@article {pmid41577348,
year = {2026},
author = {Liu, Y and Yan, X and Yang, J and Zhang, D and Fang, Y and Huang, J and Zhu, M and Li, L and Zhang, T and Zhang, Q and Jiang, F},
title = {Efficacy and safety of non-pharmacological therapies for irritable bowel syndrome with diarrhoea: protocol for systematic review and network meta-analysis.},
journal = {BMJ open},
volume = {16},
number = {1},
pages = {e105579},
doi = {10.1136/bmjopen-2025-105579},
pmid = {41577348},
issn = {2044-6055},
mesh = {Humans ; *Irritable Bowel Syndrome/therapy/complications ; Systematic Reviews as Topic ; *Diarrhea/therapy/etiology ; Network Meta-Analysis as Topic ; Quality of Life ; Research Design ; Probiotics/therapeutic use ; Meta-Analysis as Topic ; Cognitive Behavioral Therapy ; Acupuncture Therapy ; Randomized Controlled Trials as Topic ; },
abstract = {INTRODUCTION: Irritable bowel syndrome with diarrhoea (IBS-D) significantly impairs patients' quality of life. Although various non-pharmacological interventions show promise, evidence on their comparative effectiveness remains limited. This protocol outlines a systematic review and network meta-analysis designed to comprehensively evaluate and rank the efficacy and safety of guideline-recommended non-pharmacological therapies.

METHODS AND ANALYSIS: We will systematically search PubMed, Cochrane Library, Web of Science, Embase, China National Knowledge Infrastructure, Chinese Biomedical Database, Wanfang Data and VIP Database from inception to January 2025. Eligible studies will include randomised controlled trials assessing guideline-recommended non-pharmacological interventions, probiotics, acupuncture, cognitive-behavioural therapy, dietary modifications and faecal microbiota transplantation in adults diagnosed with IBS-D based on Rome III or IV criteria. The primary outcome is the Irritable Bowel Syndrome Symptom Severity Score. Secondary outcomes include the Irritable Bowel Syndrome Quality of Life Scale and Hospital Anxiety and Depression Scale. Two independent reviewers will screen studies, extract data and evaluate risk of bias using the Cochrane Risk of Bias 2.0 tool. Network meta-analysis will be performed using frequentist methods with Stata and R software. Transitivity, heterogeneity, consistency and publication bias will be assessed. Certainty of evidence will be graded using the Grading of Recommendations, Assessment, Development and Evaluations methodology, supplemented with trial sequential analysis to determine the required information size.

ETHICS AND DISSEMINATION: Ethical approval is not required for this secondary analysis as it uses published data. The results will be disseminated via peer-reviewed journals and conference presentations to inform clinical practice and guideline development.

REGISTRATION: INPLASY202470112.},
}

Humans
*Irritable Bowel Syndrome/therapy/complications
Systematic Reviews as Topic
*Diarrhea/therapy/etiology
Network Meta-Analysis as Topic
Quality of Life
Research Design
Probiotics/therapeutic use
Meta-Analysis as Topic
Cognitive Behavioral Therapy
Acupuncture Therapy
Randomized Controlled Trials as Topic

@article {pmid41575675,
year = {2026},
author = {Kopalli, SR and Wankhede, N and Rahangdale, SR and Sammeta, S and Aglawe, M and Koppula, S and Taksande, B and Upaganlawar, A and Umekar, M and Kale, M},
title = {Age-driven dysbiosis: gut microbiota in the pathogenesis and treatment of aging disorders.},
journal = {Biogerontology},
volume = {27},
number = {1},
pages = {42},
pmid = {41575675},
issn = {1573-6768},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/therapy/microbiology ; *Aging/physiology ; Animals ; Probiotics/therapeutic use ; },
abstract = {Aging, a complex physiological and molecular process, has undergone significant changes, of which gut microbiome composition has surfaced as an important key in the maintenance of neurological health. Recent studies have revealed the significant impact of age-related gut dysbiosis in the induction of neuroinflammation, metabolic syndrome, disruptions in gut-brain axis, and age-related neurological decline. Although significant studies have revealed the impact of the microbiome-gut-brain axis in individual neurological diseases, an aging-focused holistic synthesis has not yet been adequately developed. This review provides a critical assessment of the involvement of age-related dysbiosis of gut microbiota in the development and progression of neurological disorders such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis, and cognitive aging of the elderly, and to focus on age-related microbial patterns and mechanisms of dysbiosis related to neurological aging, including inflammation and immune system dysregulation, metabolic changes, oxidative stress, barrier dysfunction, and gut-brain communication through enteroendocrine, enteric neural, and vagal mechanisms, and to emphasize disease-specific and common microbial patterns of dysbiosis and beneficial and harmful microbial roles in aging diseases. This review assesses some of the latest promising therapies aimed at the microbiota, such as probiotics, prebiotics, dietary therapies, fecal microbiota transplantation, as well as pharmacological therapies, and critically discusses their limitations in terms of interindividual variability and their generalisation and applicability. Focusing on mechanistic, comparative, and translation aspects, this review offers a comprehensive approach to neurological aging due to gut microbiota and identifies gaps for future precision microbiome-based interventions.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Dysbiosis/therapy/microbiology
*Aging/physiology
Animals
Probiotics/therapeutic use

@article {pmid41575201,
year = {2026},
author = {Kleinhans, M and Lissen, A and Hewitson, L and Rijkers, GT},
title = {From fecal microbiota transplants to targeted intervention for improvement of immune checkpoint inhibition therapy: how far down the road are we?.},
journal = {Expert review of anticancer therapy},
volume = {},
number = {},
pages = {},
doi = {10.1080/14737140.2026.2621240},
pmid = {41575201},
issn = {1744-8328},
abstract = {INTRODUCTION: The outcome of immune checkpoint inhibition (ICI) therapy of cancer appears to be influenced by the gut microbiota composition of the patient. Microbiome-based therapy by fecal microbiota transplantation (FMT) appears to improve the outcome of ICI therapy. The ideal composition of the microbiota as well as treatment schedule are not yet established.

AREAS COVERED: The most recent published studies are reviewed, as well as the study designs of registered clinical trials which are ongoing. The effect of pretreatment of patients with antibiotics, aimed to improve engraftment of the transplant, is evaluated.

EXPERT OPINION: The optimal treatment schedule would be to start with FMT, followed by ICI, implying FMT should be given to ICI naive patients. Rather than donor derived FMT, defined consortia of microbiota could be preferred.},
}

@article {pmid41574864,
year = {2026},
author = {Gao, Y and Shahbaz, S and Elahi, S and Monaghan, TM and , and Kao, D},
title = {Distinct T and innate-like lymphocyte reprogramming following lyophilized fecal microbiota transplantation in recurrent C. difficile infection.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2620127},
doi = {10.1080/19490976.2026.2620127},
pmid = {41574864},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Clostridium Infections/immunology/therapy/microbiology ; Clostridioides difficile/physiology/immunology ; Male ; Female ; Middle Aged ; Immunity, Innate ; Adult ; },
abstract = {Fecal microbiota transplantation (FMT) is highly effective in preventing recurrent Clostridioides difficile infection (rCDI), yet its immunological mechanisms remain poorly defined. While bacterial engraftment and recovery of microbial diversity are central to FMT efficacy, accumulating evidence suggests that host immune reprogramming is involved. In murine models, regulatory CD4[+] T cells are indispensable for clearing C. difficile. To address this mechanistic gap, we examined systemic immune reprogramming following FMT by performing flow cytometry and single-cell RNA sequencing (scRNA-seq) on a subset of successfully treated participants from a clinical trial comparing lyophilized FMT (LFMT) with lyophilized sterile fecal filtrate (LSFF, no live bacteria) for preventing rCDI. Flow cytometry was performed on peripheral mononuclear cells from 19 LFMT recipients and 18 LSFF recipients, and scRNA-seq analysis was performed on two LFMT recipients. Although flow cytometry results did not show significant changes in the assessed markers after rCDI resolution in either treatment group, exploratory scRNA-seq in the two LFMT recipients revealed distinct LFMT-associated transcriptional signatures across adaptive and innate-like lymphocyte populations. LFMT was associated with upregulated activation and regulatory genes (CD69, STAT1, TOX, RORA, FOXP3) in CD4[+] and CD8[+] T cells, suggesting enhanced immune regulation with reduced cytotoxic gene expression (GZMB, PRF1, GNLY). Innate-like lymphocytes displayed broad activation, with natural killer cells showing increased KLRD1, PRF1, and IL2RB and mucosal-associated invariant T cells (MAIT cells) upregulating STAT1, JUN, and RORA while downregulating KLRB1 and STAT3. These transcriptional programs are consistent with recalibration of T cell homeostasis and innate-like lymphocyte activation, potentially driven by microbial restoration. Collectively, this exploratory study provides the first single-cell immune atlas of LFMT in rCDI, identifying coordinated activation of regulatory, effector, and innate immune pathways. Given the small sample size, these findings should be considered hypothesis-generating, requiring validation in larger cohorts.},
}

Humans
*Fecal Microbiota Transplantation
*Clostridium Infections/immunology/therapy/microbiology
Clostridioides difficile/physiology/immunology
Male
Female
Middle Aged
Immunity, Innate
Adult

@article {pmid41574548,
year = {2026},
author = {Li, C and Ma, J and Huang, G and Chen, B and He, C and Wu, R},
title = {Lactobacillus Regulates the Specificity of Polysaccharides Derived From Pericarpium Citri Reticulatae "Chachiensis" to Alleviate High-Fat Diet-Induced Depression-Like Behavior.},
journal = {Molecular nutrition & food research},
volume = {70},
number = {2},
pages = {e70388},
doi = {10.1002/mnfr.70388},
pmid = {41574548},
issn = {1613-4133},
support = {2024A0505090024//Guangdong and Macao cooperation project from Department of Science and Technology of Guangdong Province and Jiangmen Science and Technology Bureau/ ; 0077/2024/AGJ//Macao Science and Technology Development Fund/ ; 2520002000138//Jiangmen Key Project of Fundamental and Applied Basic Research/ ; 2024ZDJS035//Guangdong Provincial Key Disciplines Scientific Research Capacity Enhancement Project/ ; 2024ZDZX4015//Department of Education of Guangdong Province/ ; },
mesh = {Animals ; *Diet, High-Fat/adverse effects ; *Depression/etiology/drug therapy ; Gastrointestinal Microbiome/drug effects ; Male ; *Polysaccharides/pharmacology/chemistry ; *Lactobacillus/physiology ; Mice, Inbred C57BL ; Mice ; Fecal Microbiota Transplantation ; Antidepressive Agents/pharmacology ; Behavior, Animal/drug effects ; },
abstract = {Gut microbiota dysbiosis is closely linked to depression and can be modulated by dietary polysaccharides. This study aimed to characterize three polysaccharide fractions from Pericarpium Citri Reticulatae "Chachiensis" (PCRCP)-PCRCPI, PCRCPII, and PCRCPIII-and evaluate their antidepressant effects in a high-fat diet-induced mouse model. Their average molecular weights were approximately 48.9 kDa (PCRCPI), 13.7 kDa (PCRCPII), and 34.8 kDa (PCRCPIII), with a composition primarily of galacturonic acid, arabinose, galactose, and rhamnose. PCRCPI most effectively mitigated depression-like behaviors, as indicated by improved behavioral performance and neurotransmitter levels and reduced neuronal damage. The antidepressant effect of PCRCPI was contingent upon the gut microbiota, as demonstrated by the fact that fecal microbiota transplantation (FMT) from donors treated with PCRCPI conferred behavioral improvements. Mechanistically, PCRCPI treatment selectively increased the abundance of Lactobacillus species and elevated fecal levels of metabolites associated with retrograde endocannabinoid signaling, particularly 2-arachidonoylglycerol (2-AG). Subsequent colonization experiments with specific Lactobacillus strains, either alone or in combination with PCRCPI, activated hippocampal retrograde endocannabinoid signaling as revealed by transcriptomic analysis, and ameliorated depression-like phenotypes. These findings demonstrate the potential of PCRCPI as a prebiotic for alleviating diet-associated depression, through a novel microbiota-gut-brain axis mechanism targeting the endocannabinoid system.},
}

