Due to Gut Microbiome Alteration and NLRP3 Inflammasome Activation After Spinal Cord Injury: Molecular Mechanisms, Promising Treatments, and Aids from Artificial Intelligence.},
journal = {Brain sciences},
volume = {15},
number = {2},
pages = {},
doi = {10.3390/brainsci15020197},
pmid = {40002529},
issn = {2076-3425},
abstract = {Aside from its immediate traumatic effects, spinal cord injury (SCI) presents multiple secondary complications that can be harmful to those who have been affected by SCI. Among these secondary effects, gut dysbiosis (GD) and the activation of the NOD (nucleotide-binding oligomerization domain) like receptor-family pyrin-domain-containing three (NLRP3) inflammasome are of special interest for their roles in impacting mental health. Studies have found that the state of the gut microbiome is thrown into disarray after SCI, providing a chance for GD to occur. Metabolites such as short-chain fatty acids (SCFAs) and a variety of neurotransmitters produced by the gut microbiome are hampered by GD. This disrupts healthy cognitive processes and opens the door for SCI patients to be impacted by mental health disorders. Additionally, some studies have found an increased presence and activation of the NLRP3 inflammasome and its respective parts in SCI patients. Preclinical and clinical studies have shown that NLRP3 inflammasome plays a key role in the maturation of pro-inflammatory cytokines that can initiate and eventually aggravate mental health disorders after SCI. In addition to the mechanisms of GD and the NLRP3 inflammasome in intensifying mental health disorders after SCI, this review article further focuses on three promising treatments: fecal microbiome transplants, phytochemicals, and melatonin. Studies have found these treatments to be effective in combating the pathogenic mechanisms of GD and NLRP3 inflammasome, as well as alleviating the symptoms these complications may have on mental health. Another area of focus of this review article is exploring how artificial intelligence (AI) can be used to support treatments. AI models have already been developed to track changes in the gut microbiome, simulate drug-gut interactions, and design novel anti-NLRP3 inflammasome peptides. While these are promising, further research into the applications of AI for the treatment of mental health disorders in SCI is needed.},
}

@article {pmid40002492,
year = {2025},
author = {Gao, A and Lv, J and Su, Y},
title = {The Inflammatory Mechanism of Parkinson's Disease: Gut Microbiota Metabolites Affect the Development of the Disease Through the Gut-Brain Axis.},
journal = {Brain sciences},
volume = {15},
number = {2},
pages = {},
doi = {10.3390/brainsci15020159},
pmid = {40002492},
issn = {2076-3425},
support = {Grant No. 81601330-YS//National Natural Science Foundation of China/ ; Grant No. 2022CFB178-YS//Natural Science Foundation of Hubei Province/ ; },
abstract = {Parkinson's disease is recognized as the second most prevalent neurodegenerative disorder globally, with its incidence rate projected to increase alongside ongoing population growth. However, the precise etiology of Parkinson's disease remains elusive. This article explores the inflammatory mechanisms linking gut microbiota to Parkinson's disease, emphasizing alterations in gut microbiota and their metabolites that influence the disease's progression through the bidirectional transmission of inflammatory signals along the gut-brain axis. Building on this mechanistic framework, this article further discusses research methodologies and treatment strategies focused on gut microbiota metabolites, including metabolomics detection techniques, animal model investigations, and therapeutic approaches such as dietary interventions, probiotic treatments, and fecal transplantation. Ultimately, this article aims to elucidate the relationship between gut microbiota metabolites and the inflammatory mechanisms underlying Parkinson's disease, thereby paving the way for novel avenues in the research and treatment of this condition.},
}

@article {pmid40001573,
year = {2025},
author = {Mafe, AN and Büsselberg, D},
title = {Modulation of the Neuro-Cancer Connection by Metabolites of Gut Microbiota.},
journal = {Biomolecules},
volume = {15},
number = {2},
pages = {},
doi = {10.3390/biom15020270},
pmid = {40001573},
issn = {2218-273X},
support = {NPRP 14S0311-210033//QNRF/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Brain Neoplasms/metabolism/microbiology ; Animals ; Brain-Gut Axis ; Fatty Acids, Volatile/metabolism ; Bile Acids and Salts/metabolism ; Dysbiosis/metabolism/microbiology ; Tryptophan/metabolism ; Fecal Microbiota Transplantation ; Lipopolysaccharides/metabolism ; },
abstract = {The gut-brain-cancer axis represents a novel and intricate connection between the gut microbiota, neurobiology, and cancer progression. Recent advances have accentuated the significant role of gut microbiota metabolites in modulating systemic processes that influence both brain health and tumorigenesis. This paper explores the emerging concept of metabolite-mediated modulation within the gut-brain-cancer connection, focusing on key metabolites such as short-chain fatty acids (SCFAs), tryptophan derivatives, secondary bile acids, and lipopolysaccharides (LPS). While the gut microbiota's impact on immune regulation, neuroinflammation, and tumor development is well established, gaps remain in grasping how specific metabolites contribute to neuro-cancer interactions. We discuss novel metabolites with potential implications for neurobiology and cancer, such as indoles and polyamines, which have yet to be extensively studied. Furthermore, we review preclinical and clinical evidence linking gut dysbiosis, altered metabolite profiles, and brain tumors, showcasing limitations and research gaps, particularly in human longitudinal studies. Case studies investigating microbiota-based interventions, including dietary changes, fecal microbiota transplantation, and probiotics, demonstrate promise but also indicate hurdles in translating these findings to clinical cancer therapies. This paper concludes with a call for standardized multi-omics approaches and bi-directional research frameworks integrating microbiome, neuroscience, and oncology to develop personalized therapeutic strategies for neuro-cancer patients.},
}

Humans
*Gastrointestinal Microbiome
*Brain Neoplasms/metabolism/microbiology
Animals
Brain-Gut Axis
Fatty Acids, Volatile/metabolism
Bile Acids and Salts/metabolism
Dysbiosis/metabolism/microbiology
Tryptophan/metabolism
Fecal Microbiota Transplantation
Lipopolysaccharides/metabolism

@article {pmid40001396,
year = {2025},
author = {Sher, AA and Whitehead-Tillery, CE and Peer, AM and Bell, JA and Vocelle, DB and Dippel, JT and Zhang, L and Mansfield, LS},
title = {Dynamic Spread of Antibiotic Resistance Determinants by Conjugation to a Human-Derived Gut Microbiota in a Transplanted Mouse Model.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {2},
pages = {},
doi = {10.3390/antibiotics14020152},
pmid = {40001396},
issn = {2079-6382},
support = {RN031097-DEHN//Albert C. and Lois E. Dehn Chair Endowment/ ; NC1202//United States Department of Agriculture/ ; GS100019//University Distinguished Professor Endowment, Michigan State University/ ; U19AI090872//National Institutes of Health, Enterics Research Investigational Network, Cooperative Research Center/ ; Stipend to Azam A. Sher//College of Veterinary Medicine/ ; },
abstract = {BACKGROUND: Antibiotic-resistant (AR) bacteria pose an increasing threat to public health, but the dynamics of antibiotic resistance gene (ARG) spread in complex microbial communities are poorly understood. Conjugation is a predominant direct cell-to-cell mechanism for the horizontal gene transfer (HGT) of ARGs. We hypothesized that commensal Escherichia coli donor strains would mediate the conjugative transfer of ARGs to phylogenetically distinct bacteria without antibiotic selection pressure in gastrointestinal tracts of mice carrying a human-derived microbiota with undetectable levels of E. coli. Our objective was to identify a mouse model to study the factors regulating AR transfer by conjugation in the gut.

METHODS: Two donor E. coli strains were engineered to carry chromosomally encoded red fluorescent protein, and an ARG- and green fluorescent protein (GFP)-encoding broad host range RP4 conjugative plasmid. Mice were orally gavaged with two donor strains (1) E. coli MG1655 or (2) human-derived mouse-adapted E. coli LM715-1 and their colonization assessed by culture over time. Fluorescence-activated cell sorting (FACS) and 16S rDNA sequencing were performed to trace plasmid spread to the microbiota.

RESULTS: E. coli LM715-1 colonized mice for ten days, while E. coli MG1655 was not recovered after 72 h. Bacterial cells from fecal samples on days 1 and 3 post inoculation were sorted by FACS. Samples from mice given donor E. coli LM715-1 showed an increase in cells expressing green but not red fluorescence compared to pre-inoculation samples. 16S rRNA gene sequencing analysis of FACS GFP positive cells showed that bacterial families Lachnospiraceae, Clostridiaceae, Pseudomonadaceae, Rhodanobacteraceae, Erysipelotrichaceae, Oscillospiraceae, and Butyricicoccaceae were the primary recipients of the RP4 plasmid.

CONCLUSIONS: Results show this ARG-bearing conjugative RP4 plasmid spread to diverse human gut bacterial taxa within a live animal where they persisted. These fluorescent marker strategies and human-derived microbiota transplanted mice provided a tractable model for investigating the dynamic spread of ARGs within gut microbiota and could be applied rigorously to varied microbiotas to understand conditions facilitating their spread.},
}

@article {pmid40000989,
year = {2025},
author = {Zhao, M and Zhang, Y and Liu, S and Wang, F and Zhang, P},
title = {Eradication of Helicobacter pylori reshapes gut microbiota and facilitates the evolution of antimicrobial resistance through gene transfer and genomic mutations in the gut.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {90},
pmid = {40000989},
issn = {1471-2180},
support = {32201393//National Natural Science Foundation of China/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects/genetics ; Humans ; *Helicobacter pylori/genetics/drug effects ; *Drug Resistance, Bacterial/genetics ; *Anti-Bacterial Agents/pharmacology ; *Helicobacter Infections/microbiology/drug therapy ; *Gene Transfer, Horizontal ; *Feces/microbiology ; Mutation ; Metagenomics ; Klebsiella/genetics/drug effects ; Female ; Male ; Genome, Bacterial/genetics ; Adult ; Escherichia/genetics/drug effects ; Middle Aged ; Genes, Bacterial/genetics ; },
abstract = {Treating Helicobacter pylori (H. pylori) infection requires large quantities of antibiotics, thus dramatically promoting the enrichment and dissemination of antimicrobial resistance (AMR) in feces. However, the influence of H. pylori eradication on the AMR mobility and the gut microbiota evolution has yet to be thoroughly investigated. Here, a study involving 12 H. pylori-positive participants was conducted, and the pre- and post- eradication fecal samples were sequenced. Metagenomic analysis revealed that the eradication treatment drastically altered the gut microbiome, with the Escherichia and Klebsiella genera emerging as the predominant bacteria. Interestingly, the eradication treatment significantly increased the relative abundance and diversity of resistome and mobilome in gut microbiota. Eradication of H. pylori also enriched AMR genes (ARGs) conferring resistance to antibiotics not administered because of the co-location with other ARGs or mobile genetic elements (MGEs). Additionally, the Escherichia and Klebsiella genera were identified as the primary bacterial hosts of these highly transferable ARGs. Furthermore, the genomic variations associated with ARGs in Escherichia coli (E. coli) caused by the eradication treatment were profiled, including the parC, parE, and gyrA genes. These findings revealed that H. pylori eradication promoted the enrichment of ARGs and MGEs in the Escherichia and Klebsiella genera, and further facilitated bacterial evolution through the horizontal transfer of ARGs and genomic variations.},
}