Animals
*Diet, High-Fat/adverse effects
*Depression/etiology/drug therapy
Gastrointestinal Microbiome/drug effects
Male
*Polysaccharides/pharmacology/chemistry
*Lactobacillus/physiology
Mice, Inbred C57BL
Mice
Fecal Microbiota Transplantation
Antidepressive Agents/pharmacology
Behavior, Animal/drug effects

@article {pmid41574027,
year = {2026},
author = {Lin, A and Xiong, M and Jiang, A and Chen, L and Huang, L and Li, K and Wong, HZH and Zhang, J and Liu, Z and Cheng, Q and Tang, B and Zhang, P and Luo, P},
title = {Tumor Immunotherapy and Microbiome: From Bench-to-Bedside Applications.},
journal = {MedComm},
volume = {7},
number = {2},
pages = {e70454},
pmid = {41574027},
issn = {2688-2663},
abstract = {Cancer immunotherapy has emerged as a transformative therapeutic strategy that harnesses the immune system to combat malignant tumors, overcoming critical limitations such as the nonspecific cytotoxicity of conventional chemotherapy and radiotherapy and drug resistance arising from target mutations in targeted therapies. Growing evidence demonstrates that the human microbiome plays a pivotal role in modulating immune responses and influencing the efficacy of immunotherapeutic interventions. Although the impact is increasingly recognized, the molecular mechanisms and translational potential of microbiome-based strategies remain incompletely explored. This review systematically elucidates how microorganisms from distinct anatomical sites (including bacteria, fungi, and viruses residing in the gut, oral cavity, skin, respiratory tract, and urogenital tract) and intratumoral microbes modulate the tumor immune microenvironment through metabolites, immune cell priming, and antigen mimicry. Furthermore, we discuss how specific microbial signatures predict responses to immune checkpoint inhibitors (ICIs) and CAR-T cell therapy, and highlight emerging interventional strategies, including fecal microbiome transplantation (FMT), probiotics, and engineered bacteria, that demonstrate synergistic effects with immunotherapy in preclinical and clinical settings. By integrating mechanistic insights with translational advances, this review provides a comprehensive scientific foundation for microbiome-based precision immunotherapy, aimed at improving patient survival outcomes and reducing treatment-related adverse events.},
}

@article {pmid41573337,
year = {2026},
author = {Liu, J and Chen, Y and Wang, Y and Li, D and Xu, Z and Zhang, J and Qin, L and Han, B and Jing, Y and Cui, D and Zhu, Y and Xia, S and Jiang, C},
title = {Diversity of Gut Microbiota and Metabolites in Benign Prostatic Hyperplasia with Different Prostate Volumes.},
journal = {European urology open science},
volume = {84},
number = {},
pages = {40-49},
pmid = {41573337},
issn = {2666-1683},
abstract = {BACKGROUND AND OBJECTIVE: The gut microbiota, influenced by age and sex hormones, may correlate with the development and progression of benign prostatic hyperplasia (BPH). This study aims to characterize gut microbiota and metabolite profiles in BPH patients with varying prostate volumes.

METHODS: Fecal samples from BPH patients were analyzed using 16S rDNA sequencing and untargeted metabolomics. Microbial and metabolic differences were assessed via the Linear discriminant analysis Effect Size, KEGG pathway enrichment, and a mediation analysis.

KEY FINDINGS AND LIMITATIONS: We identified 26 differential amplicon sequence variants (ASVs) and 70 metabolites, with 18 microbes correlating significantly with clinical BPH indicators. The key pathways included unsaturated fatty acid and steroid hormone biosynthesis. Akkermansia (ASV549) may affect prostate volume through the regulation of intestinal amino acid metabolism and may negatively affect prostate-specific antigen levels by inhibiting heat shock protein (HSP) 90 (luminespib). Limitations include sample size and unmeasured confounders.

Gut microbiota and metabolite diversity are associated with prostate volume; further studies are warranted to elucidate the potential interventions via microbiome modulation or metabolic targeting for BPH management.

PATIENT SUMMARY: In this study, we identified the potential associations between gut and both prostate volume and benign prostatic hyperplasia symptoms. These findings suggest that dietary interventions or fecal microbiota transplantation may represent potential strategies for modulating prostate health in the future.},
}

@article {pmid41572749,
year = {2026},
author = {Ding, L and Xi, Z and Zou, Y and Li, S and Chen, D and Liu, Y and Zhao, J},
title = {Targeting the Gut Microbiota in the Treatment of Type 2 Diabetes: Dietary Interventions, Microbial Preparations, and Fecal Transplantation.},
journal = {Current diabetes reviews},
volume = {},
number = {},
pages = {},
doi = {10.2174/0115733998411102251127094217},
pmid = {41572749},
issn = {1875-6417},
abstract = {Type 2 diabetes mellitus (T2DM) is the most prevalent metabolic disease worldwide, characterized by hyperglycemia and insulin resistance (IR). Its escalating global prevalence and the associated morbidity and mortality render it a major public health concern. Conventional glucose- lowering therapies frequently entail adverse effects, hypoglycaemia risk, and fail to arrest disease progression. Emerging evidence positions the gut microbiota as a central regulator of glucose homeostasis and insulin sensitivity, suggesting that gut microbiota might be a promising target for T2DM. This review synthesizes current knowledge of microbiota-driven mechanisms, particularly those of the gut microbiota and their metabolites, that precipitate or exacerbate T2DM. It then critically evaluates microbiota-targeted interventions (dietary modulation, probiotics, prebiotics, antibiotic therapy, and fecal microbiota transplantation) as emerging therapeutic or adjunctive strategies to restore glycaemic control by modulating the gut microbial ecosystem. While clinical validation is incomplete, targeting the gut microbiota represents a promising avenue for both prevention and treatment of T2DM.},
}

@article {pmid41572742,
year = {2026},
author = {Patil, S and Doshi, G},
title = {Gut Microbiota in the Hepato-Cardiorenal Axis: Microbial Metabolites, Inflammation, and Emerging Therapeutic Targets.},
journal = {Current pharmaceutical design},
volume = {},
number = {},
pages = {},
doi = {10.2174/0113816128413464251209115653},
pmid = {41572742},
issn = {1873-4286},
abstract = {INTRODUCTION: To sustain systemic homeostasis, the gut microbiota manages immunological, metabolic, and inflammatory processes. Multiorgan diseases, especially those impacting the liver, kidney, and cardiovascular system through the hepato-cardiorenal axis, have been strongly associated with dysbiosis.

METHODS: A comprehensive literature search was conducted using PubMed, Scopus, Web of Science, Science Direct, and Google Scholar, with the focus on articles till 2025. Eligible sources included clinical trials, systematic reviews, and peer-reviewed academic publications that discussed metabolites, gut microbiota, and treatment approaches for diseases of the liver, kidney, and heart. A qualitative synthesis of the data indicated important mechanisms and potential treatments.

RESULTS: SCFAs have anti-inflammatory and intestinal barrier integrity-enhancing qualities, whereas uremic toxins and TMAO promote oxidative stress, fibrosis, and vascular dysfunction. Hepatic steatosis, insulin resistance, and systemic inflammation are all affected by the dysbiosis-induced bile acid imbalance. Microbiotatargeted therapies include fecal microbiota transplantation, fiber- or polyphenol-rich diets, probiotics, prebiotics, synbiotics, and pharmacological modification of bile acid or TMAO pathways, which have potential but need more comprehensive validation.

DISCUSSION: The findings show that, among other factors, gut metabolites-such as uremic toxins, bile acids, TMAO, and SCFAs - are key players in mediating inflammation and metabolic dysregulation across the hepato-cardiorenal axis. However, the lack of consistent treatment protocols and differences in microbiome composition limit the practical application of preclinical research that has clearly demonstrated the existence of mechanistic links. Future research should focus on long-term clinical outcomes, biomarker identification, and precise microbiome modifications to establish causation and improve therapy effectiveness.

CONCLUSION: The gut microbiota significantly influences the hepato-cardiorenal axis through metabolitemediated signalling. While therapeutic modulation shows promise, precision medicine approaches and highquality randomized trials are essential to tackle multi-organ metabolic and inflammatory diseases.},
}

@article {pmid41572325,
year = {2026},
author = {Su, SH and Lu, DD and Wu, YF and Huang, XS and Zhang, L},
title = {Fecal microbiota transplantation promotes Wnt3a-mediated hippocampal neurogenesis in a rat model of chronic cerebral hypoperfusion.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-025-07631-8},
pmid = {41572325},
issn = {1479-5876},
support = {81974209//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Limited data support the beneficial effects of fecal microbiota transplantation (FMT) against intracranial ischemic injury under chronic cerebral hypoperfusion (CCH). However, a comprehensive understanding is lacking, hindering its clinical translation. In the present study, we evaluated microbial, metabolic, cellular, and behavioral alterations to explore the roles and mechanisms of FMT in hippocampal neurogenesis under CCH.

METHODS: Rats underwent bilateral common carotid artery occlusion to induce CCH. Intestinal microbiota (IM) and fecal/hippocampal metabolites were assessed by 16S ribosomal RNA sequencing and untargeted liquid chromatography-mass spectrometry, respectively. Potential molecular pathways and differentially expressed genes in the hippocampus were identified by RNA sequencing and verified by western blot, immunofluorescence, and dual-luciferase reporter assays. Neurogenesis was quantified by BrdU/DCX, BrdU/nestin, BrdU/GFAP, and BrdU/NeuN labeling. Cognitive function was evaluated with the Morris water maze.

RESULTS: FMT altered IM composition by enriching Verrucomicrobiae, Ruminococcaceae, Akkermansiaceae, Turicibacter, Akkermansia, Verrucomicrobiales, Oscillospirales, Verrucomicrobiota, and Akkermansia_muciniphila. These shifts were associated with significantly elevated metabolites in tryptophan- and arginine-related pathways, including fecal L-tryptophan and hippocampal L-arginine, L-glutamine, indolepyruvate, indoleacetaldehyde, and kynurenic acid. Furthermore, FMT potentiated the Wnt3a/β-catenin/Neurog2/BDNF pathway, promoting hippocampal neurogenesis. FMT-induced activation of Wnt3a/β-catenin/Neurog2 signaling also up-regulated hippocampal C3 expression, contributing to neurogenesis and cognitive recovery under CCH.

CONCLUSION: These findings provide evidence that FMT exerts protective effects against CCH insult through Wnt3a-mediated neurogenesis.},
}

@article {pmid41571673,
year = {2026},
author = {Bautista, J and Lamas-Maceiras, M and Hidalgo-Tinoco, C and Guerra-Guerrero, A and Betancourt-Velarde, A and López-Cortés, A},
title = {Gut microbiome-driven colorectal cancer via immune, metabolic, neural, and endocrine axes reprogramming.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-025-00883-8},
pmid = {41571673},
issn = {2055-5008},
abstract = {Colorectal cancer (CRC) is a leading cause of cancer mortality worldwide and is increasingly recognized as the outcome of complex host-microbe interactions. Beyond established genetic and environmental drivers, the gut microbiome has emerged as a causal and mechanistic contributor to CRC initiation, progression, and therapy response. This review synthesizes current molecular, ecological, and translational evidence to explain how gut microbial communities reprogram immune, metabolic, neural, and endocrine networks within the tumor microenvironment. CRC-associated dysbiosis is characterized by enrichment of pathobionts such as Fusobacterium nucleatum, pks[+] Escherichia coli, and enterotoxigenic Bacteroides fragilis, and by loss of protective, short-chain-fatty-acid-producing commensals. These microbes promote carcinogenesis through genotoxin-induced DNA damage, epithelial barrier disruption, metabolic rewiring, and chronic inflammation that collectively sustain immune suppression and tumor growth. Defined mutational signatures from bacterial metabolites, including colibactin, cytolethal distending toxin, and indolimines, now directly link microbial exposures to human cancer genomes. By integrating these findings, this review conceptualizes CRC as a biofilm-structured, microbiome-driven ecosystem disease, where polymicrobial consortia coordinate barrier breakdown, immune evasion, and metabolic cooperation. Finally, we highlight emerging microbiota-targeted strategies, including dietary modulation, pre- and probiotics, postbiotics, bacteriophage therapy, engineered live biotherapeutics, and fecal microbiota transplantation, that translate these insights into precision prevention and therapy. Through this integrative framework, the review aims to reposition the microbiome from a correlative feature to a tractable determinant of CRC pathogenesis and treatment response.},
}