*Gastrointestinal Microbiome/drug effects/genetics
Humans
*Helicobacter pylori/genetics/drug effects
*Drug Resistance, Bacterial/genetics
*Anti-Bacterial Agents/pharmacology
*Helicobacter Infections/microbiology/drug therapy
*Gene Transfer, Horizontal
*Feces/microbiology
Mutation
Metagenomics
Klebsiella/genetics/drug effects
Female
Male
Genome, Bacterial/genetics
Adult
Escherichia/genetics/drug effects
Middle Aged
Genes, Bacterial/genetics

@article {pmid39999537,
year = {2025},
author = {Dhanasekaran, D and Venkatesan, M and Sabarathinam, S},
title = {Efficacy of microbiome-targeted interventions in obesity management- A comprehensive systematic review.},
journal = {Diabetes & metabolic syndrome},
volume = {19},
number = {2},
pages = {103208},
doi = {10.1016/j.dsx.2025.103208},
pmid = {39999537},
issn = {1878-0334},
abstract = {BACKGROUND: Obesity is a global health crisis linked to numerous chronic diseases. The gut microbiome plays a crucial role in human metabolism, and emerging evidence suggests that modulating the microbiome may offer novel therapeutic avenues for obesity management.

OBJECTIVE: This systematic review aimed to assess the efficacy and safety of microbiome-targeted interventions, including probiotics, prebiotics, synbiotics, and fecal microbiota transplantation, in improving body composition, metabolic parameters, and inflammatory markers in overweight and obese adults.

METHODS: A comprehensive search of PubMed, Scopus, and ScienceDirect was conducted to identify relevant studies published between 2005 and 2023. Included studies were assessed for methodological quality and risk of bias using the Cochrane Collaboration tool.

RESULTS: Body composition: Most studies demonstrated significant reductions in body weight, Body mass index, and body fat percentage.

METABOLIC PARAMETERS: Improvements were observed in lipid profiles (reduced cholesterol, triglycerides) and glucose metabolism (improved insulin sensitivity).

INFLAMMATORY MARKERS: Significant reductions were observed in inflammatory markers such as Interleukins (IL-6, IL-8) and C-reactive protein.

MICROBIAL COMPOSITION: Interventions generally led to shifts in microbial composition, with increases in beneficial bacteria such as Bifidobacterium and Lactobacillus.

ADVERSE EVENTS: Adverse events were generally minimal and limited.

CONCLUSION: This review provides strong evidence that microbiome-targeted interventions can effectively improve body composition, metabolic parameters, and inflammatory markers in individuals with obesity. Further research is needed to optimize intervention strategies, identify specific microbial targets, and translate these findings into effective clinical applications.},
}

@article {pmid39999013,
year = {2025},
author = {Tashkent, Y and Choo, JM and Richard, A and Wang, Z and Calzadilla-Bertot, L and Vasil, E and Miller, S and Taylor, SL and Ivey, KL and Woodman, R and Adler, B and Ayonrinde, OT and Olynyk, JK and Beilin, LJ and Mori, TA and Wigg, AJ and Muller, KR and Adams, LA and Rogers, GB},
title = {Steatotic Liver Disease in Younger Adults is Associated With Altered Gut Microbiology.},
journal = {Liver international : official journal of the International Association for the Study of the Liver},
volume = {45},
number = {3},
pages = {e70032},
pmid = {39999013},
issn = {1478-3231},
support = {//Gastroenterological Society of Australia/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; Male ; Adult ; Female ; Cross-Sectional Studies ; *Feces/microbiology ; Magnetic Resonance Imaging ; Fatty Liver/microbiology/diagnostic imaging ; },
abstract = {BACKGROUND AND AIMS: Steatotic liver disease (SLD) is a leading cause of chronic liver disease worldwide. As SLD pathogenesis has been linked to gut microbiome alterations, we aimed to identify SLD-associated gut microbiome features early in SLD development by utilising a highly characterised cohort of community-dwelling younger adults.

METHODS AND RESULTS: At age 27 years, 588 participants of the Raine Study Generation 2 underwent cross-sectional assessment. Hepatic steatosis was quantified using a validated magnetic resonance imaging (MRI) volumetric liver fat fraction (VLFF) equation (HepaFat). Of the 588 participants, 488 (83%) were classified as having 'no SLD' (VLFF ≤ 3.55%), 76 (12.9%) with 'mild-moderate' SLD (VLFF: 3.56%-13.4%) and 24 (4.10%) with 'severe' SLD (VLFF > 13.4%). Stool microbiome profiling identified an association between severe SLD and lower microbiota alpha diversity (observed features [p = 0.015], Pielou evenness [p = 0.001] and Shannon diversity [p = 0.002]) compared to no SLD. Faecal microbiota composition differed significantly between no SLD and both mild-moderate (p = 0.004) and severe SLD groups (p = 0.001). There was no significant difference in microbiota dispersion between SLD groups. Reduced relative abundance of short-chain fatty acid producing bacteria, and higher levels of proinflammatory bacterial taxa, were both significantly associated with severe SLD (q < 0.05).

CONCLUSIONS: SLD in younger adults is associated with reduced intestinal microbial diversity and a pattern of bacterial taxa depletion that is consistent with other chronic inflammatory conditions. Our characterisation of gut microbiome characteristics in early SLD development provides a potential basis for risk identification and reduction.

TRIAL REGISTRATION: The Raine Study is registered in the Australian New Zealand Clinical Trials Registry (ACTRN12617001599369).},
}

Humans
*Gastrointestinal Microbiome
Male
Adult
Female
Cross-Sectional Studies
*Feces/microbiology
Magnetic Resonance Imaging
Fatty Liver/microbiology/diagnostic imaging

@article {pmid39998920,
year = {2025},
author = {Lundgrin, EL and Hatipoglu, B},
title = {Trending Modalities in Type 2 Diabetes Prevention.},
journal = {The Journal of clinical endocrinology and metabolism},
volume = {110},
number = {Supplement_2},
pages = {S187-S192},
doi = {10.1210/clinem/dgaf040},
pmid = {39998920},
issn = {1945-7197},
support = {//This work was supported by the Deborah and Ronald Ratner Fund/ ; //Mary B. Lee Chair/ ; },
mesh = {Humans ; *Diabetes Mellitus, Type 2/prevention & control ; *Prediabetic State/therapy ; Hypoglycemic Agents/therapeutic use ; Fecal Microbiota Transplantation ; Incretins/therapeutic use ; Gastrointestinal Microbiome ; Life Style ; },
abstract = {CONTEXT: Prediabetes now affects a substantial proportion of the population, marking a growing group of individuals at increased risk for the development of type 2 diabetes (T2D). Given the profound effect of T2D on an individual's morbidity and mortality, T2D prevention is of critical importance.

EVIDENCE ACQUISITION: We searched PubMed and Ovid MEDLINE databases for recent systematic reviews, meta-analyses, and original research articles pertaining to prediabetes and the prevention of T2D.

EVIDENCE SYNTHESIS: T2D prevention strategies have focused on intensive lifestyle modification as well as numerous medications that ultimately improve insulin resistance. Recently, a better understanding of the gut microbiome's role in diabetes progression has suggested a possible preventive role for fecal transplant. Finally, multiple incretin pharmaceutical agents have been developed that show promise in the prevention and treatment of T2D.

CONCLUSION: The number of novel ways to prevent T2D is rapidly growing. A thorough understanding of the indications, outcomes, and limitations of these new therapies is critical for all who care for individuals with diabetes.},
}

Humans
*Diabetes Mellitus, Type 2/prevention & control
*Prediabetic State/therapy
Hypoglycemic Agents/therapeutic use
Fecal Microbiota Transplantation
Incretins/therapeutic use
Gastrointestinal Microbiome
Life Style

@article {pmid39998294,
year = {2025},
author = {Wolfe, TM and Jo, J and Pinkham, NV and Garey, KW and Walk, ST},
title = {The impact of ibezapolstat and other Clostridioides difficile infection-relevant antibiotics on the microbiome of humanized mice.},
journal = {Antimicrobial agents and chemotherapy},
volume = {},
number = {},
pages = {e0160424},
doi = {10.1128/aac.01604-24},
pmid = {39998294},
issn = {1098-6596},
abstract = {Ibezapolstat (IBZ) is a competitive inhibitor of the bacterial Pol IIIC enzyme in clinical development for the treatment of Clostridioides difficile infection (CDI). Previous studies demonstrated that IBZ carries a favorable microbiome diversity profile compared to vancomycin (VAN). However, head-to-head comparisons with other CDI antibiotics have not been done. The purpose of this study was to compare microbiome changes associated with IBZ to other clinically used CDI antibiotics. Groups of germ-free (GF) mice received a fecal microbiota transplant from one of two healthy human donors and were subsequently exposed to either IBZ, VAN, fidaxomicin (FDX), metronidazole (MET), or no antibiotic (control). 16S rRNA encoding gene sequencing of temporally collected stool samples was used to compare the gut microbiome perturbations between treatment and no-drug control groups. Among the tested antibiotics, the most significant change in microbiome diversity was observed in MET-treated mice. Each antibiotic had a unique effect, but changes in alpha and beta diversities following FDX- and IBZ-treated groups were less pronounced than those observed in VAN- or MET-treated groups. By the end of therapy, both IBZ and FDZ increased the relative abundance of Bacteroidota (phylum), with IBZ additionally increasing the relative abundance of Actinomycetota (phylum). In microbiome-humanized mice, IBZ and FDX had smaller effects on gut microbiome diversity than VAN and MET. Notable differences were observed between the microbiome of IBZ- and FDX-treated groups, which may allow for differentiation of these two antibiotics in future studies.},
}