@article {pmid41571448,
year = {2026},
author = {Cakir, RC and Belen, NH and Yildirim, S and Avci, S and Dincer, A and Kazan, MK and Celik, O and Aslaner, A and Eyvaz, K and Cakir, T},
title = {Effect of Ileal Feces Transplantation in Preventing Diversion Colitis and Its Complications Due to Protective Loop Ileostomy in Rectal Cancer Cases.},
journal = {Journal of investigative surgery : the official journal of the Academy of Surgical Research},
volume = {39},
number = {1},
pages = {2609429},
doi = {10.1080/08941939.2025.2609429},
pmid = {41571448},
issn = {1521-0553},
mesh = {Humans ; *Ileostomy/adverse effects/methods ; Male ; Middle Aged ; Female ; *Rectal Neoplasms/surgery ; Prospective Studies ; Aged ; *Colitis/prevention & control/etiology/pathology ; Ileum/surgery ; *Postoperative Complications/prevention & control/etiology ; Treatment Outcome ; *Fecal Microbiota Transplantation/methods ; Adult ; Feces ; },
abstract = {To evaluate the effectiveness of fecal transplantation (FT) in preventing the development of diversion colitis (DC) and reducing its complications in patients who underwent protective loop ileostomy (PLI) following low anterior resection for rectal cancer. The study was prospectively conducted at Tertiary Hospital. Seventeen patients who underwent PLI were assigned to the FT group (FT+), and 19 patients served as the control group (FT-). In the FT+ group, ileal content was delivered to the efferent loop via a catheter placed during surgery. Both groups were evaluated postoperatively through biopsies taken for histopathological examination. In the FT+ group, significant reductions were observed in parameters specific to DC, such as the severity of inflammation, ulceration, goblet cell loss, and crypt abscesses, compared to the FT- group (p < 0.05). The epithelial structure and crypt organization in the FT+ group were closer to normal. FT is an effective and easily applicable method for preventing DC development and reducing the severity of inflammatory changes in patients undergoing PLI. The technique is low-cost, has high patient compliance, and aligns with methods reported in the literature for DC prevention.},
}

Humans
*Ileostomy/adverse effects/methods
Male
Middle Aged
Female
*Rectal Neoplasms/surgery
Prospective Studies
Aged
*Colitis/prevention & control/etiology/pathology
Ileum/surgery
*Postoperative Complications/prevention & control/etiology
Treatment Outcome
*Fecal Microbiota Transplantation/methods
Adult
Feces

@article {pmid41571367,
year = {2026},
author = {Lin, Y and Jiang, Z and Yu, Z and Huang, T and Gui, W and Wang, Z and Li, F and Xiao, P and Li, C and Liu, E},
title = {Honokiol attenuates diabetes by enriching Akkermansia muciniphila andregulating tryptophan metabolism in mice.},
journal = {Chinese journal of natural medicines},
volume = {24},
number = {1},
pages = {59-72},
doi = {10.1016/S1875-5364(26)61077-1},
pmid = {41571367},
issn = {1875-5364},
mesh = {Animals ; *Lignans/administration & dosage/pharmacology ; *Tryptophan/metabolism ; Gastrointestinal Microbiome/drug effects ; Mice ; *Biphenyl Compounds/administration & dosage/pharmacology ; Male ; Mice, Inbred C57BL ; *Hypoglycemic Agents/administration & dosage ; Glucagon-Like Peptide 1/metabolism ; *Akkermansia/drug effects ; Receptors, Aryl Hydrocarbon/metabolism ; *Diabetes Mellitus, Experimental/drug therapy/metabolism/microbiology ; Humans ; *Diabetes Mellitus/drug therapy/metabolism/microbiology ; Fecal Microbiota Transplantation ; Allyl Compounds ; Phenols ; },
abstract = {Diabetes mellitus (DM) is a chronic disease influenced by gut microbiome disturbances. Honokiol (HON), a low oral bioavailability compound from Magnolia officinalis bark, has demonstrated potential as a treatment for DM. This research investigates the effects of HON on gut microbiota and host metabolism to elucidate its mechanism of action in DM. After 8 weeks of intervention through fecal microbiota transplantation (FMT) or antibiotic treatment, HON improved glucose tolerance and lipid metabolism in a gut microbiota-dependent manner. Specifically, HON administration significantly increased Akkermansia muciniphila (AKK) abundance and modulated tryptophan (TRP) metabolism, as evidenced by 16S ribosomal ribonucleic acid (rRNA) gene sequencing and untargeted/targeted metabolomics analysis. Notably, research revealed that AKK metabolized TRP into tryptamine (TA) and other metabolites in vitro. Both AKK and TA activated the aryl hydrocarbon receptor (AHR) pathway, increasing circulating glucagon-like peptide-1 (GLP-1) levels and ameliorating diabetes-related symptoms in DM mice. These findings indicate that HON's hypoglycemic effect primarily stems from AHR-GLP-1 pathway activation through targeted modulation of AKK and microbial TRP metabolite TA, potentially enhancing HON's clinical applications.},
}

Animals
*Lignans/administration & dosage/pharmacology
*Tryptophan/metabolism
Gastrointestinal Microbiome/drug effects
Mice
*Biphenyl Compounds/administration & dosage/pharmacology
Male
Mice, Inbred C57BL
*Hypoglycemic Agents/administration & dosage
Glucagon-Like Peptide 1/metabolism
*Akkermansia/drug effects
Receptors, Aryl Hydrocarbon/metabolism
*Diabetes Mellitus, Experimental/drug therapy/metabolism/microbiology
Humans
*Diabetes Mellitus/drug therapy/metabolism/microbiology
Fecal Microbiota Transplantation
Allyl Compounds
Phenols

@article {pmid41570877,
year = {2026},
author = {Wang, Y and Wang, X and Gan, B and Jia, T and Xu, T and Xu, H},
title = {Ferroptosis and Hepatic Fibrosis induced by Cooperative Exposure to Polylactic Acid Nanoplastics and Copper: Emphasis on Gut Microbiota Dysbiosis.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {},
number = {},
pages = {127698},
doi = {10.1016/j.envpol.2026.127698},
pmid = {41570877},
issn = {1873-6424},
abstract = {Co-exposure to polylactic acid nanoplastics (PLA-NPs) and copper (Cu) in the environment poses a health risk, yet their combined toxic effects remain poorly understood. This study investigated the synergistic hepatotoxicity and underlying mechanisms, focusing on the gut-liver axis, in a mouse model of subacute exposure. Results demonstrated that co-exposure caused significant synergistic effects, including exacerbated changes in body weight (BW), increased hepatic index ratio, and severe liver injury marked by elevated Aspartate Aminotransferase/Alanine Aminotransferase/Alkaline Phosphatase (AST/ALT/AKP) activities and histopathological damage. Crucially, co-exposure synergistically induced hepatic ferroptosis (evidenced by dysregulated Glutathione (GSH), Malondialdehyde (MDA), and iron homeostasis), disrupted lipid metabolism, and promoted oxidative stress. These hepatic injuries were indeced by intestinal barrier damage and gut microbiota dysbiosis, characterized by reduced beneficial Lactobacillus murinus. The fecal microbiota transplantation (FMT) experiment definitively confirmed the causal role of gut microbiota, as transferring microbiota from donor mice to healthy recipients recapitulated the key hepatointestinal injuries. This study demonstrates that co-exposure to PLA-NPs and Cu induces synergistic hepatotoxicity primarily mediated through gut microbiota disruption and gut-liver axis dysfunction, leading to hepatic ferroptosis and fibrosis. These findings highlight the critical role of the gut microbiome in modulating the synergistic toxicity of environmental contaminants and provide new insights into the health risks of mixed pollutant exposure.},
}

@article {pmid41570815,
year = {2026},
author = {Tong, T and Huang, X and Li, L and Hu, M and Zhu, X and Zhu, B and Ma, Y and Ning, L and Jiang, Y and Zhang, Y and Zhou, Y and Wang, Z and Ding, J and Zhao, Y and Xuan, B and Zhang, Y and Xiao, X and Fang, JY and Hong, J and Yin, Y and Liu, F and Chen, H},
title = {Microbial metabolite FAD mobilizes adipocyte lipid remodeling to enhance cancer immunotherapy efficacy.},
journal = {Cell metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmet.2025.12.012},
pmid = {41570815},
issn = {1932-7420},
abstract = {Crosstalk between gut microbiota and adipose tissue critically shapes immunotherapy responses in patients with cancer. An obesity-associated microbial signature enriched in riboflavin-producing taxa was identified, along with increased microbial riboflavin biosynthesis pathway and elevated levels of flavin adenine dinucleotide (FAD), in obese responders to immune checkpoint blockade (ICB). In diet-induced obese (DIO) mice, fecal microbiota transplantation (FMT), administration of Lachnospiraceae bacterium, or FAD supplementation significantly enhanced the therapeutic efficacy of anti-PD-1 therapy. These interventions increased the cytotoxicity of tumor-infiltrating CD8[+] T cells via mesenteric adipocyte-driven synthesis of polyunsaturated fatty acids (PUFAs). Inhibiting fatty acid desaturase 2 (FADS2) eliminated the benefits of FAD, underscoring a critical role for adipocyte-intrinsic lipid remodeling in mediating immune responses. Clinically, elevated systemic levels of PUFAs, particularly docosahexaenoic acid (DHA), were positively correlated with intratumoral CD8[+] T cell infiltration and favorable immunotherapy outcomes. Dietary DHA supplementation improved ICB responses in lean mice. This study highlights that a microbiota-adipose axis shapes antitumor immunity, enabling potential personalized metabolic and microbial immunotherapy strategies.},
}

@article {pmid41570783,
year = {2026},
author = {Ding, J and Xu, F and Chen, D and Xi, J and Gao, F and Chen, L and Wang, B and Dou, X and Qiu, J and He, G},
title = {Qing Hua Yu Du formula ameliorates alcoholic hepatic fibrosis by regulating MAPK/TLR4-MyD88 inflammatory pathways, restoring hepatic metabolism and modulating gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {152},
number = {},
pages = {157830},
doi = {10.1016/j.phymed.2026.157830},
pmid = {41570783},
issn = {1618-095X},
abstract = {BACKGROUND: Alcohol-induced liver injury (ALI) and subsequent hepatic fibrosis pose significant global health burdens, with limited effective therapeutic options. Traditional Chinese Medicine (TCM) formulas, such as Qing Hua Yu Du (QHYD) formula, have shown potential in treating alcoholic hepatic fibrosis in clinical, but their therapeutic effects, and underlying mechanisms remain incompletely characterized. Additionally, the interplay between hepatic inflammation, metabolic disorders, and gut-liver axis dysregulation in ALI-related fibrosis necessitates comprehensive validation across multiple models.

PURPOSE: This study aimed to evaluate the therapeutic effects of QHYD formula on alcohol-CCl₄-induced alcoholic hepatic fibrosis in diverse models (alcohol-CCl₄, acute binge alcohol, and cell models), explore its mechanisms involving inflammatory signaling, hepatic metabolism, and gut microbiota, validate the key metabolite l-histidine's role, and assess its safety profile.

METHODS: The QHYD formula's chemical composition was characterized using advanced high-performance liquid chromatography (HPLC) fingerprinting for quality control and ultra-high-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UHPLC-Q/TOF-MS) for constituent identification. Male C57BL/6 mice were assigned to normal, model, QHYD (2.7, 4.05, 5.4 g/kg/day), and fecal microbiota transplantation (FMT) groups. Acute binge alcohol and AML-12 cell models were used for supplementary validation. Liver injury was evaluated by plasma biochemical markers (ALT/AST/GGT/TC/TG) and histological staining (H&E/Masson). Inflammatory pathways (MAPK/TLR4-MyD88), metabolic changes, and gut microbiota were analyzed via Western blot, ELISA, transcriptomics, metabolomics, and 16S rRNA sequencing. l-histidine's mechanism was validated in LX-2 cells using qRT-PCR and immunofluorescence. Acute/chronic toxicity assays were conducted to assess safety.

RESULTS: HPLC confirmed QHYD's batch consistency, and UHPLC-Q/TOF-MS identified 82 constituents. QHYD significantly ameliorated liver injury and fibrosis in alcohol-CCl₄ and acute binge alcohol models, reduced plasma TC/TG, and inhibited Col1a1/α-SMA expression. It suppressed MAPK/TLR4-MyD88 signaling, restored protein digestion/absorption pathway (upregulating l-histidine), and modulated gut microbiota richness/composition. FMT experiments confirmed QHYD-modulated gut microbiota directly mediated anti-fibrotic effects. l-histidine dose-dependently inhibited HSC activation via the NF-κB-TIMP1 axis.

CONCLUSION: QHYD ameliorates alcoholic hepatic fibrosis through multi-targeted mechanisms: inhibiting MAPK/TLR4-MyD88 inflammatory pathways, restoring hepatic metabolism via l-histidine, and modulating gut microbiota. Its favorable safety profile and efficacy across diverse models support QHYD as a promising therapeutic candidate, with l-histidine serving as a key mediating metabolite.},
}

@article {pmid41569851,
year = {2026},
author = {Kabil, AK and Cait, A and Reynolds, LA and Chopra, S and Bilenky, M and Moksa, M and Li, Y and Cait, J and Hernaez, DC and Scott, RW and Fogarty, E and Finlay, BB and Mohn, WW and Hirst, M and Hughes, MR and McNagny, KM},
title = {Early-life microbiota skews long-term gene expression and chromatin states of bone marrow hematopoietic precursors.},
journal = {Cell reports},
volume = {45},
number = {2},
pages = {116871},
doi = {10.1016/j.celrep.2025.116871},
pmid = {41569851},
issn = {2211-1247},
abstract = {Early life is a critical window during which the gut microbiota sculpts immunity and long-term susceptibility to allergic disease. Using neonatal antibiotic administration and bone marrow transplantation assays, we show that depletion of short-chain fatty acid (SCFA)-producing bacteria alters gene expression in hematopoietic stem and progenitor cells (HSPCs) and imprints a persistent, transplantable atopic immune phenotype. Bone marrow transplants from exposed mice generate recipients with elevated serum immunoglobulin E (IgE), downstream increased IgE bound to basophils, and exacerbated allergic lung inflammation following papain challenge. Depletion of SCFA-producing bacteria also impairs recovery from chemotherapy-induced myelosuppression and increases DNA damage in long-term HSPCs in an antibiotic-specific manner. Histone 3 lysine 27 (H3K27) chromatin immunoprecipitation sequencing (ChIP-seq) analyses further reveal differential histone acetylation in HSPCs, consistent with an SCFA-mediated epigenetic regulatory mechanism. Collectively, these findings establish a link between gut microbiota composition, hematopoiesis, and long-term immune function, offering a mechanistic explanation for microbiota-driven susceptibility to atopic disease and hematopoietic dysfunction.},
}

@article {pmid41569045,
year = {2026},
author = {Yao, G and Zhang, T and Qin, Z and Wang, Y and Gu, J and He, C and Jin, J},
title = {Corn silk extract as a prebiotic exerts antihypertensive effects via gut microbiota modulation in hypertensive rats.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0144225},
doi = {10.1128/spectrum.01442-25},
pmid = {41569045},
issn = {2165-0497},
abstract = {UNLABELLED: Corn silk extract (CSE), a traditional medicinal food rich in polysaccharides, flavonoids, and saponins, has been used as a natural antihypertensive agent, but its mechanism remains unclear. This study aimed to evaluate whether CSE can lower blood pressure through gut microbiota modulation. Spontaneously hypertensive rats received oral CSE for 4 weeks, followed by a 4-week drug-free observation. The treatment significantly reduced blood pressure, increased microbial diversity, decreased the Firmicutes/Bacteroidetes ratio, and enriched beneficial genera, such as Akkermansia and Lactobacillus. These changes were accompanied by reduced serum lipopolysaccharide and pro-inflammatory cytokines, elevated nitric oxide (NO) levels, and restored endothelial function. Permutational multivariate analysis of variance (PERMANOVA) and correlation analyses showed that microbiota and inflammatory markers were more strongly associated with blood pressure improvements than urinary indices. Structural equation modeling suggested a potential mechanistic pathway involving gut microbiota-inflammation-NO regulation. Importantly, fecal microbiota transplantation using post-treatment donor samples reproduced the antihypertensive and anti-inflammatory effects, confirming the microbiota's critical mediating role. These findings provide the first experimental evidence that CSE functions as a prebiotic to improve gut microbial balance and vascular health, offering a promising natural strategy for microbiota-targeted blood pressure control.

IMPORTANCE: This study identifies corn silk extract (CSE) as a novel plant-derived prebiotic with antihypertensive effects mediated through gut microbiota modulation. Using a spontaneously hypertensive rat model, we demonstrated that CSE reshapes gut microbial composition, enhances microbial diversity, and promotes beneficial genera while reducing systemic inflammation and restoring nitric oxide (NO)-mediated vascular function. Importantly, fecal microbiota transplantation confirmed the causal role of gut microbiota in mediating these effects. These findings highlight a gut microbiota-inflammation-NO axis as a key pathway through which CSE regulates blood pressure. As a safe, accessible, and food-compatible intervention, CSE represents a promising strategy for non-pharmacological blood pressure management and broadens the application scope of prebiotics in cardiovascular health.},
}

@article {pmid41568946,
year = {2026},
author = {Huang, P and Cao, L and Cao, T and Wang, X and Cui, S and Jiang, S and Chen, H and Di, L and Li, S and Huang, L},
title = {Intermittent Fasting Alleviates Anesthesia/Surgery-Induced Delirium-Like Behavior in Aged Mice by Remodeling Gut Microbiota.},
journal = {CNS neuroscience & therapeutics},
volume = {32},
number = {1},
pages = {e70748},
pmid = {41568946},
issn = {1755-5949},
support = {//Hebei Medical University Postdoctoral Fund/ ; PD2025007//Postdoctoral Research Support Program for Clinical Medicine of Hebei Medical University/ ; H2022206586//the S&T Program of Hebei/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Fasting/physiology ; Mice ; Mice, Inbred C57BL ; Male ; *Delirium/prevention & control/etiology ; Hippocampus/ultrastructure/metabolism ; Fecal Microbiota Transplantation ; *Anesthesia/adverse effects ; Aging ; Mitochondria/metabolism ; Fatty Acids, Volatile/metabolism ; *Postoperative Complications/prevention & control ; Intermittent Fasting ; },
abstract = {BACKGROUND: Postoperative delirium (POD) is a serious complication in elderly patients, associated with prolonged recovery and adverse outcomes. Recent evidence links POD to mitochondrial dysfunction. While intermittent fasting (IF) has been shown to enhance mitochondrial function and exert neuroprotective effects, potentially through gut microbiota modulation, its ability to prevent POD and the underlying mechanisms remain unclear.

METHODS: We examined the effects of preoperative IF on delirium-like behavior in aged mice following anesthesia/surgery. Assessments included neurobehavioral tests, gut microbiota composition, fecal shortchain fatty acids (SCFAs), hippocampal synaptic and mitochondrial ultrastructure via transmission electron microscopy, mitochondrial function, and related molecular markers. To establish causality, fecal microbiota transplantation and SCFA supplementation experiments were conducted.

RESULTS: Preoperative IF significantly attenuated anesthesia/surgery-induced delirium-like behaviors. Mechanistically, IF reshaped the gut microbiota and preserved SCFA levels, which collectively maintained hippocampal mitochondrial homeostasis. Both fecal microbiota transplantation and SCFA supplementation replicated the protective effects of IF, confirming the causal role of gut microbiota and its metabolites.

CONCLUSION: These findings demonstrate that preoperative intermittent fasting mitigates delirium-like behavior by modulating the gut microbiota-SCFA-mitochondrial axis, highlighting its potential as a non-pharmacological strategy to enhance neurocognitive resilience and prevent POD in elderly surgical patients.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Fasting/physiology
Mice
Mice, Inbred C57BL
Male
*Delirium/prevention & control/etiology
Hippocampus/ultrastructure/metabolism
Fecal Microbiota Transplantation
*Anesthesia/adverse effects
Aging
Mitochondria/metabolism
Fatty Acids, Volatile/metabolism
*Postoperative Complications/prevention & control
Intermittent Fasting

@article {pmid41568321,
year = {2026},
author = {Yahyapour, A and Najafi, A and Ahmadi, A and Salarizadeh, N},
title = {Immunoprotective and neuroprotective properties of gut microbiome in psoriasis.},
journal = {Journal of translational autoimmunity},
volume = {12},
number = {},
pages = {100348},
pmid = {41568321},
issn = {2589-9090},
abstract = {Psoriasis impacts nearly 100 million people globally and is associated with neuropsychiatric comorbidities such as depression and anxiety. With gut microbiome dysbiosis serving as a primary pathophysiological factor, the gut-brain-skin axis provides a crucial framework for understanding this relationship. This review evaluates the mechanisms of the gut-brain-skin axis in psoriasis pathophysiology and assesses the therapeutic potential of microbiome-based treatments, combining preclinical, clinical, and multi-omics data. Patients with psoriasis show specific gut dysbiosis patterns, including reduced microbial diversity, lower SCFA-producing bacteria (especially Faecalibacterium and Akkermansia), and increased pro-inflammatory bacteria. This microbial imbalance damages intestinal barrier integrity, triggers systemic inflammation, activates cutaneous Th17 pathways, and induces neuroinflammation through blood-brain barrier disruption. Axis communication occurs through immune-inflammatory mechanisms mediated by SCFAs and neuroendocrine pathways involving microbially-derived neurotransmitters (GABA, serotonin, dopamine). Metagenomic research indicates functional deficiencies in neurotransmitter and SCFA synthesis pathways are more significant than taxonomic alterations. Machine learning models can utilize these functional features to identify patients at risk for neuropsychiatric comorbidities and predict treatment response. Recent randomized controlled trials demonstrate that targeted interventions (probiotics, prebiotics, postbiotics, fecal microbiota transplantation) significantly improve Psoriasis Area and Severity Index scores, inflammatory markers, and microbiota composition. The evidence supports a shift toward integrated microbiome strategies, emphasizing functional approaches including mitochondrial therapies, psychobiotics, precision nutrition, and multi-omics-guided therapies.},
}

@article {pmid41568320,
year = {2025},
author = {Perry, S and Pillarisetti, L and Gelfman, T and Agrawal, DK},
title = {Gut-Brain Axis in Inflammatory Bowel Disease: Pathogenesis and Therapeutics.},
journal = {Archives of internal medicine research},
volume = {8},
number = {4},
pages = {339-345},
pmid = {41568320},
issn = {2688-5654},
support = {R25 AI179582/AI/NIAID NIH HHS/United States ; },
abstract = {Inflammatory Bowel Disease (IBD), encompassing Crohn's disease and ulcerative colitis, is a chronic inflammatory disorder of the gastrointestinal tract driven by complex interactions between genetic susceptibility, environmental triggers, microbial dysbiosis, and immune dysregulation. The gut microbiome, composed primarily of Firmicutes and Bacteroidetes, plays a crucial role in maintaining intestinal barrier integrity, immune balance, and neuroimmune signaling. Disruption of this microbial ecosystem is characterized by loss of beneficial short chain fatty acid producing bacteria and expansion of pathogenic species which promotes mucosal inflammation, cytokine release, and neuroimmune signaling that can disrupt mental health through the gut-brain axis. Emerging evidence links microbial metabolites, vagal tone, and the hypothalamic-pituitary-adrenal axis in a feedback loop that perpetuates inflammation and alters mood regulation. Current therapeutic approaches include diet modification, osteopathic manipulative treatments, fecal microbiota transplantation and phage therapy. This article focuses on understanding mechanisms linking dysbiosis, immune activation, and neuroinflammation to guide future interventions. A holistic model addressing the gut-brain axis holds the greatest promise for improving outcomes and personalizing care for IBD.},
}

@article {pmid41568166,
year = {2026},
author = {Lu, M and Guo, S and Nie, Z and Ji, J and Wang, Y and Jiang, X and Zhang, L and Xiang, B and Wu, W and Ji, J and Zou, J and Ding, X and Yu, X},
title = {Differences in gut microbiota composition are an important reason for lower serum p-cresol sulfate levels in anuric peritoneal dialysis patients compared to hemodialysis patients.},
journal = {Current research in microbial sciences},
volume = {10},
number = {},
pages = {100548},
pmid = {41568166},
issn = {2666-5174},
abstract = {BACKGROUND: Patients with end-stage kidney disease (ESKD) accumulate toxic metabolites that contribute to severe clinical complications. Peritoneal dialysis (PD) and hemodialysis (HD) exhibit distinct capacites for toxin clearance. Furthermore, the gut microbiota plays a significant role in toxin generation and is modulated by dialysis modality. This study aimed to compare gut microbiota composition and serum metabolite profiles between PD and HD patients, and to investigate their association with uremic toxin production.