@article {pmid39996827,
year = {2025},
author = {Lu, D and Ma, X and Tao, K and Lei, H},
title = {Advancements in the Pathogenesis, Diagnosis, and Therapeutic Implications of Intestinal Bacteria.},
journal = {Current issues in molecular biology},
volume = {47},
number = {2},
pages = {},
pmid = {39996827},
issn = {1467-3045},
support = {2024AFB070//Hubei Natural Science Foundation/ ; 2023XHYN043//Science Foundation of Union Hospital/ ; 82403220//National Natural Science Foundation of China/ ; },
abstract = {Intestinal bacteria form one of the most complex microbial communities in the human body, playing a crucial role in maintaining host health and contributing to the development of various diseases. Here, we provide a comprehensive overview of the composition and function of intestinal bacteria, the factors affecting their homeostasis, and their association and mechanisms with a range of diseases (e.g., inflammatory bowel diseases, colorectal cancer, metabolic diseases). Additionally, their advanced potential in disease diagnosis and treatment is highlighted. Therapies, such as chemotherapy, radiotherapy, and immunotherapy, are significantly impacted by intestinal bacteria, with research indicating that bacteria can enhance chemoimmunotherapy efficiency by affecting T cell recruitment and immune cell infiltration. Fecal microbiota transplantation has emerged as a promising option for treating recurrent Clostridium difficile infections and certain metabolic and neurological disorders. Gut bacteria-related serum metabolites serve as non-invasive indicators for diagnosing CRC, while fecal immunochemical tests offer promising applications in CRC screening. Future research is needed to better understand the causal relationships between intestinal bacteria and diseases, develop more precise diagnostic tools, and evaluate the effectiveness and safety of microbiome-targeted therapies in clinical treatment. This study provides deeper insights into the role of intestinal bacteria in human health and disease, providing a scientific basis for innovative therapeutic strategies that have the potential to transform the landscape of healthcare.},
}

@article {pmid39996549,
year = {2025},
author = {Yu, YS and Weng, YT and Wu, CW and Tzeng, YS},
title = {Successful Perianal Wound Treatment Using the Fecal Management System: A Report of 2 Cases.},
journal = {Annals of plastic surgery},
volume = {94},
number = {3S Suppl 1},
pages = {S87-S89},
doi = {10.1097/SAP.0000000000004197},
pmid = {39996549},
issn = {1536-3708},
mesh = {Humans ; Female ; Aged ; Young Adult ; *Wound Healing/physiology ; Negative-Pressure Wound Therapy/methods ; Debridement/methods ; Anal Canal/injuries/surgery ; Skin Transplantation/methods ; Burns/therapy ; Treatment Outcome ; Colostomy/methods ; },
abstract = {BACKGROUND: Fecal diversion is important for healing of perianal wounds. However, traditional fecal diversion with colostomy is associated with risks of general anesthesia and requires healthy abdominal skin for stoma creation. Alternative methods of fecal diversion are needed.

AIM AND OBJECTIVES: We aimed to illustrate an effective alternate method of fecal diversion in patients with perianal wounds by reporting 2 patients with perianal wounds who were successfully treated using the fecal management system.

MATERIALS AND METHODS: The first patient was a 79-year-old female with a grade IV sacral pressure injury who underwent operative debridements and vacuum-assisted wound closure. The second patient was a 21-year-old female with extensive perianal burn wounds who underwent a series of debridements, wound dressing changes, and split-thickness skin grafts. The fecal management system was utilized for fecal diversion in both patients.

RESULTS: Satisfactory wound healing was achieved in each patient using the fecal management system for fecal diversion.

CONCLUSIONS: Based on our 2 patients and previous studies that have reported successful treatment of perianal wounds using the fecal management system, this system is feasible to use and effective. We suggest its use in patients with perianal wounds, particularly those in whom colostomy is not preferable or contraindicated.},
}

Humans
Female
Aged
Young Adult
*Wound Healing/physiology
Negative-Pressure Wound Therapy/methods
Debridement/methods
Anal Canal/injuries/surgery
Skin Transplantation/methods
Burns/therapy
Treatment Outcome
Colostomy/methods

@article {pmid39996473,
year = {2025},
author = {Wang, X and Hu, M and Wu, W and Lou, X and Gao, R and Ma, T and Dheen, ST and Cheng, J and Xiong, J and Chen, X and Wang, J},
title = {Indole derivatives ameliorated the methamphetamine-induced depression and anxiety via aryl hydrocarbon receptor along "microbiota-brain" axis.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2470386},
doi = {10.1080/19490976.2025.2470386},
pmid = {39996473},
issn = {1949-0984},
mesh = {Animals ; Mice ; *Receptors, Aryl Hydrocarbon/metabolism/genetics ; *Methamphetamine/adverse effects ; *Depression/chemically induced/metabolism/drug therapy ; *Indoles/pharmacology/metabolism ; *Anxiety/microbiology ; *Gastrointestinal Microbiome/drug effects ; *Brain-Gut Axis/drug effects ; Male ; Humans ; *Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; Bacteria/classification/genetics/metabolism/isolation & purification ; Tryptophan/metabolism ; Brain/metabolism ; Mice, Knockout ; Adult ; Substance Withdrawal Syndrome/drug therapy/metabolism ; },
abstract = {In addition to the high neurotoxicity, depression, and anxiety are the most prominent characteristics of methamphetamine (Meth) withdrawal. Studies to date on the issue of Meth-associated depression and anxiety are focused on the brain, however, whether peripheral homeostasis, especially the "microbiota-gut" axis participates in these adverse outcomes, remains poorly understood. In the current study, with the fecal microbiota transplantation (FMT) assay, the mice received microbiota from Meth withdrawal mice displayed marked depression and anxiety behaviors. The 16S rRNA sequencing results showed that Meth withdrawal contributed to a striking reduction of Akkermansia, Bacteroides, Faecalibaculum, Desulfovibrio, and Anaerostipes, which are known to be associated with tryptophan (TRP) metabolism. Noteworthily, the substantial decreases of the indole derivatives from the TRP metabolic pathway, including IAA, IPA, ILA, IET, IArA, IAld, and TRM were observed in the serum of both Meth abusing humans and mice during Meth withdrawal with the UHPLC-MS/MS analysis. Combining the high and low TRP diet mouse model, the mice with high TRP diet obviously impeded Meth-associated depression and anxiety behaviors, and these results were further strengthened by the evidence that administration of IPA, IAA, and indole dramatically ameliorated the Meth induced aberrant behaviors. Importantly, these protective effects were remarkably counteracted in aryl hydrocarbon receptor knockout (AhR KO) mice, underlining the key roles of microbiota-indoles-AhR signaling in Meth-associated depression and anxiety. Collectively, the important contribution of the present work is that we provide the first evidence that peripheral gut homeostasis disturbance but not limited to the brain, plays a key role in driving the Meth-induced depression and anxiety in the periods of withdrawal, especially the microbiota and the indole metabolic disturbance. Therefore, targeting AhR may provide novel insight into the therapeutic strategies for Meth-associated psychological disorders.},
}

Animals
Mice
*Receptors, Aryl Hydrocarbon/metabolism/genetics
*Methamphetamine/adverse effects
*Depression/chemically induced/metabolism/drug therapy
*Indoles/pharmacology/metabolism
*Anxiety/microbiology
*Gastrointestinal Microbiome/drug effects
*Brain-Gut Axis/drug effects
Male
Humans
*Mice, Inbred C57BL
Fecal Microbiota Transplantation
Bacteria/classification/genetics/metabolism/isolation & purification
Tryptophan/metabolism
Brain/metabolism
Mice, Knockout
Adult
Substance Withdrawal Syndrome/drug therapy/metabolism

@article {pmid39996135,
year = {2025},
author = {Sehgal, K and Berry, P and Cho, J and Saffouri, G and Dierkhising, RA and Battaglioli, E and Kashyap, PC and Pardi, D and Khanna, S},
title = {Body mass index changes after fecal microbiota transplantation for recurrent Clostridioides difficile infection.},
journal = {Therapeutic advances in gastroenterology},
volume = {18},
number = {},
pages = {17562848251321121},
pmid = {39996135},
issn = {1756-283X},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is a successful therapy for Clostridioides difficile infection (CDI). FMT from overweight donors is speculated to influence the recipient's body mass index (BMI) after administration for CDI.

OBJECTIVES: We investigated changes in the recipient's BMI after FMT in relation to the donor's BMI.

DESIGN: We conducted a retrospective cohort study involving patients who underwent FMT for recurrent CDI at Mayo Clinic between 2012 and 2019.

METHODS: We analyzed demographic and donor data for patients undergoing FMT at Mayo Clinic (2012-2019). Recipient BMI (pre- and post-FMT) and donor BMI were extracted from medical records. Mixed-effects linear regression was used to evaluate the impact of donor BMI, donor BMI category, recipient baseline BMI, time before and after FMT, and interactions between these variables on overall BMI change and BMI change per month. Kaplan-Meier curves were used to assess BMI changes (⩾5 units) based on the last recorded post-FMT BMI.

RESULTS: We analyzed data from 401 patients with recorded BMI measurements before and after FMT. The median age of the recipients at the time of FMT was 59.1 years (interquartile range (IQR): 40.5-70.1 years), with 61.6% being female. The median BMI for recipients prior to FMT was 26.7 kg/m² (IQR: 22.7-31.6 kg/m²), while the median BMI of the donors was 24.5 kg/m[2] (IQR: 23.9-27.5 kg/m[2]). Stool from donors with a normal BMI was used for 58.2% of recipients, while 41.8% received stool from pre-obese donors. Donor BMI data were missing for 3.2% of recipients. Donor BMI was not significantly associated with changes in recipient BMI; for each 1-unit increase in donor BMI, a 0.01-unit monthly increase was observed (95% confidence interval: -0.0003, 0.02; p = 0.11). The log-rank test for BMI increases (⩾+5) and decreases (⩽-5) revealed no significant differences among the donor BMI groups (Chi-squared = 4.4, p = 0.1 for increases, Chi-squared = 2, p = 0.4 for decreases).