METHODS: This single-center, cross-sectional study included 100 anuric ESKD patients (50 PD and 50 HD) matched for age, gender, and dialysis duration. Fecal and serum samples were collected and analyzed using 16S rRNA gene sequencing and non-targeted metabolomics. To validate the gut microbiota-serum metabolite relationship, fecal microbiota transplantation (FMT) was performed in germ-free CKD mice.

RESULTS: No significant differences in alpha diversity were observed between PD and HD groups (all indices P > 0.05), but beta diversity analysis revealed distinct gut microbial compositions (ANOSIM R = 0.093, P = 0.001), with PD patients showing higher abundance of opportunistic pathogens and lower abundance of beneficial bacteria. Non-targeted metabolomics identified 314 significantly different metabolites between the two groups, including significantly lower levels of p-cresyl sulfate (PCS) in PD patients (PD:19.16(7.24,53.83), HD:70.21(26.75,96.79), P < 0.001), with altered metabolic pathways such as tyrosine, tryptophan, and phenylalanine metabolism. FMT experiments in CKD germ-free mice confirmed higher serum PCS levels in HD recipients than in PD recipients (PD:30,456.02±4598.39, HD:45,025.00±4513.59, P < 0.05), supporting the role of gut microbiota in toxin production.

CONCLUSION: PD and HD patients show distinct gut microbiota and serum metabolite profiles, with notably lower PCS levels in PD patients. These differences are associated with variations in gut microbiota. Animal experiments provide additional evidence suggesting a potential causal relationship. Modulating gut microbiota may represent a promising therapeutic approach to decrease uremic toxin production in dialysis patients.},
}

@article {pmid41567684,
year = {2025},
author = {Lanas, A and Alvarez-Mercado, AI},
title = {Editorial: Improving the gut microbiome: applications of fecal transplantation in disease, volume II.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1758943},
doi = {10.3389/fmed.2025.1758943},
pmid = {41567684},
issn = {2296-858X},
}

@article {pmid41566359,
year = {2026},
author = {Ko, H and Kim, CJ and Choi, S and Noh, J and Kim, SW and Lee, J and Byun, S and Lee, H and Park, JC and Park, HE and Sharma, A and Park, M and Park, J and Lee, CG and Cha, KH and Im, SH},
title = {Commensal microbe-derived butyrate enhances T follicular helper cell function to boost mucosal vaccine efficacy.},
journal = {Microbiome},
volume = {14},
number = {1},
pages = {37},
pmid = {41566359},
issn = {2049-2618},
support = {RS-2024-00414820//Ministry of Education, Science and Technology/ ; 2Z07251//Korea Institute of Science and Technology/ ; RS-2024-00345575//Ministry of Science and ICT, South Korea/ ; },
mesh = {Animals ; Mice ; *T Follicular Helper Cells/immunology/drug effects ; *Gastrointestinal Microbiome/immunology ; *Butyrates/metabolism ; Peyer's Patches/immunology ; *Immunity, Mucosal ; Mice, Inbred C57BL ; Immunoglobulin A, Secretory/immunology ; Cell Differentiation ; Immunoglobulin A/immunology ; *T-Lymphocytes, Helper-Inducer/immunology ; Female ; B-Lymphocytes/immunology ; },
abstract = {BACKGROUND: The gut microbiota plays an essential role in mucosal immunity, with secretory immunoglobulin A (IgA) acting as a key effector in neutralizing pathogens and maintaining host-microbiota homeostasis. IgA production occurs via T cell-dependent (TD) and -independent pathways, with T follicular helper (Tfh) cells driving high-affinity, antigen-specific IgA responses. However, the specific microbial taxa and metabolites that regulate Tfh-mediated IgA responses under steady-state conditions remain poorly understood. This study investigated how gut microbiota-derived signals shape Tfh responses and IgA production, with implications for enhancing mucosal vaccine efficacy.

RESULTS: We demonstrate that Peyer's patches (PP)-derived Tfh cells exhibit superior IgA-inducing capacity compared to splenic Tfh cells. RNA sequencing revealed distinct transcriptional profiles in PP-Tfh cells, including upregulation of the genes associated with Tfh differentiation and activation (Bcl6, Cd40lg, Maf), T-B cell interactions (Il21, Sh2d1a, Fyn), and migration (Ccr6, Cxcr5). Functionally, PP-Tfh cells formed larger T-B cell contact areas and induced significantly higher IgA secretion in co-culture than their splenic counterparts. Microbiota depletion experiments revealed that eliminating neomycin-depleted bacteria reduced fecal IgA levels and diminished PP-Tfh cell frequencies. Fecal microbiota transplantation from neomycin-treated mice restored both IgA production and Tfh responses in germ-free (GF) mice. Bioinformatic analysis (PICRUSt2 and LEfSe) identified butyrate-producing Lachnospiraceae and Ruminococcaceae as key drivers of the Tfh-IgA axis. Butyrate supplementation enhanced Tfh differentiation and IgA⁺ germinal center B cell development in vitro and increased fecal IgA levels in vivo. Mechanistically, butyrate promoted IgA production via GPR43 signaling, as its effect was lost in co-cultures with Gpr43[⁻/⁻] Tfh cells. Moreover, treatment with tributyrin, a butyrate prodrug, enhanced vaccine-induced IgA and protected mice against Salmonella Typhimurium infection, reducing bacterial burden and tissue damage. These findings define a functional microbiota-Tfh-IgA axis sustained by neomycin-depleted, butyrate-producing bacteria.

CONCLUSIONS: Our study underscores the crucial role of the gut microbiota, particularly neomycin-depleted butyrate producing taxa, in regulating PP-Tfh cell function and IgA production. Butyrate emerges as a metabolite linking microbial metabolism to Tfh differentiation and IgA class switching. Together, these findings establish a microbiota-metabolite-Tfh cell axis essential for mucosal immune homeostasis and suggest novel strategies for enhancing vaccine efficacy and protection against enteric infections. Video Abstract.},
}

Animals
Mice
*T Follicular Helper Cells/immunology/drug effects
*Gastrointestinal Microbiome/immunology
*Butyrates/metabolism
Peyer's Patches/immunology
*Immunity, Mucosal
Mice, Inbred C57BL
Immunoglobulin A, Secretory/immunology
Cell Differentiation
Immunoglobulin A/immunology
*T-Lymphocytes, Helper-Inducer/immunology
Female
B-Lymphocytes/immunology

@article {pmid41564102,
year = {2026},
author = {Pu, X and Liu, B and Dong, L and Yuan, M and Jin, S and Jiang, X},
title = {Fecal microbiota transplantation ameliorates radiation-induced lung injury by reshaping gut metabolic homeostasis to activate FAM134B-mediated ER-phagy.},
journal = {PLoS pathogens},
volume = {22},
number = {1},
pages = {e1013786},
pmid = {41564102},
issn = {1553-7374},
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; Mice ; *Gastrointestinal Microbiome/physiology ; *Endoplasmic Reticulum/metabolism ; *Lung Injury/therapy/metabolism/etiology/microbiology ; Homeostasis ; Mice, Inbred C57BL ; Male ; Pancreatitis-Associated Proteins/metabolism ; *Membrane Proteins/metabolism ; },
abstract = {Radiation-induced lung injury (RILI) is a serious complication of thoracic radiotherapy, with limited effective treatment options. This study demonstrates that fecal microbiota transplantation (FMT) confers protection against RILI through modulation of the gut-lung axis. In a total lung irradiation (TLI) mouse model, FMT significantly alleviated pulmonary histopathological injury, inflammatory responses, oxidative stress, and collagen deposition during fibrogenesis. Concurrently, FMT improved intestinal motility, enhanced mucosal barrier integrity, and restored TLI-induced dysbiosis in gut microbiota diversity and community structure. Metabolomic analysis revealed that TLI significantly disrupted the metabolism of unsaturated fatty acids and arachidonic acid (AA), whereas FMT partially restored these metabolic networks. Transcriptomic and ultrastructural analyses indicated that RILI suppressed endoplasmic reticulum (ER) protein processing and induced ER swelling, while FMT promoted protective ER-phagy and facilitated restoration of ER morphology. Integrated multi-omics analysis further identified the AA metabolism as a key component of FMT-mediated protection, with its alterations closely associated with pulmonary tissue repair. Further in vivo and in vitro experiments demonstrated that AA binds to and activates the nuclear receptor PPARγ, leading to transcriptional upregulation of FAM134B, promoting protective ER-phagy and ameliorating RILI. In summary, this study highlights the bidirectional gut-lung axis as a therapeutic target in RILI progression and intervention, and reveals that FMT confers protection through metabolic remodeling and activation of the PPARγ-FAM134B-mediated ER-phagy pathway, providing a mechanistic basis for potential clinical translation.},
}

Animals
*Fecal Microbiota Transplantation/methods
Mice
*Gastrointestinal Microbiome/physiology
*Endoplasmic Reticulum/metabolism
*Lung Injury/therapy/metabolism/etiology/microbiology
Homeostasis
Mice, Inbred C57BL
Male
Pancreatitis-Associated Proteins/metabolism
*Membrane Proteins/metabolism

@article {pmid41562083,
year = {2025},
author = {Liu, J and Hong, W and Sun, Z and Zhang, S and Xue, C and Dong, N},
title = {The gut-lung axis: effects and mechanisms of gut microbiota on pulmonary diseases.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1693964},
pmid = {41562083},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; *Lung/immunology/metabolism/microbiology ; Dysbiosis/immunology ; *Lung Diseases/microbiology/immunology/metabolism/therapy/etiology ; Fatty Acids, Volatile/metabolism ; Fecal Microbiota Transplantation ; },
abstract = {The proposal of the gut-lung axis has profoundly reshaped our understanding of the mechanisms underlying respiratory diseases. As a crucial component of this axis, the gut microbiota plays a central role in pulmonary immune regulation through inter-organ communication mediated by metabolic products. However, a systematic integration of mechanisms explaining how gut microbes achieve precise cross-organ immune regulation remains elusive. Existing research predominantly focuses on descriptive observations, such as the association between early-life microbiota dysbiosis and an increased risk of asthma and chronic obstructive pulmonary disease (COPD), as well as the frequent occurrence of acute respiratory distress syndrome (ARDS) and pulmonary fibrosis (PF), often accompanied by gut microbiome disruption. This paper focuses on three key gut microbial metabolites-short-chain fatty acids (SCFAs), tryptophan metabolites, and polyamines (PAs)-to examine their roles in immune regulation, maintenance of barrier function, and modulation of metabolic signaling networks. Based on the latest experimental and clinical evidence, this study systematically elucidates how dysbiosis of the gut microbiota, a key component of the gut-lung axis, crosses physiological barriers to exacerbate pulmonary inflammation. Regarding intervention strategies, probiotics, fecal microbiota transplantation (FMT), and CRISPR-Cas systems have demonstrated significant therapeutic potential in restoring gut microbial balance. Finally, this paper outlines future research directions, emphasizing the need to further explore non-invasive microbial sampling techniques, molecular interaction mechanisms of the gut-lung axis, and personalized microbiome-based diagnostic and therapeutic strategies to provide new insights for the prevention and treatment of respiratory diseases involving gut microbiota.},
}

Humans
*Gastrointestinal Microbiome/immunology
Animals
*Lung/immunology/metabolism/microbiology
Dysbiosis/immunology
*Lung Diseases/microbiology/immunology/metabolism/therapy/etiology
Fatty Acids, Volatile/metabolism
Fecal Microbiota Transplantation

@article {pmid41561086,
year = {2025},
author = {Zhang, MY and Chen, SY and Lin, YH and Yuan, XX},
title = {Gut microbiota modulation in gastrointestinal disorders: current evidence and therapeutic perspectives.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1740322},
pmid = {41561086},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Gastrointestinal Diseases/therapy/microbiology ; Probiotics/therapeutic use ; Animals ; Fecal Microbiota Transplantation ; Gastrointestinal Tract/microbiology ; Phage Therapy ; Dysbiosis/therapy ; },
abstract = {Gut microbiome medicine is a promising field in functional medicine, offering personalized treatment strategies for gastrointestinal disorders. Advanced metagenomic and metabolomic technologies have revealed the gut microbiome's systemic influence, extending to distant organs like the brain and lungs. While small molecules and genes facilitate these effects, the gut microbiota's greatest abundance and activity are concentrated in the gastrointestinal tract, particularly in the distal regions. The balance of microbial communities in the small and large intestines is crucial for gastrointestinal health. However, the dominance of pathogenic bacteria can disrupt this balance, leading to tissue damage and contributing to gastrointestinal disorders. Emerging interventions, such as probiotics, fecal microbiota transplantation, and dietary enrichment with short-chain fatty acids, show potential in restoring microbial balance, enhancing immune function, and potentially protecting against carcinogenesis. Current evidence from clinical trials and animal models supports the therapeutic role of gut microbiome modulation in reversing gastrointestinal disorders. However, variability in study outcomes highlights the need for further research to standardize these approaches for clinical practice. This review underscores the gut microbiome's pivotal role in gastrointestinal health and the therapeutic promise of functional medicine in addressing these disorders. This review also explores emerging interventions, such as phage therapy and engineered microbes, and provides comparative analyses of microbiota signatures and therapeutic approaches across different gastrointestinal disorders.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Gastrointestinal Diseases/therapy/microbiology
Probiotics/therapeutic use
Animals
Fecal Microbiota Transplantation
Gastrointestinal Tract/microbiology
Phage Therapy
Dysbiosis/therapy

@article {pmid41561085,
year = {2025},
author = {Bu, W and Chen, Z and Liu, B and Jia, X},
title = {Gut microbiota and its metabolism in autism spectrum disorder: from pathogenesis to therapy.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1687691},
pmid = {41561085},
issn = {2235-2988},
mesh = {Humans ; *Autism Spectrum Disorder/therapy/microbiology/metabolism ; *Gastrointestinal Microbiome/physiology ; Fecal Microbiota Transplantation ; Dysbiosis/microbiology ; Probiotics ; Animals ; Brain-Gut Axis ; Prebiotics/administration & dosage ; },
abstract = {Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder characterized by social communication deficits and repetitive behaviors. Studies show that nearly half of ASD patients have gastrointestinal symptoms such as abdominal pain and diarrhea, indicating the important role of gut microbiota in its pathogenesis. This review finds that ASD patients exhibit reduced gut microbiota diversity and imbalanced Bacteroidetes/Firmicutes ratio, with abnormal microbial structure affecting neurobehavior through the gut-brain axis. Abnormalities in gut microbiota metabolites (short-chain fatty acids, phenolic compounds, bile acids, amino acids, etc.) are key mediators, which can exacerbate symptoms by affecting BBB permeability, neuroinflammation, and neurotransmitter balance. The gut-brain axis regulates ASD through mechanisms including the HPA axis, vagus nerve, immune pathways, and barrier functions. Gut microbiota-targeted interventions (exercise, dietary intervention, fecal microbiota transplantation, prebiotics/probiotics, etc.) can alleviate gastrointestinal and behavioral symptoms of ASD by regulating microbiota balance and improving metabolic environment. However, there are still issues such as unclear metabolite regulation mechanisms and significant individual differences in interventions. Future studies should combine multi-omics and artificial intelligence to identify core targets, develop personalized plans, and promote clinical translation.},
}

Humans
*Autism Spectrum Disorder/therapy/microbiology/metabolism
*Gastrointestinal Microbiome/physiology
Fecal Microbiota Transplantation
Dysbiosis/microbiology
Probiotics
Animals
Brain-Gut Axis
Prebiotics/administration & dosage

@article {pmid41491103,
year = {2026},
author = {Bryant, JA and Vulić, M and Walsh, EA and Allen, EG and Beauchemin, NJ and Chafee, ME and Diao, L and Fenn, K and Ford, KA and Hasson, BR and Litcofsky, KD and Lombardo, MJ and Martinez, A and O'Brien, EJ and Straub, TJ and Sykes, SM and Marshall, LF and Winkler, JA and McGovern, BH and Ford, CB and Wortman, JR and Henn, MR},
title = {The impact of an oral purified microbiome therapeutic on the gastrointestinal microbiome.},
journal = {Nature medicine},
volume = {32},
number = {1},
pages = {186-196},
pmid = {41491103},
issn = {1546-170X},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Clostridium Infections/microbiology/therapy/prevention & control ; Clostridioides difficile/pathogenicity ; Administration, Oral ; Male ; Female ; Double-Blind Method ; Feces/microbiology ; Middle Aged ; Bacillota ; Adult ; *Fecal Microbiota Transplantation/methods ; Aged ; },
abstract = {VOWST (VOWST oral spores, VOS; fecal microbiota spores, live-brpk, formerly SER-109) is an FDA-approved, orally administered consortium of purified Firmicutes spores developed to prevent recurrent Clostridioides difficile infection (CDI). Although 86.7% (26/30) of patients with recurrent CDI did not experience a subsequent recurrence over 8 weeks in an open-label phase 1b study, a subsequent double-blind phase 2 study (NCT02437487) did not demonstrate a significant benefit over placebo (rate of recurrence at 8 weeks in SER-109 versus placebo: 44.1% versus 53.3%). These discordant outcomes were hypothesized to be due to suboptimal dosing. This hypothesis was addressed in a pivotal phase 3 trial (NCT03183128) using an approximately tenfold higher dose. In phase 3, only 12% of VOS-treated patients versus 40% of placebo patients recurred by week 8 (relative risk 0.32, P < 0.001). Here in this follow-up post hoc analysis, across-trial comparisons confirmed that the higher, efficacious phase 3 dose is associated with improved pharmacokinetics, assessed by VOS engraftment (patients with available samples: phase 1b: 28, phase 2: 79, phase 3: 170). In-depth phase 3 analyses revealed that VOS significantly altered microbial composition, significantly enriching the diversity and abundance of Firmicutes species and reducing the prevalence and abundance of C. difficile and opportunistic pathogens (for example, Enterobacteriaceae species). Consistent with these taxonomic changes, significant changes in key bioactive metabolites were observed, including depletion of conjugated and deconjugated primary bile acids, enrichment of secondary bile acids and increases in short-chain and medium-chain fatty acids. In vitro, VOS batches produced these C. difficile-inhibiting metabolites. These findings on the pharmacology of VOS underscore the importance of rapidly restoring key protective functions of the microbiome in patients with recurrent CDI to achieve durable prevention of recurrence, as observed in the phase 3 study; they also highlight the need to include the microbiome in the clinical management of CDI. ClinicalTrials.gov registrations: NCT02437487 and NCT03183128 .},
}

Humans
*Gastrointestinal Microbiome/drug effects
*Clostridium Infections/microbiology/therapy/prevention & control
Clostridioides difficile/pathogenicity
Administration, Oral
Male
Female
Double-Blind Method
Feces/microbiology
Middle Aged
Bacillota
Adult
*Fecal Microbiota Transplantation/methods
Aged

@article {pmid41398688,
year = {2025},
author = {Zhong, W and Feng, R and Liang, H and Hu, J and Zhou, S and Liu, D and Li, S and Liao, G and Liao, J and Yang, S and Zhang, Y and Xiao, X and Qian, J and Chen, H and Fan, L and Li, M and Zhao, M and Chen, J and Liu, Y},
title = {Longitudinal profiling of gut microbiota dynamics in kidney transplant recipients.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {91},
pmid = {41398688},
issn = {1479-5876},
support = {No. 2022A1515012304 & 2023A1515110205//Basic and Applied Basic Research Foundation of Guangdong Province/ ; No. 82170764 & 82403882//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: The gut microbiota undergoes substantial alterations in kidney transplant recipients, which are linked to postoperative complications and renal function recovery. However, the underlying mechanisms of these associations remain unclear.

METHODS: We conducted a prospective, longitudinal cohort study at our center. Fecal samples were collected from 88 kidney transplant recipients at multiple time points before and after surgery. The gut microbiota dynamics were profiled using 16S rRNA sequencing.

RESULTS: Significant shifts in gut microbiota diversity and composition were observed following transplantation. At 30 days post-surgery, a significant enrichment of Enterobacteriaceae was associated with an increased risk of urinary tract infections (UTIs) and a concomitant reduction in multiple peripheral blood lymphocyte subsets. While Enterobacteriaceae enrichment was not correlated with renal function, patients with an estimated glomerular filtration rate (eGFR) greater than 30 mL/min/1.73 m² at 30 days post-transplantation exhibited a marked increase in Bifidobacterium.

CONCLUSIONS: Our findings suggest that post-transplant enrichment of Enterobacteriaceae may be associated with an increased incidence of UTIs and immune dysregulation. In contrast, Bifidobacterium may play a beneficial role in supporting renal function recovery. These results highlight specific gut microbiota taxa as potential biomarkers or targets for improving outcomes in kidney transplant recipients.

GRAPHICAL ABSTRACT: [Image: see text]

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12967-025-07465-4.},
}

@article {pmid41561048,
year = {2025},
author = {Wang, L and Chen, S and Cai, X and Zheng, Y and Zheng, C and Yao, Y},
title = {The influence of immune regulation mediated by intestinal microbiota on postmenopausal osteoporosis and intervention strategies.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1720484},
pmid = {41561048},
issn = {1664-2392},
mesh = {Humans ; *Osteoporosis, Postmenopausal/immunology/microbiology/therapy ; *Gastrointestinal Microbiome/immunology ; Female ; Animals ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {Postmenopausal osteoporosis (PMO) is a common metabolic bone disease characterized by reduced bone mass and deteriorated bone microarchitecture, leading to an increased risk of fractures. In recent years, growing evidence has highlighted the role of gut microbiota and its immune-mediated regulation in the pathogenesis and progression of PMO. The gut microbiota modulates host immune responses, influencing the balance between bone resorption and bone formation. Estrogen deficiency after menopause disrupts gut microbiota composition, induces systemic inflammation, and promotes osteoclast activation, accelerating bone loss. Moreover, specific microbial communities and their metabolites, such as short-chain fatty acids (SCFAs), regulate bone metabolism by modulating immune cells, including T cells, B cells, and macrophages. Various microbiota-targeted interventions, such as probiotics, prebiotics, and fecal microbiota transplantation (FMT), have shown potential in improving bone health. However, several challenges remain, including individual variability in microbiota composition, the long-term effects of interventions, and their clinical applicability. Further investigations into the gut microbiota-mediated immune regulation of PMO may provide novel insights and therapeutic strategies for osteoporosis prevention and treatment.},
}

Humans
*Osteoporosis, Postmenopausal/immunology/microbiology/therapy
*Gastrointestinal Microbiome/immunology
Female
Animals
Probiotics/therapeutic use
Fecal Microbiota Transplantation