CONCLUSION: The lack of impact of donor BMI on BMI changes post-FMT suggests that these changes are more dependent on the recipient's metabolic profile. Prospective, controlled trials are required to analyze these results more comprehensively.},
}

@article {pmid39996003,
year = {2025},
author = {Ren, K and Yong, C and Jin, Y and Rong, S and Xue, K and Cao, B and Wei, H},
title = {Unraveling the microbial mysteries: gut microbiota's role in ulcerative colitis.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1519974},
pmid = {39996003},
issn = {2296-861X},
abstract = {Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by persistent inflammation of the colon. Recent research has highlighted the significant role of gut microbiota in the pathogenesis and treatment of UC. This review aims to provide a comprehensive overview of the current understanding of the relationship between gut microbiota and UC. We discuss the involvement of gut microbiota in the onset of UC, including the dysbiosis observed in patients and its potential mechanisms. Additionally, the role of extra-intestinal microbiota in UC pathogenesis is explored, which has been less studied but is gaining attention. The influence of gut microbiota on the efficacy of biological immunotherapy for UC is also examined, highlighting how microbial composition can influence treatment outcomes. Furthermore, we review microbiota transplantation, and their potential benefits in UC management. Finally, we consider the combined use of antibiotics and biological agents in UC treatment, discussing their synergistic effects and potential drawbacks. This review underscores the importance of gut microbiota in UC and suggests that targeting microbial communities could offer new avenues for effective treatment.},
}

@article {pmid39995913,
year = {2025},
author = {Morshedbak, M and Rahimi, K and Tabandeh, MR},
title = {Effect of fecal microbiota transplantation on ulcerative colitis model in rats: The gut-brain axis.},
journal = {Heliyon},
volume = {11},
number = {3},
pages = {e42430},
pmid = {39995913},
issn = {2405-8440},
abstract = {STUDY OBJECTIVES: The impact of fecal microbiota transplantation (FMT) on the TLR4/MYD88/NF-kB signaling pathway in the colon in the ulcerative colitis model, as well as the incidence of anxiety behaviors caused by the colitis model was investigated.

METHODS: Twenthy four ats were induced with ulcerative colitis using a 4 % acetic acid solution administered intrarectally and were subsequently treated with prednisolone and FMT. The study examined several indicators, such as TLR4, MYD88, and NF-κB mRNA expression, along with oxidative stress factors. Additionally, it examined the relationship between anxiety-related behaviors and colitis and assessed the pro-inflammatory cytokines in the hippocampus.

RESULTS: FMT led to lower disease score index and improved colon tissue pathology findings. This was associated with reduced mRNA expression of TLR4, MYD88, and NF-κB, as well as lower levels of TOS, and higher levels of TAC, GSH, and GSSG in colon tissues. FMT was found to reduce anxiety in both the open field and elevated plus maze tests. Additionally, levels of IL-6 and TNF-a were decreased in the hippocampus.

CONCLUSIONS: FMT suppressed acetic acid-induced colitis by inhibiting the TLR4/MYD88/NF-kB signaling pathway. FMT reduced anxiety in open field and plus maze tests, and resulted in decreased levels of IL-6 and TNF-a in the hippocampus.},
}

@article {pmid39994836,
year = {2025},
author = {Wan, J and Zhou, J and Wang, Z and Liu, D and Zhang, H and Xie, S and Wu, K},
title = {Recent advances in epidemiology, pathogenesis, diagnosis, and treatment of inflammatory bowel disease: Insights from the past two years.},
journal = {Chinese medical journal},
volume = {},
number = {},
pages = {},
pmid = {39994836},
issn = {2542-5641},
abstract = {Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease, is a chronic inflammation of the gastrointestinal tract with unknown etiology. The cause of IBD is widely considered multifactorial, with prevailing hypotheses suggesting that the microbiome and various environmental factors contribute to inappropriate activation of the mucosal immune system in genetically susceptible individuals. Although the incidence of IBD has stabilized in Western countries, it is rapidly increasing in newly industrialized countries, particularly China, making IBD a global disease. Significant changes in multiple biomarkers before IBD diagnosis during the preclinical phase provide opportunities for earlier diagnosis and intervention. Advances in technology have driven the development of telemonitoring tools, such as home-testing kits for fecal calprotectin, serum cytokines, and therapeutic drug concentrations, as well as wearable devices for testing sweat cytokines and heart rate variability. These tools enable real-time disease activity assessment and timely treatment strategy adjustments. A wide range of novel drugs for IBD, including interleukin-23 inhibitors (mirikizumab, risankizumab, and guselkumab) and small-molecule drugs (etrasimod and upadacitinib), have been introduced in the past few years. Despite these advancements, approximately one-third of patients remain primary non-responders to the initial treatment, and half eventually lose response over time. Precision medicine integrating multi-omics data, advanced combination therapy, and complementary approaches, including stem cell transplantation, psychological therapies, neuromodulation, and gut microbiome modulation therapy, may offer solutions to break through the therapeutic ceiling.},
}

@article {pmid39994634,
year = {2025},
author = {Almheiri, RT and Hajjar, B and Alkhaaldi, SMI and Rabeh, N and Aljoudi, S and Abd-Elrahman, KS and Hamdan, H},
title = {Beyond weight loss: exploring the neurological ramifications of altered gut microbiota post-bariatric surgery.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {223},
pmid = {39994634},
issn = {1479-5876},
mesh = {Humans ; *Bariatric Surgery ; *Gastrointestinal Microbiome ; *Weight Loss ; *Nervous System Diseases/microbiology ; Animals ; },
abstract = {This review discusses findings related to neurological disorders, gut microbiota, and bariatric surgery, focusing on neurotransmitters, neuroendocrine, the pathophysiology of bacteria contributing to disorders, and possible therapeutic interventions. Research on neurotransmitters suggests that their levels are heavily influenced by gut microbiota, which may link them to neurological disorders such as Alzheimer's disease, Parkinson's disease, Multiple sclerosis, Depression, and Autism spectrum disorder. The pathophysiology of bacteria that reach and influence the central nervous system has been documented. Trends in microbiota are often observed in specific neurological disorders, with a prominence of pro-inflammatory bacteria and a reduction in anti-inflammatory types. Furthermore, bariatric surgery has been shown to alter microbiota profiles similar to those observed in neurological disorders. Therapeutic interventions, including fecal microbiota transplants and probiotics, have shown potential to alleviate neurological symptoms. We suggest a framework for future studies that integrates knowledge from diverse research areas, employs rigorous methodologies, and includes long-trial clinical control groups.},
}

Humans
*Bariatric Surgery
*Gastrointestinal Microbiome
*Weight Loss
*Nervous System Diseases/microbiology
Animals

@article {pmid39991465,
year = {2025},
author = {Ahmadi, A and Kouhsari, E and Razavi, S and Mohamadzadeh, N and Besharat, S and Vakili, MA and Amiriani, T},
title = {Comparative analysis of dominant gut microbiota in Inflammatory Bowel Disease patients and healthy individuals: A case-control study.},
journal = {New microbes and new infections},
volume = {64},
number = {},
pages = {101567},
pmid = {39991465},
issn = {2052-2975},
abstract = {BACKGROUND: Chronic inflammation in the gut might be linked to microbiota dysbiosis.

OBJECTIVE: This study aimed to investigate alterations in the gut microbiota composition of adult IBD patients compared to healthy controls.

METHODS: This case-control study investigated the relationship between faecal microbiota composition and IBD in adults. Real-time qPCR analysis using bacterial 16S rRNA gene quantified the abundance of six key bacterial groups (Firmicutes, Lactobacillus spp., Bifidobacterium spp., Fusobacterium spp., Bacteroides fragilis, and Faecalibacterium prausnitzii) in faecal samples from 30 IBD patients (13 Crohn's disease, 17 ulcerative colitis) and 30 healthy controls. A correlation matrix was employed to assess relationships between these bacteria.

RESULTS: Real-time qPCR revealed significant differences (p-value <0.05) in the abundance of several bacterial groups between IBD patients and healthy controls. Firmicutes, Fusobacterium spp., and B. fragilis were significantly more abundant (p-value <0.05) in IBD patients compared to controls. Conversely, Lactobacillus spp. and F. prausnitzii were both significantly less abundant (p-value <0.05) in IBD patients. While some bacterial groups exhibited trends toward higher abundance in either CD or UC patients, these differences were not statistically significant (p-value >0.111). The correlation matrix analysis revealed specific co-occurrence patterns: Bacteroides showed a strong negative correlation with Prevotella, more abundant in healthy controls, suggesting a shift in dominance in IBD patients. Lactobacillus spp. and F. prausnitzii exhibited a positive correlation in healthy individuals, indicating their potential cooperative role in maintaining gut homeostasis.

CONCLUSION: This study identified significant alterations in gut microbiota composition in adult IBD patients compared to healthy controls, with notable differences in the abundance of specific bacterial groups. These findings suggest that gut microbiota dysbiosis may play a critical role in IBD pathogenesis. The identification of specific bacterial imbalances provides a foundation for developing microbiota-based therapies, such as probiotics, prebiotics, and fecal microbiota transplantation, as potential interventions for restoring microbial balance and mitigating disease progression. Further research is needed to translate these insights into targeted therapeutic strategies and to explore their effectiveness in clinical settings.},
}

@article {pmid39989875,
year = {2025},
author = {Bednárik, DS and Földvári-Nagy, KC and Simon, V and Rancz, A and Gede, N and Veres, DS and Paraskevopoulos, P and Schnabel, T and Erőss, B and Hegyi, P and Lenti, K and Földvári-Nagy, L},
title = {Comparative effectiveness of different therapies for Clostridioides difficile infection in adults: a systematic review and network meta-analysis of randomized controlled trials.},
journal = {The Lancet regional health. Europe},
volume = {49},
number = {},
pages = {101151},
pmid = {39989875},
issn = {2666-7762},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) is a leading cause of healthcare-associated diarrhea, with substantial morbidity and mortality. CDI is a severe and growing problem with numerous treatment options. We evaluated the effectiveness of all therapies in recurrent and non-recurrent infections and their prevention.

METHODS: This network meta-analysis and systematic review of randomized controlled trials (RCTs) compared all CDI therapies and preventions. We included RCTs published until 19 August 2024 and focused on adult population. We performed a systematic search in MEDLINE, EMBASE, and Cochrane Central Register of Controlled Trials. Inclusion criteria were patients: adults (>16) treated against CDI; study type: randomized controlled trial; outcome: cure rate, recurrence or effectiveness of prevention. Any publication not meeting all criteria was considered to be ineligible and excluded. We applied random-effects meta-analysis using frequentist methods. We reported our main results as odds ratios (as a symmetric effect size measure, OR) with 95% confidence interval (95% CI). We used the Cochrane risk-of-bias tool to assess the risk of bias. Our study protocol was preregistered in PROSPERO (CRD42022371210).

FINDINGS: We assessed 73 RCTs with 28 interventions, involving 27,959 patients (49.2% female) in five networks. Fecal microbiota transplantation (FMT) was the most effective treatment in terms of the cure rate overall (P-score: 0.9952) and in recurrent cases (P-score: 0.9836). In recurrent cases, fidaxomicin (P-score: 0.6734) showed significantly greater effectiveness than vancomycin (P-score: 0.3677) and tolevamer (P-score: 0.0365). For non-recurrent CDI treatments ridinilazole, fidaxomicin, FMT and nitazoxanide were equally effective. Ridinilazole (P-score: 0.7671) and fidaxomicin (P-score: 0.7627) emerged as the most effective in preventing recurrence. Probiotics were not effective in preventing CDI, since network meta-analyses did not show significant differences between probiotics and placebo. In probiotics' subgroups pairwise meta-analyses Lactobacillaceae proved to be significantly more effective in prevention than placebo. Oral and colonoscopic FMT administration methods were equally effective. The study-level aggregated risk of bias of the publications included ranged from low to high. We observed relevant heterogeneity among studies in therapeutic doses, treatment durations, and follow-up times.

INTERPRETATION: The superiority of FMT in the treatment of CDI highlights the potential for increased use of FMT in clinical settings. Further research on optimizing FMT protocols and exploring its long-term safety and efficacy in larger samples is needed. Our findings suggest that the preventive use of probiotics might be questioned.

FUNDING: None.},
}

@article {pmid39989768,
year = {2025},
author = {Reddi Sree, R and Kalyan, M and Anand, N and Mani, S and Gorantla, VR and Sakharkar, MK and Song, BJ and Chidambaram, SB},
title = {Newer Therapeutic Approaches in Treating Alzheimer's Disease: A Comprehensive Review.},
journal = {ACS omega},
volume = {10},
number = {6},
pages = {5148-5171},
pmid = {39989768},
issn = {2470-1343},
abstract = {Alzheimer's disease (AD) is an aging-related irreversible neurodegenerative disease affecting mostly the elderly population. The main pathological features of AD are the extracellular Aβ plaques generated by APP cleavage through the amyloidogenic pathway, the intracellular neurofibrillary tangles (NFT) resulting from the hyperphosphorylated tau proteins, and cholinergic neurodegeneration. However, the actual causes of AD are unknown, but several studies suggest hereditary mutations in PSEN1 and -2, APOE4, APP, and the TAU genes are the major perpetrators. In order to understand the etiology and pathogenesis of AD, various hypotheses are proposed. These include the following hypotheses: amyloid accumulation, tauopathy, inflammation, oxidative stress, mitochondrial dysfunction, glutamate/excitotoxicity, cholinergic deficiency, and gut dysbiosis. Currently approved therapeutic interventions are donepezil, galantamine, and rivastigmine, which are cholinesterase inhibitors (ChEIs), and memantine, which is an N-methyl-d-aspartate (NMDA) antagonist. These treatment strategies focus on only symptomatic management of AD by attenuating symptoms but not regeneration of neurons or clearance of Aβ plaques and hyperphosphorylated Tau. This review focuses on the pathophysiology, novel therapeutic targets, and disease-altering treatments such as α-secretase modulators, active immunotherapy, passive immunotherapy, natural antioxidant products, nanomaterials, antiamyloid therapy, tau aggregation inhibitors, transplantation of fecal microbiota or stem cells, and microtubule stabilizers that are in clinical trials or still under investigation.},
}

@article {pmid39989751,
year = {2025},
author = {Arantes, JA and Di Pietro, R and Ratté, M and Arroyo, LG and Leclère, M and Costa, MC},
title = {Changes in bacterial viability after preparation and storage of fecal microbiota transplantation solution using equine feces.},
journal = {PeerJ},
volume = {13},
number = {},
pages = {e18860},
pmid = {39989751},
issn = {2167-8359},
mesh = {Animals ; Horses/microbiology ; *Feces/microbiology ; *Fecal Microbiota Transplantation/methods ; *Microbial Viability/drug effects ; Cryoprotective Agents/pharmacology ; Freezing ; Glycerol/pharmacology ; Cryopreservation/methods ; Bacteria/drug effects ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) has been used as a treatment option for horses (Equus caballus) with gastrointestinal diseases. Several preparation and conservation protocols to improve bacterial survival have been studied in other species.

METHODS: This study aimed to evaluate the impact of oxygen exposure and different protectant solutions on bacterial viability before and after freezing using horse feces. Fecal samples from 10 healthy horses were aliquoted and diluted in cryoprotectant solutions containing antioxidants (n = 40) or 10% glycerol (n = 40). Half of the aliquots from each dilution condition were prepared inside an anaerobic chamber, while the other half were prepared under ambient air conditions. Each sample was also analyzed fresh and after freezing at -20 °C for 90 days. Bacterial viability was assessed using flow cytometry. A mixed linear model and the Friedman and Wilcoxon tests were used depending on data distribution.

RESULTS: Freeze-thawing decreased bacterial viability by 47% (mean ± SD: 51 ± 27% before, 27 ± 8% after; p < 0.001). Glycerol was superior to the cryoprotectant after freezing (32 ± 8% glycerol, 24 ± 8% cryoprotectant; p < 0.001). Oxygen exposure did not affect viability (p = 0.13). There was no statistical difference between protectant solutions in fresh samples (p = 0.16).

CONCLUSIONS: Fresh FMT solutions may be better for treating horses with dysbiosis, but if freezing cannot be avoided, glycerol should be used to dilute feces.},
}

Animals
Horses/microbiology
*Feces/microbiology
*Fecal Microbiota Transplantation/methods
*Microbial Viability/drug effects
Cryoprotective Agents/pharmacology
Freezing
Glycerol/pharmacology
Cryopreservation/methods
Bacteria/drug effects

@article {pmid39988618,
year = {2025},
author = {Liang, Y and Du, M and Li, X and Gao, J and Li, Q and Li, H and Li, J and Gao, X and Cong, H and Huang, Y and Li, X and Wang, L and Cui, J and Gan, Y and Tu, H},
title = {Upregulation of Lactobacillus spp. in gut microbiota as a novel mechanism for environmental eustress-induced anti-pancreatic cancer effects.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2470372},
doi = {10.1080/19490976.2025.2470372},
pmid = {39988618},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome ; Animals ; Mice ; Humans ; *Pancreatic Neoplasms/microbiology/immunology/therapy/pathology ; *Lactobacillus/physiology ; *Killer Cells, Natural/immunology ; *Carcinoma, Pancreatic Ductal/microbiology/immunology/therapy/pathology ; Fecal Microbiota Transplantation ; Mice, Inbred C57BL ; Tumor Microenvironment/immunology ; Up-Regulation ; Male ; Female ; Feces/microbiology ; Probiotics/administration & dosage/pharmacology ; Limosilactobacillus reuteri/physiology ; Cell Line, Tumor ; },
abstract = {Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy with limited effective treatment options. Emerging evidence links enriched environment (EE)-induced eustress to PDAC inhibition. However, the underlying mechanisms remain unclear. In this study, we explored the role of gut microbiota in PDAC-suppressive effects of EE. We demonstrated that depletion of gut microbiota with antibiotics abolished EE-induced tumor suppression, while fecal microbiota transplantation (FMT) from EE mice significantly inhibited tumor growth in both subcutaneous and orthotopic PDAC models housed in standard environment. 16S rRNA sequencing revealed that EE enhanced gut microbiota diversity and selectively enriched probiotic Lactobacillus, particularly L. reuteri. Treatment with L. reuteri significantly suppressed PDAC tumor growth and increased natural killer (NK) cell infiltration into the tumor microenvironment. Depletion of NK cells alleviated the anti-tumor effects of L. reuteri, underscoring the essential role of NK cell-mediated immunity in anti-tumor response. Clinical analysis of PDAC patients showed that higher fecal Lactobacillus abundance correlated with improved progression-free and overall survival, further supporting the therapeutic potential of L. reuteri in PDAC. Overall, this study identifies gut microbiota as a systemic regulator of PDAC under psychological stress. Supplementation of psychobiotic Lactobacillus may offer a novel therapeutic strategy for PDAC.},
}

*Gastrointestinal Microbiome
Animals
Mice
Humans
*Pancreatic Neoplasms/microbiology/immunology/therapy/pathology
*Lactobacillus/physiology
*Killer Cells, Natural/immunology
*Carcinoma, Pancreatic Ductal/microbiology/immunology/therapy/pathology
Fecal Microbiota Transplantation
Mice, Inbred C57BL
Tumor Microenvironment/immunology
Up-Regulation
Male
Female
Feces/microbiology
Probiotics/administration & dosage/pharmacology
Limosilactobacillus reuteri/physiology
Cell Line, Tumor

@article {pmid39984137,
year = {2025},
author = {Dai, J and Yang, J and Han, S and Li, N and Wang, S and Xia, S and Kim, HH and Jun, Y and Lee, S and Kitagawa, Y and Xie, F and Yang, L and Shen, S and Chen, L and Turner, DP and Hodin, RA and Martyn, JAJ and Mao, J and You, Z},
title = {Deficiency of intestinal alkaline phosphatase affects behavior and microglia activity in mice.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.bbi.2025.02.006},
pmid = {39984137},
issn = {1090-2139},
abstract = {The gut microbiota plays crucial roles in the development and functions of the central nervous system (CNS) as well as in modulation of neurobehavior in heath and disease. The gut brush border enzyme intestinal alkaline phosphatase (IAP) is an important positive regulator of gut microbial homeostasis. In mice, IAP is encoded by Akp3 gene, which is specifically expressed in the duodenum of the small intestine. IAP deficiency alters gut bacterial composition and gut barrier function. Decreased IAP activity has been observed in aging, gut inflammatory diseases, and metabolic disorders. We hypothesized that this enzyme could also play an important role in modulating neurobehavior. We performed deep sequencing of gut bacterial 16S rRNA and found that IAP deficiency changed gut microbiota composition at various taxonomic levels. Using targeted metabolomic analysis, we also found that IAP deficiency resulted in changes of gut bacteria-derived metabolites in serum and brain metabolism. Neurobehavioral analyses revealed that Akp3[-/-] (IAP knockout) mice had decreased basal nociception thresholds, increased anxiety-like behavior, and reduced locomotor activity. Furthermore, Akp3[-/-] mice had more pronounced brain microglial phagocytic activity, together with an increase in the activated microglia population. Fecal microbiota transplantation from wildtype to Akp3[-/-] mice partially improved neurobehavior and reduced brain microglial phagocytic activity in Akp3[-/-] mice. This study demonstrates that deficiency of the endogenous gut-derived host factor IAP induces behavioral phenotype changes (nociception; motor activity, and anxiety) and affects brain microglia activity. Changes in the gut microbiota induced by knocking down Akp3 contribute to behavioral changes, which is probably mediated by microglia activity modulated by the gut bacteria-derived metabolites.},
}