@article {pmid41560593,
year = {2026},
author = {Reddy, N and Lau, K and Naman, J and Lu, K and McGillivary, E and Salmasi, A and Liss, M and Stewart, T},
title = {Killing cancer takes guts: lessons learned from the manipulation of gut microbiome and immunotherapy for the future of urothelial carcinoma.},
journal = {Oncoimmunology},
volume = {15},
number = {1},
pages = {2611458},
doi = {10.1080/2162402X.2025.2611458},
pmid = {41560593},
issn = {2162-402X},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immunotherapy/methods ; Immune Checkpoint Inhibitors/therapeutic use ; Fecal Microbiota Transplantation ; Animals ; Probiotics/therapeutic use ; *Carcinoma, Transitional Cell/therapy/immunology/microbiology ; *Urinary Bladder Neoplasms/therapy/immunology/microbiology ; },
abstract = {Urothelial carcinoma (UC) remains a common cancer with significant morbidity and mortality worldwide. Immune checkpoint inhibitors (ICIs) have helped revolutionize the treatment of UC, and there is growing evidence suggesting the crucial role of the gut microbiome in immune system function influences immunotherapy outcomes in this disease. Herein, we review the preclinical basis for how manipulation of the gut microbiome may alter the efficacy of immunotherapy for patients with cancer, highlight interventions optimizing gut microbiome diversity currently in use, review recent and ongoing clinical trials supporting the role of the gut microbiome in improving immunotherapy outcomes, and discuss clinical implications to improve outcomes for UC patients with immunotherapy in the real world. There is growing evidence that suggests that specific gut microbiome compositions significantly modulate the host immune system and response to ICIs. Early studies have shown that certain microbial taxa enhance antitumor immunity by influencing T cell priming, dendritic cell activation, and cytokine production. Fecal microbiota transplantation (FMT), probiotic supplementation, and dietary modulation have emerged as promising methods to alter microbiomes to improve immunotherapy outcomes. Taxa from positive immunotherapy responders across a variety of cancers demonstrate beneficial effects when transplanted into both treatment-naive or prior nonresponders. Increasing evidence suggests that the gut microbiome plays a crucial role in cancer care, particularly when patients are treated with immunotherapy. Future studies are needed to better understand the underlying mechanisms. While some studies are currently underway to explore gut manipulation for patients with UC, more studies are needed to investigate the potential to convert nonresponders into responders through microbiome manipulation.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
*Immunotherapy/methods
Immune Checkpoint Inhibitors/therapeutic use
Fecal Microbiota Transplantation
Animals
Probiotics/therapeutic use
*Carcinoma, Transitional Cell/therapy/immunology/microbiology
*Urinary Bladder Neoplasms/therapy/immunology/microbiology

@article {pmid41560360,
year = {2026},
author = {Zhang, J and Wang, Z and Li, S and Luo, C and Li, H and Ma, S and Wang, P and Liu, H and Sun, L and Yin, Y and Zhang, W and Wang, Q},
title = {Phocaeicola coprophilus-Derived 6-Methyluracil Attenuates Radiation-Induced Intestinal Fibrosis by Suppressing the IDO1-Kynurenine-AHR Axis.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e18502},
doi = {10.1002/advs.202518502},
pmid = {41560360},
issn = {2198-3844},
support = {JDYY15202429//Youth Development Fund of the First Hospital of Jilin University/ ; JDYY-DEP-2022006//Doctor of Excellence Program (DEP), The First Hospital of Jilin University/ ; YDZJ202402012CXJD//Department of Science and Technology of Jilin Province/ ; 82330017//National Natural Science Foundation of China/ ; 82270610//National Natural Science Foundation of China/ ; 20240484505//Beijing Nova Program/ ; 2024ZD0530100//Noncommunicable Chronic Diseases-National Science and Technology Major Project/ ; },
abstract = {Therapeutic options for radiation-induced intestinal fibrosis (RIF) remain limited. This study reveals that intestinal kynurenine (Kyn) is persistently elevated after radiation and correlates with fibrosis severity in both murine models and human rectal cancer samples. Exogenous Kyn exacerbated RIF, whereas inhibition of indoleamine 2,3-dioxygenase 1 (IDO1) attenuated fibrotic progression. Mechanistically, Kyn activates the aryl hydrocarbon receptor (AHR) to promote fibroblast activation and fibrosis. Antibiotic depletion of gut microbiota abrogates radiation-induced IDO1-Kyn upregulation and protects against RIF. Conversely, fecal microbiota transplantation from irradiated mice recapitulates the elevated IDO1-Kyn phenotype. Metagenomic analysis identify radiation-induced depletion of Phocaeicola coprophilus (P. coprophilus), whose abundance inversely correlates with Kyn levels. Supplementation with live P. coprophilus suppresses IDO1-Kyn signaling and ameliorates RIF. Untargeted metabolomics further show that radiation reduces 6-methyluracil, a metabolite derived from P. coprophilus. Exogenous 6-methyluracil replenishment inhibits repression of the IDO1-Kyn axis and mitigates fibrosis. Together, these findings define a microbiota-metabolite-host pathway in which radiation depletes P. coprophilus, leading to loss of 6-methyluracil and derepression of the IDO1-Kyn-AHR axis, thereby driving fibrogenesis. Restoration of either P. coprophilus or its metabolite 6-methyluracil represents a promising therapeutic strategy against RIF.},
}

@article {pmid41558030,
year = {2026},
author = {Fan, C and Hayase, T and Chang, CC and Glover, IK and Flores, II and McDaniel, LK and Ortega, MR and Sanchez, CA and El-Himri, RK and Brown, AN and Karmouch, JL and Jamal, MA and Ahmed, SS and Halsey, TM and Jin, Y and Tsai, WB and Prasad, R and Enkhbayar, A and Mohammed, A and Schmiester, M and Damania, AV and Ajami, NJ and Wargo, JA and Peterson, CB and Rondon, G and Al-Juhaishi, T and Alousi, AM and Molldrem, JJ and Champlin, RE and Shpall, EJ and Martens, E and Arias, CA and Jenq, RR and Hayase, E},
title = {Fecal carbohydrate-degrading bacteria are associated with reduced incidence of lower gastrointestinal GVHD.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2025016780},
pmid = {41558030},
issn = {2473-9537},
abstract = {Lower gastrointestinal graft-versus-host disease (LGI-GVHD) carries morbidity and mortality for patients undergoing allogeneic hematopoietic stem cell transplantation (allo-HSCT), with critical contributions from the intestinal microbiome. In a retrospective cohort of metagenomic sequencing of allo-HSCT patient stool (n = 90), we found that a reduction in specific Parabacteroides and Bacteroides species around the time of engraftment contributes to LGI-GVHD risk. Given the known diverse carbohydrate degrading functionality of these bacteria, we investigated gene abundances for Carbohydrate-Active enZyme (CAZyme) and found that Parabacteroides merdae, Parabacteroides distasonis and Bacteroides ovatus abundances were significantly correlated with CAZymes in patients who did not develop LGI-GVHD compared to those who did. The specific gene abundances of xylosidase, which contribute to the degradation of xylose-containing polysaccharides, were significantly associated with reduced risk of LGI-GVHD. Together, these findings show the importance of carbohydrate degrading functionality of putative beneficial bacteria in mediating risk of LGI-GVHD.},
}

@article {pmid41557194,
year = {2026},
author = {Hayashi, A and Okamoto, T and Takahashi, T and Sato, Y and Ueda, Y},
title = {Pitfalls in the differential diagnosis of diarrhea after kidney transplantation: challenges in identifying Yersinia enterocolitica infection.},
journal = {CEN case reports},
volume = {15},
number = {1},
pages = {25},
pmid = {41557194},
issn = {2192-4449},
mesh = {Humans ; *Kidney Transplantation/adverse effects ; Male ; *Yersinia enterocolitica/isolation & purification ; *Yersinia Infections/diagnosis/drug therapy ; Diagnosis, Differential ; Adolescent ; *Diarrhea/diagnosis/etiology/microbiology ; Anti-Bacterial Agents/therapeutic use ; Feces/microbiology ; Colonoscopy ; Immunocompromised Host ; Abdominal Pain/etiology ; },
abstract = {We present the case of a 14-year-old boy with a history of kidney transplantation due to focal segmental glomerulosclerosis who developed severe diarrhea and abdominal pain following an episode of antibody-mediated rejection. Despite stable kidney function, the patient required increased immunosuppressive therapy, raising concerns regarding possible drug-induced enteritis or infections. Initial investigations, including stool tests for common pathogens and imaging, failed to identify the causative agent. Colonoscopy revealed thickening of the terminal ileum and aphthae in the colon; however, common infections, such as cytomegalovirus and Epstein-Barr virus, were excluded. Given the persistence of symptoms and worsening ultrasound findings showing enlarged lymph nodes and mucosal thickening, Yersinia enterocolitica infection was suspected. Special stool culture media for Yersinia spp. confirmed the infection, and the patient responded well to antibiotic therapy. Our case highlights several challenges in diagnosing gastrointestinal infections in kidney transplant recipients, including the non-specific nature of symptoms and the difficulty in distinguishing between drug-induced enteritis, viral or bacterial infections, and other transplant-related complications. This underscores the importance of considering rare pathogens, such as Yersinia, in the differential diagnosis of gastrointestinal symptoms in immunocompromised transplant patients, including pediatric patients, and emphasizes the need for specialized diagnostic techniques, such as stool culture on selective media, to confirm the diagnosis.},
}

Humans
*Kidney Transplantation/adverse effects
Male
*Yersinia enterocolitica/isolation & purification
*Yersinia Infections/diagnosis/drug therapy
Diagnosis, Differential
Adolescent
*Diarrhea/diagnosis/etiology/microbiology
Anti-Bacterial Agents/therapeutic use
Feces/microbiology
Colonoscopy
Immunocompromised Host
Abdominal Pain/etiology

@article {pmid41557025,
year = {2026},
author = {Alnaggar, M and Chen, Y and Wang, C and Wang, S and Zhu, F and Lin, Y and Abdu, FA and Gong, L},
title = {Synergistic Effect of Fecal Microbiota Transplantation, γδT Cell Immunotherapy, and Pembrolizumab in Refractory Advanced Pancreatic Cancer: A Case Report.},
journal = {Journal of gastrointestinal cancer},
volume = {57},
number = {1},
pages = {23},
pmid = {41557025},
issn = {1941-6636},
support = {KJZD20230923115110020//Shenzhen Major Scientific and Technological Project./ ; },
mesh = {Humans ; Male ; *Antibodies, Monoclonal, Humanized/therapeutic use/pharmacology ; Aged ; *Pancreatic Neoplasms/therapy/pathology/immunology ; *Fecal Microbiota Transplantation/methods ; *Antineoplastic Agents, Immunological/therapeutic use ; *Immunotherapy/methods ; Combined Modality Therapy ; },
abstract = {BACKGROUND: Pancreatic cancer (PC) remains one of the most lethal malignancies with limited treatment options, particularly in advanced stages. Emerging immunotherapeutic strategies, such as Gamma Delta (γδ) T cell therapy paired with microbiota management, have demonstrated promise.

CASE PRESENTATION: We report a case of a 75-year-old male diagnosed with advanced-stage and poorly differentiated PC who demonstrated significant clinical improvement following a novel therapeutic approach combining fecal microbiota transplantation (FMT), γδ T cell therapy, and pembrolizumab. Initial chemotherapy and radiotherapy were discontinued due to adverse effects. Pre-treatment the CA19-9 (1206 U/mL), tumor markers were significantly elevated with CEA, CA15-3 and CA125 all within normal limits. No pathogenic mutations (e.g., BRCA1/2, PALB2) were identified. A comprehensive assessment revealed tumor progression, immunosuppression, and gut microbiota dysbiosis, resulting in FMT and γδ T cell therapy being introduced alongside pembrolizumab.

OUTCOMES: The combination therapy resulted in the clearance of circulating tumor cells (CTCs), normalization of CA19-9 to 72 U/mL, improved clinical symptoms, and a marked reduction in tumor size, as confirmed by CT. Tolerability was excellent with no serious adverse events occurred.