@article {pmid39983749,
year = {2025},
author = {Davido, B and Merrick, B and Kuijper, E and Benech, N and Biehl, LM and Corcione, S and , },
title = {How can the gut microbiome be targeted to fight multidrug-resistant organisms?.},
journal = {The Lancet. Microbe},
volume = {},
number = {},
pages = {101063},
doi = {10.1016/j.lanmic.2024.101063},
pmid = {39983749},
issn = {2666-5247},
abstract = {The rise of antimicrobial resistance presents a challenge to public health, undermines the efficacy of antibiotics, and compromises the management of infectious diseases. Gut colonisation by multidrug-resistant organisms, such as multidrug-resistant Enterobacterales and vancomycin-resistant enterococci, is associated with increased morbidity and mortality rates, as well as health-care costs. Of late, the role of the gut microbiome in combating colonisation by multidrug-resistant organisms, which could precede invasive infection, has garnered interest. Innovative interventions, including faecal microbiota transplantation, probiotics, phage therapy, and bacterial consortia, represent potential preventive or therapeutic options to counteract colonisation by multidrug-resistant organisms. In this Personal View, we have synthesised the current findings on these interventions and elucidated their potential as solutions to the crisis of antimicrobial resistance.},
}

@article {pmid39981255,
year = {2025},
author = {Yao, K and Zheng, L and Chen, W and Xie, Y and Liao, C and Zhou, T},
title = {Characteristics, pathogenic and therapeutic role of gut microbiota in immunoglobulin A nephropathy.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1438683},
pmid = {39981255},
issn = {1664-3224},
mesh = {*Glomerulonephritis, IGA/microbiology/therapy/immunology/drug therapy ; Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Dysbiosis ; Immunity, Mucosal ; Immunoglobulin A/immunology ; },
abstract = {Immunoglobulin A nephropathy (IgAN) is the most prevalent glomerulonephritis in the world, and it is one of the leading causes of end-stage kidney disease. It is now believed that the pathogenesis of IgAN is the mesangial deposition of immune complex containing galactose-deficient IgA1, resulting in glomerular injury. Current treatments for IgAN include supportive care and immunosuppressive therapy. A growing number of studies found that the gut microbiota in IgAN was dysregulated. Gut microbiota may be involved in the development and progression of IgAN through three main aspects: destruction of intestinal barrier, changes in metabolites and abnormal mucosal immunity. Interestingly, therapies by modulating the gut microbiota, such as fecal microbiota transplantation, antibiotic treatment, probiotic treatment, Chinese herbal medicine Zhen Wu Tang treatment, gluten-free diet, and hydroxychloroquine treatment, can improve IgAN. In this review, the alteration of gut microbiota in IgAN, potential pathogenic roles of gut microbiota on IgAN and potential approaches to treat IgAN by modulating the gut microbiota are summarized.},
}

*Glomerulonephritis, IGA/microbiology/therapy/immunology/drug therapy
Humans
*Gastrointestinal Microbiome/immunology
Animals
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Dysbiosis
Immunity, Mucosal
Immunoglobulin A/immunology

@article {pmid39979990,
year = {2025},
author = {Xie, H and Zhang, H and Zhou, L and Chen, J and Yao, S and He, Q and Li, Z and Zhou, Z},
title = {Fecal microbiota transplantation promotes functional recovery in mice with spinal cord injury by modulating the spinal cord microenvironment.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {210},
pmid = {39979990},
issn = {1479-5876},
support = {202201010803//Science and Technology Project Foundation of Guangzhou City/ ; 2024A03J1068//Science and Technology Project Foundation of Guangzhou City/ ; },
mesh = {Animals ; *Spinal Cord Injuries/therapy/physiopathology/microbiology ; *Recovery of Function ; *Spinal Cord/pathology/physiopathology ; *Fecal Microbiota Transplantation ; *Mice, Inbred C57BL ; Gastrointestinal Microbiome ; Cellular Microenvironment ; Female ; Mice ; Axons ; RNA, Ribosomal, 16S/genetics ; Inflammation/pathology ; },
abstract = {BACKGROUND: spinal cord injury (SCI) disrupts the gut microbiota, worsening the injury's impact. Fecal microbiota transplantation (FMT) is increasingly recognized as a promising strategy to improve neural function post-SCI, yet its precise mechanisms are still far from clear. The present study aims to elucidate how FMT influences motor function recovery and its underlying mechanisms utilizing a SCI mouse model.

METHODS: Mice with SCI received FMT from healthy donors. We used 16 S rRNA amplicon sequencing to analyze the alterations of gut microbes. Pathological alterations in the spinal cord tissue, including neuronal survival, axonal regeneration, cell proliferation, and neuroinflammation, were assessed among experimental groups. Additionally, RNA sequencing (RNA-seq) was used to explore alterations in relevant signaling pathways.

RESULTS: Significant shifts in gut microbiota composition following SCI were observed through 16 S rRNA analysis. On day 7 post-SCI, the FMT group exhibited a significantly higher diversity of gut microbiota compared to the ABX group, with the composition in the FMT group more closely resembling that of healthy mice. FMT promoted neuronal survival and axonal regeneration, leading to notable improvements in motor function compared to control mice. Immunofluorescence staining showed increased neuronal survival, alleviated extracellular matrix (ECM) deposition, diminished glial scar formation, and reduced inflammation in FMT-treated mice. RNA-seq analysis indicated that FMT induced transcriptomic changes associated with material metabolism, ECM remodeling, and anti-inflammatory responses.

CONCLUSIONS: FMT restored gut microbiota balance in SCI mice, mitigated inflammation, and promoted ECM remodeling, establishing an optimal environment for neural recovery. These findings demonstrated that FMT may represent a valuable approach to enhance functional recovery following SCI.},
}

Animals
*Spinal Cord Injuries/therapy/physiopathology/microbiology
*Recovery of Function
*Spinal Cord/pathology/physiopathology
*Fecal Microbiota Transplantation
*Mice, Inbred C57BL
Gastrointestinal Microbiome
Cellular Microenvironment
Female
Mice
Axons
RNA, Ribosomal, 16S/genetics
Inflammation/pathology

@article {pmid39978693,
year = {2025},
author = {Jiang, Y and Shi, L and Qu, Y and Ou, M and Du, Z and Zhou, Z and Zhou, H and Zhu, H},
title = {Multi-omics analysis reveals mechanisms of FMT in Enhancing antidepressant effects of SSRIs.},
journal = {Brain, behavior, and immunity},
volume = {126},
number = {},
pages = {176-188},
doi = {10.1016/j.bbi.2025.02.011},
pmid = {39978693},
issn = {1090-2139},
abstract = {OBJECTIVE: This study explores the behavioral and molecular biological impacts of Fecal Microbiota Transplantation (FMT) on depressive mice unresponsive to treatment with Selective Serotonin Reuptake Inhibitors (SSRIs).

METHODS: Healthy male C57BL/6 mice were used to establish a depression model through chronic restraint stress, treated with fluoxetine, and categorized into Response and Non-response groups. An FMT treatment was added to the Non-response group. Behavioral tests were conducted to assess symptoms of depression. The gut microbiome, plasma metabolites, and hippocampal tissue gene expression and function changes were analyzed using 16S rRNA gene sequencing, LC-MS, and RNA sequencing.

RESULTS: FMT significantly improved the depressive symptoms in SSRIs-resistant mice. There was a partial restoration in the diversity and structure of the gut microbiota in the FMT group. Compared to the Non-response group, significant changes were noted in the metabolomic profiles of the FMT group, identifying various differential metabolites. Functional annotations indicated that these metabolites are involved in multiple metabolic pathways. In the Non-response group, certain gene expression levels were significantly restored. GO and KEGG enrichment analyses revealed that these differential genes mainly involve cytokine activity, receptor signaling regulation, and NOD-like receptor signaling pathways. Joint analysis suggested that FMT may exert its effects through an increase in the abundance of g__Paraprevotella, leading to decreased baicalin content and increased Tal2 expression.

CONCLUSION: FMT has potential in improving depressive symptoms unresponsive to SSRIs treatment. Its mechanism may be related to the modulation of the gut microbiota and its metabolites, subsequently affecting gene expression.},
}

@article {pmid39978276,
year = {2025},
author = {Luo, X and Cheng, P and Fang, Y and Wang, F and Mao, T and Shan, Y and Lu, Y and Wei, Z},
title = {Yinzhihuang formula modulates the microbe‒gut‒liver axis and bile acid excretion to attenuate cholestatic liver injury.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {139},
number = {},
pages = {156495},
doi = {10.1016/j.phymed.2025.156495},
pmid = {39978276},
issn = {1618-095X},
abstract = {BACKGROUND: Cholestatic liver injury is a hepatobiliary disorder primarily characterized by cholestasis, which significantly contributes to liver damage. The Yinzhihuang (YZH) oral preparation is an effective clinical treatment for cholestatic liver injury; however, the specific mechanism of action has not been clarified.

PURPOSE: This study investigated YZH's pharmacological mechanisms associated with the microbe‒gut‒liver axis in cholestatic mice, offering new perspectives for the treatment of cholestasis.

METHODS: YZH's protective effects were evaluated by evaluating serum liver injury indices and liver staining in an alpha-nephthyl isothiocyanate (ANIT)-induced intrahepatic cholestasis mouse model. Colon hematoxylin‒eosin (H&E) and alcian blue staining and FITC‒dextran leakage assays were performed to assess intestinal barrier integrity. Fluorescence in situ hybridization was employed to analyze bacterial translocation. Additionally, 16S rRNA sequencing, fecal microbiota transplantation, and bile acid metabolomics analysis were conducted to examine the relationships among the microbiome, bile acid metabolism, and YZH formula.

RESULTS: We found that YZH administration alleviated symptoms of ANIT-induced hepatic pathological injury and fibrosis. In addition, YZH reduced the transfer of gut bacteria to liver tissue by maintaining an intact intestinal barrier. Notably, YZH influenced the intestinal microbiota composition, upregulated the abundance of bile acid metabolism-associated probiotic bacteria, including Clostridiales, Lachnospiraceae and Bifidobacterium pseudolongum; and downregulated the abundance of Escherichia-Shigella and Serratia, thereby promoting bile acid excretion.

CONCLUSION: YZH protects against cholestatic liver damage by promoting bile excretion and maintaining intestinal mucosal barrier integrity. Furthermore, YZH alleviates cholestasis in a gut microbiota-dependent manner, and upregulation of probiotics may be crucial for YZH's influence on bile acid metabolism.},
}

@article {pmid39975140,
year = {2025},
author = {Oppenheimer, M and Tao, J and Moidunny, S and Roy, S},
title = {Anxiety-like behavior during protracted morphine withdrawal is driven by gut microbial dysbiosis and attenuated with probiotic treatment.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.01.29.633224},
pmid = {39975140},
issn = {2692-8205},
abstract = {The development of anxiety during protracted opioid withdrawal heightens the risk of relapse into the cycle of addiction. Understanding the mechanisms driving anxiety during opioid withdrawal could facilitate the development of therapeutics to prevent negative affect and promote continued abstinence. Our lab has previously established the gut microbiome as a driver of various side effects of opioid use, including analgesic tolerance and somatic withdrawal symptoms. We therefore hypothesized that the gut microbiome contributes to the development of anxiety-like behavior during protracted opioid withdrawal. In this study, we first established a mouse model of protracted morphine withdrawal, characterized by anxiety-like behavior and gut microbial dysbiosis. Next, we used fecal microbiota transplantation (FMT) to show that gut dysbiosis alone is sufficient to induce anxiety-like behavior. We further demonstrate that probiotic therapy during morphine withdrawal attenuates the onset of anxiety-like behavior, highlighting its therapeutic potential. Lastly, we examined transcriptional changes in the amygdala of morphine-withdrawn mice treated with probiotics to explore mechanisms by which the gut-brain axis mediates anxiety-like behavior. Our results support the use of probiotics as a promising therapeutic strategy to prevent gut dysbiosis and associated anxiety during opioid withdrawal, with potential implications for improving treatment outcomes in opioid recovery programs.},
}

@article {pmid39975029,
year = {2025},
author = {Zhang, XS and Wang, Y and Sun, H and Zerbe, C and Falcone, E and Bhattacharya, S and Zhang, M and Gao, Z and Diaz-Rubio, ME and Bharj, D and Patel, D and Pan, S and Ro, G and Grenard, J and Armstrong, A and Yin, YS and Dominguez-Bello, MG and Holland, S and Su, X and Blaser, MJ},
title = {Gut microbiota phospholipids regulate intestinal gene expression and can counteract the effects of antibiotic treatment.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {39975029},
issn = {2692-8205},
abstract = {The gut microbiome influences immune and metabolic homeostasis. Our research using non-obese diabetic (NOD) mice revealed that early-life antibiotic exposure remodels the gut microbiome affecting metabolism and accelerating type 1 diabetes (T1D) incidence, with cecal material transplant (CMT) mitigating the damage. Now examining murine intestinal lipidomic profiles, we identified 747 compounds. Comparing the lipidomic profiles of cecal contents of conventional and germ-free mice and their diets, we identified 87 microbially-produced lipids reduced by antibiotic exposure but CMT-restored. Parallel analysis of human fecal lipid profiles after azithromycin-exposure showed significant alterations with substantial overlap with mice. In vitro co-culture with mouse macrophages or small intestinal epithelial cells and human colonic epithelial cells identified phospholipids that repress inflammation through the NFκB pathway. Oral administration of these phospholipids to antibiotic-treated NOD mice reduced expression of ileal genes involved in early stages of T1D pathogenesis. These findings indicate potential therapeutic anti-inflammatory roles of microbially-produced lipids.},
}

@article {pmid39974080,
year = {2025},
author = {McCann, JR and Yang, C and Bihlmeyer, N and Tang, R and Truong, T and An, J and Jawahar, J and Ilkayeva, O and Muehlbauer, M and Hu, ZZ and Dressman, H and Poppe, L and Granek, J and David, LA and Shi, P and Balikcioglu, PG and Shah, S and Armstrong, SC and Newgard, CB and Seed, PC and Rawls, JF},
title = {Branched chain amino acid metabolism and microbiome in adolescents with obesity during weight loss therapy.},
journal = {medRxiv : the preprint server for health sciences},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.02.03.25321363},
pmid = {39974080},
abstract = {BACKGROUND: Towards improving outcomes for adolescents with obesity, we aimed to define metabolic and microbiome phenotypes at baseline and post-weight loss intervention.

METHODS: The Pediatric Obesity Microbiome and Metabolism Study enrolled 220 adolescents aged 10-18 with severe obesity (OB) and 67 healthy weight controls (HWC). Blood, stool, and clinical measures were collected at baseline and after a 6-month intervention for the OB group. Serum metabolomic and fecal microbiome data were analyzed for associations with BMI, insulin resistance, and inflammation. Fecal microbiome transplants were performed on germ-free mice using samples from both groups to assess weight gain and metabolomic changes.

RESULTS: Adolescents with OB exhibited elevated serum branched-chain amino acids (BCAA) but reduced ketoacid metabolites (BCKA) compared to HWC. This pattern was sex- and age-dependent, unlike adults with OB, who showed elevated levels of both. The fecal microbiomes of adolescents with OB and HWC had similar diversity but differed in membership and functional potential. FMT from OB and HWC donors had similar effects on mouse body weight, with specific taxa linked to weight gain in FMT recipients. Longitudinal analysis identified metabolic and microbial features correlated with changes in health measures during the intervention.

CONCLUSION: Adolescents with OB have unique metabolomic adaptations and microbiome signatures compared to their HWC counterparts and adults with OB.

TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT03139877 (Observational Study) and NCT02959034 (Repository).

FUNDING SOURCES: American Heart Association Grants: 17SFRN33670990, 20PRE35180195National Institute of Diabetes and Digestive and Kidney Diseases Grant: R24-DK110492.},
}

@article {pmid39973149,
year = {2025},
author = {Zhang, T and Liu, S and Liu, S and Zhao, P and Zhang, C and Wang, X and Meng, Y and Lu, Y},
title = {Oleanolic Acid Alleviates Hyperuricemia via Gut Microbiota Control the Integrity of Gut Barrier and the Expressions of Urate Transporter in Mice.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.4c09270},
pmid = {39973149},
issn = {1520-5118},
abstract = {Hyperuricemia (HUA) is a globally prevalent metabolic disorder characterized by an imbalance in uric acid (UA) production and excretion. In this study, we found that oleanolic acid (OA), a natural pentacyclic triterpene, effectively reduced HUA and associated kidney injury in C57BL/6J mice. A 12-week OA treatment significantly and dose-dependently reduced UA and creatinine levels in serum and urine while suppressing hepatic xanthine oxidase activity in HUA mice. Mechanistic analysis revealed that OA modulates the expression of urate transporters including ABCG2, GLUT9, and URAT1 in the kidney and small intestine. Furthermore, OA restored gut microbiota imbalances, increased short-chain fatty acid production, and enhanced the expressions of intestinal tight junction proteins in HUA mice, thereby improving gut barrier integrity in HUA mice. Consequently, fecal microbiota transplantation (FMT) was employed to illustrate the major mediating role of gut microbiota in OA's alleviation of HUA in mice. Recipient HUA mice transplanted with feces from OA-treated HUA mice exhibited significantly lower blood and urinary UA levels, reduced kidney inflammation, and improved gut microbiota balance compared to those receiving feces from untreated HUA mice (p < 0.05). Additionally, FMT normalized urate transporter expression and reinforced intestinal tight junctions in recipient mice. These findings underscore that OA mitigates HUA primarily by modulating gut microbiota, regulating urate transporter expression, and reinforcing gut barrier integrity, offering novel insights into its preventive potential for managing HUA and related complications.},
}

@article {pmid39971913,
year = {2025},
author = {Cune, D and Pitasi, CL and Rubiola, A and Jamma, T and Simula, L and Boucher, C and Fortun, A and Adoux, L and Letourneur, F and Saintpierre, B and Donnadieu, E and Terris, B and Bossard, P and Chassaing, B and Romagnolo, B},
title = {Inhibition of Atg7 in intestinal epithelial cells drives resistance against Citrobacter rodentium.},
journal = {Cell death & disease},
volume = {16},
number = {1},
pages = {112},
pmid = {39971913},
issn = {2041-4889},
mesh = {*Citrobacter rodentium ; Animals ; *Autophagy-Related Protein 7/metabolism/genetics ; Mice ; *Enterobacteriaceae Infections/immunology/microbiology/pathology ; *Gastrointestinal Microbiome ; *Intestinal Mucosa/microbiology/immunology/metabolism/pathology ; *Autophagy ; Epithelial Cells/metabolism/microbiology/immunology ; Mice, Inbred C57BL ; Colitis/microbiology/immunology/pathology ; },
abstract = {Autophagy, a cytoprotective mechanism in intestinal epithelial cells, plays a crucial role in maintaining intestinal homeostasis. Beyond its cell-autonomous effects, the significance of autophagy in these cells is increasingly acknowledged in the dynamic interplay between the microbiota and the immune response. In the context of colon cancer, intestinal epithelium disruption of autophagy has been identified as a critical factor influencing tumor development. This disruption modulates the composition of the gut microbiota, eliciting an anti-tumoral immune response. Here, we report that Atg7 deficiency in intestinal epithelial cells shapes the intestinal microbiota leading to an associated limitation of colitis induced by Citrobacter rodentium infection. Mice with an inducible, intestinal epithelial-cell-specific deletion of the autophagy gene, Atg7, exhibited enhanced clearance of C. rodentium, mitigated hyperplasia, and reduced pathogen-induced goblet cell loss. This protective effect is linked to a higher proportion of neutrophils and phagocytic cells in the early phase of infection. At later stages, it is associated with the downregulation of pro-inflammatory pathways and an increase in Th17 and Treg responses-immune responses known for their protective roles against C. rodentium infection, modulated by specific gut microbiota. Fecal microbiota transplantation and antibiotic treatment approaches revealed that the Atg7-deficiency-shapped microbiota, especially Gram-positive bacteria, playing a central role in driving resistance to C. rodentium infection. In summary, our findings highlight that inhibiting autophagy in intestinal epithelial cells contributes to maintaining homeostasis and preventing detrimental intestinal inflammation through microbiota-mediated colonization resistance against C. rodentium. This underscores the central role played by autophagy in shaping the microbiota in promoting immune-mediated resistance against enteropathogens.},
}

*Citrobacter rodentium
Animals
*Autophagy-Related Protein 7/metabolism/genetics
Mice
*Enterobacteriaceae Infections/immunology/microbiology/pathology
*Gastrointestinal Microbiome
*Intestinal Mucosa/microbiology/immunology/metabolism/pathology
*Autophagy
Epithelial Cells/metabolism/microbiology/immunology
Mice, Inbred C57BL
Colitis/microbiology/immunology/pathology

@article {pmid39971742,
year = {2025},
author = {Akagbosu, CO and McCauley, KE and Namasivayam, S and Romero-Soto, HN and O'Brien, W and Bacorn, M and Bohrnsen, E and Schwarz, B and Mistry, S and Burns, AS and Perez-Chaparro, PJ and Chen, Q and LaPoint, P and Patel, A and Krausfeldt, LE and Subramanian, P and Sellers, BA and Cheung, F and Apps, R and Douagi, I and Levy, S and Nadler, EP and Hourigan, SK},
title = {Gut microbiome shifts in adolescents after sleeve gastrectomy with increased oral-associated taxa and pro-inflammatory potential.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2467833},
pmid = {39971742},
issn = {1949-0984},
support = {R25 DK096944/DK/NIDDK NIH HHS/United States ; },
mesh = {*Gastrointestinal Microbiome ; Adolescent ; Humans ; *Gastrectomy/adverse effects ; Animals ; Female ; Male ; *Feces/microbiology ; Mice ; Inflammation/microbiology ; Bacteria/classification/isolation & purification/genetics/metabolism ; Th17 Cells/immunology ; T-Lymphocytes, Regulatory/immunology ; Bariatric Surgery ; Metabolome ; Obesity, Morbid/surgery/microbiology ; Child ; Leukocyte L1 Antigen Complex/analysis/metabolism ; },
abstract = {Bariatric surgery is highly effective in achieving weight loss in children and adolescents with severe obesity, however the underlying mechanisms are incompletely understood, and gut microbiome changes are unknown. Here, we show that adolescents exhibit significant gut microbiome and metabolome shifts several months after laparoscopic vertical sleeve gastrectomy (VSG), with increased alpha diversity and notably with enrichment of oral-associated taxa. To assess causality of the microbiome/metabolome changes in phenotype, pre-VSG and post-VSG stool was transplanted into germ-free mice. Post-VSG stool was not associated with any beneficial outcomes such as adiposity reduction compared pre-VSG stool. However, post-VSG stool exhibited a potentially inflammatory phenotype with increased intestinal Th17 and decreased regulatory T cells. Concomitantly, we found elevated fecal calprotectin and an enrichment of proinflammatory pathways in a subset of adolescents post-VSG. We show that in some adolescents, microbiome changes post-VSG may have inflammatory potential, which may be of importance considering the increased incidence of inflammatory bowel disease post-VSG.},
}

*Gastrointestinal Microbiome
Adolescent
Humans
*Gastrectomy/adverse effects
Animals
Female
Male
*Feces/microbiology
Mice
Inflammation/microbiology
Bacteria/classification/isolation & purification/genetics/metabolism
Th17 Cells/immunology
T-Lymphocytes, Regulatory/immunology
Bariatric Surgery
Metabolome
Obesity, Morbid/surgery/microbiology
Child
Leukocyte L1 Antigen Complex/analysis/metabolism

@article {pmid39969373,
year = {2024},
author = {Li, Q and Obi, E and Marciniak, A and Newman, R and Whittle, I and Kufakwaro, J},
title = {Clinical and economic outcomes associated with fidaxomicin in comparison to vancomycin, metronidazole, and FMT: A systematic literature review.},
journal = {Medicine},
volume = {103},
number = {52},
pages = {e39219},
pmid = {39969373},
issn = {1536-5964},
mesh = {Humans ; *Vancomycin/therapeutic use/economics ; *Fidaxomicin/therapeutic use ; *Metronidazole/therapeutic use/economics ; *Clostridium Infections/economics/drug therapy/therapy ; *Anti-Bacterial Agents/therapeutic use/economics ; *Fecal Microbiota Transplantation/economics ; Cost-Benefit Analysis ; Treatment Outcome ; },
abstract = {BACKGROUND: There are an estimated half a million cases of Clostridioides difficile infection (CDI), in the United States annually. Fidaxomicin, vancomycin, and metronidazole are commonly used for CDI treatment, with fidaxomicin recommended by clinical guidelines as the preferred treatment for initial and recurrent CDI. This systematic literature review aimed to explore clinical and economic outcomes associated with fidaxomicin use with or without comparison to vancomycin, metronidazole, or fecal microbiota transplantation (FMT).

METHODS: The EMBASE, Medline, EconLit, and Evidence Based Medicine Reviews databases were searched from January 1st, 2012 to December 6th, 2022, as fidaxomicin was first approved for adult use in 2011. Identified publications were assessed and extracted by 2 independent reviewers.

RESULTS: Seventy-nine publications were included. Articles reporting at least 50 patients with follow-up ≤90 days were selected to obtain comparable outcome definitions (N = 14). Sustained clinical cure rate at 30- and 60-days follow-up was higher among fidaxomicin-treated patients (70.0-75.1% and 63.2-78.9%; N = 3) than vancomycin (45.1-58.2% and 38.9-50.0%; N = 3). Lower recurrence rates were reported post-fidaxomicin treatment compared to vancomycin, however the ranges overlapped at 30-, 60-, and 90-days follow-up. Limited outcomes for comparators metronidazole and FMT were identified. Healthcare resource use data were limited, with 2 studies reporting direct costs finding that fidaxomicin use-associated savings were driven by reduced hospital admission-related costs. Fidaxomicin was cost-effective in 14 of 21 economic analyses (11 vs vancomycin). Three studies reported vancomycin or FMT as more cost-effective than fidaxomicin. Fidaxomicin was consistently cost-effective or cost-saving among patients receiving concomitant antibiotics, and patients with cancer or renal impairment. Ten publications reported that the higher acquisition cost of fidaxomicin was offset by reduced recurrence and hospital readmission costs.

CONCLUSIONS: Fidaxomicin was clinically effective compared to vancomycin. Fidaxomicin is often reported as cost-effective, consistently within high-risk subpopulations.},
}

Humans
*Vancomycin/therapeutic use/economics
*Fidaxomicin/therapeutic use
*Metronidazole/therapeutic use/economics
*Clostridium Infections/economics/drug therapy/therapy
*Anti-Bacterial Agents/therapeutic use/economics
*Fecal Microbiota Transplantation/economics
Cost-Benefit Analysis
Treatment Outcome

@article {pmid39968682,
year = {2025},
author = {Yu, RL and Weber, HC},
title = {Irritable bowel syndrome, the gut microbiome, and diet.},
journal = {Current opinion in endocrinology, diabetes, and obesity},
volume = {},
number = {},
pages = {},
doi = {10.1097/MED.0000000000000905},
pmid = {39968682},
issn = {1752-2978},
abstract = {PURPOSE OF REVIEW: To provide an update of recent studies exploring the role of the gut microbiota and diet in the pathogenesis and treatment of irritable bowel syndrome (IBS).

RECENT FINDINGS: The human gut microbiome has been recognized as an important, active source of signaling molecules that explain in part the disorder of the gut brain interaction (DGBI) in IBS. Subsequent changes in the metabolome such as the production of short-chain fatty acids (SCFA) and serotonin are associated with IBS symptoms. Dietary components are recognized as important triggers of IBS symptoms and a diet low in fermentable oligo-, di-, monosaccharides, and polyols (FODMAPs) has been shown effective and safe, even when used long-term. Fecal microbiota transplantation (FMT) in IBS has not shown sustained and effective IBS symptom reduction in controlled clinical trials.

SUMMARY: This update elucidates recent developments in IBS as it relates to clinical trial results targeting dietary and gut microbiota interventions. The gut microbiome is metabolically active and affects the bi-directional signaling of the gut-brain axis.},
}

@article {pmid39773539,
year = {2025},
author = {Zeng, J and Zhao, D and Way, G and Fagan, A and Fuchs, M and Puri, P and Davis, BC and Wang, X and Gurley, EC and Hylemon, PB and Fan, JG and Sikaroodi, M and Gillevet, PM and Zhou, H and Bajaj, JS},
title = {Intestinal mucosal mitochondrial oxidative phosphorylation worsens with cirrhosis progression and is ameliorated with fecal microbiota transplantation.},
journal = {JCI insight},
volume = {10},
number = {4},
pages = {},
doi = {10.1172/jci.insight.186649},
pmid = {39773539},
issn = {2379-3708},
mesh = {*Fecal Microbiota Transplantation/methods ; *Intestinal Mucosa/microbiology/metabolism/pathology ; *Oxidative Phosphorylation ; *Liver Cirrhosis/therapy/metabolism/microbiology/pathology ; *Disease Progression ; *Mitochondria/metabolism ; Humans ; Male ; *Gastrointestinal Microbiome ; Animals ; Mice ; Middle Aged ; Female ; },
abstract = {Cirrhosis, the end-stage of liver disease, progresses through altered gut-liver axis and microbial change. Here we show that intestinal mucosal mitochondrial oxidative phosphorylation, which affects intestinal barrier worsens with cirrhosis progression. This is ameliorated with fecal microbiota transplantation.},
}

*Fecal Microbiota Transplantation/methods
*Intestinal Mucosa/microbiology/metabolism/pathology
*Oxidative Phosphorylation
*Liver Cirrhosis/therapy/metabolism/microbiology/pathology
*Disease Progression
*Mitochondria/metabolism
Humans
Male
*Gastrointestinal Microbiome
Animals
Mice
Middle Aged
Female

@article {pmid39968343,
year = {2025},
author = {Sun, T and Song, B and Li, B},
title = {Gut microbiota and atrial cardiomyopathy.},
journal = {Frontiers in cardiovascular medicine},
volume = {12},
number = {},
pages = {1541278},
pmid = {39968343},
issn = {2297-055X},
abstract = {Atrial cardiomyopathy is a multifaceted heart disease characterized by structural and functional abnormalities of the atria and is closely associated with atrial fibrillation and its complications. Its etiology involves a number of factors, including genetic, infectious, immunologic, and metabolic factors. Recent research has highlighted the critical role of the gut microbiota in the pathogenesis of atrial cardiomyopathy, and this is consistent with the gut-heart axis having major implications for cardiac health. The aim of this work is to bridge the knowledge gap regarding the interactions between the gut microbiota and atrial cardiomyopathy, with a particular focus on elucidating the mechanisms by which gut dysbiosis may induce atrial remodeling and dysfunction. This article provides an overview of the role of the gut microbiota in the pathogenesis of atrial cardiomyopathy, including changes in the composition of the gut microbiota and the effects of its metabolites. We also discuss how diet and exercise affect atrial cardiomyopathy by influencing the gut microbiota, as well as possible future therapeutic approaches targeting the gut-heart axis. A healthy gut microbiota can prevent disease, but ecological dysbiosis can lead to a variety of symptoms, including the induction of heart disease. We focus on the pathophysiological aspects of atrial cardiomyopathy, the impact of gut microbiota dysbiosis on atrial structure and function, and therapeutic strategies exploring modulation of the microbiota for the treatment of atrial cardiomyopathy. Finally, we discuss the role of gut microbiota in the treatment of atrial cardiomyopathy, including fecal microbiota transplantation and oral probiotics or prebiotics. Our study highlights the importance of gut microbiota homeostasis for cardiovascular health and suggests that targeted interventions on the gut microbiota may pave the way for innovative preventive and therapeutic strategies targeting atrial cardiomyopathy.},
}