CONCLUSION: This case suggests that FMT combined with γδ T cell therapy may be a promising immunotherapeutic strategy for advanced PC. Further studies are needed to validate these findings.},
}

Humans
Male
*Antibodies, Monoclonal, Humanized/therapeutic use/pharmacology
Aged
*Pancreatic Neoplasms/therapy/pathology/immunology
*Fecal Microbiota Transplantation/methods
*Antineoplastic Agents, Immunological/therapeutic use
*Immunotherapy/methods
Combined Modality Therapy

@article {pmid41556761,
year = {2026},
author = {Xu, J and Han, Z and Xue, Q and Wang, H and Song, J and Li, Y and Zhang, Y and Wang, D and Hu, M},
title = {Limosilactobacillus mucosae attenuates hyperlipidemic periodontitis via the gut-oral axis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2617699},
doi = {10.1080/19490976.2026.2617699},
pmid = {41556761},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Periodontitis/microbiology/therapy ; Mice ; Humans ; *Hyperlipidemias/microbiology/complications/therapy ; Male ; Mice, Inbred C57BL ; Dysbiosis/microbiology ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Claudin-1/metabolism/genetics ; *Probiotics/administration & dosage ; },
abstract = {The link between hyperlipidemia and periodontitis is well-established, but the underlying mechanisms remain incompletely understood. Here, we reveal a critical role for a 'gut-oral' axis in mediating this interaction. Integrating multi-omics analyses of clinical samples and mouse models, we identified that a significant reduction of intestinal Limosilactobacillus mucosae is a key feature of hyperlipidemic periodontitis (HPD). Fecal microbiota transplantation established a causal link between this gut dysbiosis and exacerbated periodontitis. Mechanistically, oral administration of live L. mucosae ameliorates HPD by restoring intestinal levels of the key metabolite, glycerophosphocholine (α-GPC). Notably, supplementation with α-GPC alone recapitulated this protective effect by upregulating the tight junction protein Claudin-1 (CLDN1) in periodontal tissue. This reinforcement of the epithelial barrier curtailed inflammatory infiltration and restored bone homeostasis. Our findings uncover a protective ' L. mucosae-α-GPC-CLDN1' axis, providing mechanistic insight into how gut microbiota mediates metabolism-associated inflammation and proposing a potential therapeutic strategy for HPD.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Periodontitis/microbiology/therapy
Mice
Humans
*Hyperlipidemias/microbiology/complications/therapy
Male
Mice, Inbred C57BL
Dysbiosis/microbiology
Disease Models, Animal
Fecal Microbiota Transplantation
Claudin-1/metabolism/genetics
*Probiotics/administration & dosage

@article {pmid41555858,
year = {2026},
author = {Wu, Z and Yang, Z and Lyu, C and Sun, B and Zhang, R and Li, H and Chen, J},
title = {Gut microbiota and neoadjuvant chemoradiotherapy in locally advanced rectal cancer: a review of current evidence and emerging insights.},
journal = {Therapeutic advances in medical oncology},
volume = {18},
number = {},
pages = {17588359251413948},
pmid = {41555858},
issn = {1758-8340},
abstract = {Locally advanced rectal cancer (LARC) presents a significant burden on lower gastrointestinal diseases, with current treatment strategies primarily involving neoadjuvant chemoradiotherapy (nCRT) followed by radical surgery. However, patient responses to nCRT exhibit significant variability, highlighting the need for personalized therapeutic approaches. Emerging evidence suggests that the gut microbiota plays a critical role in influencing both treatment outcomes and toxicity in LARC patients. Intestinal dysbiosis has been linked to LARC progression and may affect the efficacy and adverse effects of nCRT. This narrative review critically evaluates the current literature on the relationship between gut microbiota and nCRT in LARC. Certain microbial taxa, such as Alistipes spp., Akkermansia muciniphila, and Faecalibacterium prausnitzii, have been associated with enhanced therapeutic responses, while others, such as Fusobacterium nucleatum and Enterotoxigenic Bacteroides fragilis, may contribute to treatment resistance and exacerbate adverse effects. We also discuss novel mechanisms by which specific gut microbiota and their metabolites modulate nCRT response distinct from conventional immune regulation, alongside emerging strategies for microbiota modulation, including dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation. Despite challenges in standardizing microbiota analysis and fully understanding the precise mechanisms, microbiota-targeted interventions offer a promising avenue for personalized treatment in LARC, with the potential to improve patient outcomes and quality of life.},
}

@article {pmid41382117,
year = {2025},
author = {Wang, Y and Bai, Z and Sun, J and Gong, Q and Miao, W and Niu, Z and Li, X and Xu, J and Lai, Z},
title = {Intestinal congestion-driven gut dysbiosis: a cross-disease hemodynamic mechanism in liver cirrhosis and heart failure.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {79},
pmid = {41382117},
issn = {1479-5876},
support = {SYYYRC-2022006//First Hospital of Shanxi Medical University/ ; 202103021224408//Natural Science Foundation of Shanxi Province/ ; 202203021221248//Natural Science Foundation of Shanxi Province/ ; 202204010931008//Shanxi Provincial Science and Technology Department/ ; YDZJSX2021B012//Shanxi Provincial Science and Technology Department/ ; 82470693//Innovative Research Group Project of the National Natural Science Foundation of China/ ; 2023065//Health Commission of Shanxi Province/ ; },
abstract = {BACKGROUND: Intestinal congestion is a common pathophysiological feature of both liver cirrhosis and heart failure (HF). This study aimed to investigate whether intestinal congestion induces similar gut microbiota and metabolite alterations under both conditions, and to identify key microbial and metabolic signatures.

METHODS: We analyzed 117 cirrhosis patients (uncomplicated cirrhosis, cirrhosis with hepatocellular carcinoma, transjugular intrahepatic portosystemic shunt, and liver transplantation), 75 HF patients, and 31 healthy controls (CG). We performed 16S rRNA sequencing on all samples to assess gut microbial diversity, and subjected six representative samples per group to metagenomic sequencing. We conducted untargeted metabolomics on 30 fecal samples each from the uncomplicated cirrhosis, HF with reduced ejection fraction (HFrEF), and CG groups to profile intestinal metabolites, followed by correlation analyses among representative taxa, clinical characteristics, and key metabolites.

RESULTS: Intestinal congestion of different etiologies exhibits similar alterations in the gut microbiota, particularly in patients with uncomplicated cirrhosis and HFrEF. Alterations in Bacteroides were closely associated with the severity of congestion. Veillonella and Lactobacillales were enriched in cirrhotic patients, whereas Coprococcus was uniquely abundant in HFs. Metabolomic analysis revealed significant reductions in tripeptides, anti-inflammatory compounds, and prostaglandin analogs in patients with intestinal congestion. Musacin D and neopterin may serve as potential noninvasive biomarkers for HF and cirrhosis, respectively.

CONCLUSION: Intestinal congestion is associated with gut microbiota dysbiosis and metabolic disturbances in cirrhosis and HFs, with specific microbes and metabolites showing potential predictive value for distinguishing underlying diseases.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12967-025-07547-3.},
}

@article {pmid41344924,
year = {2026},
author = {Raso, T and D'Arcangelo, G and Renzo, S and Strisciuglio, C and Colucci, A and Saccomani, MD and Bramuzzo, M and Bravin, F and Sansotta, N and Russo, G and Lionetti, P and Zullo, A and Oliva, S},
title = {Diagnostic accuracy of non-invasive tests for helicobacter pylori infection in children: A multicenter retrospective study by SIGENP.},
journal = {Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver},
volume = {58},
number = {1},
pages = {82-87},
doi = {10.1016/j.dld.2025.11.013},
pmid = {41344924},
issn = {1878-3562},
mesh = {Humans ; *Helicobacter Infections/diagnosis ; Retrospective Studies ; Female ; Male ; *Helicobacter pylori/isolation & purification ; Child ; Breath Tests ; Child, Preschool ; Sensitivity and Specificity ; Adolescent ; Italy ; *Feces/chemistry/microbiology ; *Antigens, Bacterial/analysis ; Predictive Value of Tests ; Urea/analysis ; Infant ; },
abstract = {BACKGROUND: Helicobacter pylori (H. pylori) infection remains prevalent in children, with significant clinical implications. While endoscopy with biopsy is the gold standard for diagnosis, non-invasive tests such as the stool antigen test (SAT) and urea breath test (UBT) may offer alternatives.

OBJECTIVES: To assess the diagnostic accuracy of SAT and UBT in children with suspected H. pylori infection and identify clinical predictors of infection.

METHODS: This retrospective multicenter study included pediatric patients undergoing endoscopy for suspected H. pylori across six Italian centers. Histological analysis served as the reference standard. Diagnostic metrics of SAT and UBT were calculated. Demographic and clinical factors were analyzed to identify independent predictors.

RESULTS: Of 256 patients, 150 (58.6 %) had confirmed infection. SAT showed higher sensitivity [94 % (95 % CI: 0.87-0.97)] than UBT [87 % (CI: 0.64-0.98)] but lower specificity [55 % vs 67 %], with lower PPV (64 % vs 78 %) and higher NPV (91 % vs 80 %). Independent predictors for H. pylori infection included family history [OR 4.4], positive SAT [OR 16.29], and non-Caucasian ethnicity [OR 4.3].

CONCLUSIONS: SAT demonstrates high sensitivity and NPV, supporting its role as a screening tool. In children without alarm symptoms, a negative SAT may safely exclude infection and help avoid unnecessary endoscopy.},
}

Humans
*Helicobacter Infections/diagnosis
Retrospective Studies
Female
Male
*Helicobacter pylori/isolation & purification
Child
Breath Tests
Child, Preschool
Sensitivity and Specificity
Adolescent
Italy
*Feces/chemistry/microbiology
*Antigens, Bacterial/analysis
Predictive Value of Tests
Urea/analysis
Infant

@article {pmid41555353,
year = {2026},
author = {Yu, C and Qian, Y and Zhou, Y and Sang, Y and Huang, W and Yang, L and Lu, L and Rong, X and Wu, H and Shi, Y and Kong, X},
title = {Deficiency of osteopontin in gut epithelial cells enhances intestinal integrity by promoting gut renewal through the JAK3/STAT4 pathway in acetaminophen (APAP)-induced acute liver injury.},
journal = {Cell communication and signaling : CCS},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12964-026-02675-9},
pmid = {41555353},
issn = {1478-811X},
support = {82405136//National Natural Science Foundation of China/ ; 82370582//National Natural Science Foundation of China/ ; PKJ2022-Y42//Shanghai Pudong New Area Science and Technology Development Fund Institutional Public Welfare Research Special Program Healthcare Project/ ; 201940352//The Scientific Program of Shanghai Municipal Health Commission/ ; 22ZR1428100//the Science and Technology Commission of Shanghai Municipality/ ; },
abstract = {Gut barrier dysfunction is a key feature of acute liver injury (ALI) and leads to systemic immune responses (SIRS). Our previous studies have demonstrated that knockout of osteopontin (OPN) modulates antimicrobial peptide expression and reduces intestinal flora, thereby ameliorating sepsis. In this study, we employed an acetaminophen (APAP)-induced hepatotoxicity model, the leading cause of acute liver failure (ALF) worldwide, to investigate the role of intestinal epithelial-derived OPN in gut barrier integrity during ALF. We found that intestinal epithelial-specific OPN knockout mice (Opn[△][IEC]) exhibited significant protection against APAP-induced liver injury and reduced gut barrier leakage. Fecal transplantation experiments revealed that mice receiving feces from Opn[△][IEC] mice showed increased resistance to APAP-induced liver injury and enhanced immune defense. Mechanistically, transcriptome analysis of the gut barrier indicated that OPN exacerbated gut barrier damage by inhibiting gut self-renewal via the JAK3/STAT4 signaling pathway. Epithelial-derived OPN may play a critical role in compromising gut barrier integrity and may be a target for suppressing inflammation and ameliorating ALI.},
}

@article {pmid41554975,
year = {2026},
author = {Garzón, E and Galindo, V and Harary, Y and Teman, A and Yavits, L},
title = {Integrated BSI bacteria identifier-on-chip using approximate k-mer matching.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-36497-z},
pmid = {41554975},
issn = {2045-2322},
abstract = {Acute graft-versus-host (GVHD) is a deadly disease that can be treated through fecal microbiota transplantation. However, such treatment is often followed by life-threatening bloodstream infections (BSI). Rapid detection of BSI-causing bacteria is critical in preventing BSI-related deaths. PC-CAM is a pathogen identification system-on-chip designed to assist in avoiding BSI by real-time detection of pathogen bacterial genomes using k-mer matching. The core of PC-CAM is an Approximate search-capable (Hamming distance tolerant) Content Addressable Memory (ACAM). PC-CAM was designed and manufactured in a commercial 65nm process. We use PC-CAM for real-time detection of bacteria in blood and stool samples of GVHD patients and evaluate PC-CAM bacteria identification efficiency, performance, silicon area, and power consumption based on silicon measurements. PC-CAM is capable of classifying 960K short DNA reads/sec within a silicon area of 2.38mm[Formula: see text] consuming about 1.27mW. We envision PC-CAM as a platform deployed at points of care to provide real-time, accurate, privacy-preserving, easy-to-operate, and energy-efficient pathogen classification.},
}

@article {pmid41553256,
year = {2026},
author = {Linn, A and Boton, N and Beekmann, SE and Kociolek, L and Sandora, TJ and Polgreen, PM and Lee, MSL and Mehrotra, P},
title = {Pediatric Infectious Diseases Physicians' Preferences for Management of Clostridioides difficile Infection: An Emerging Infections Network (EIN) Survey.},
journal = {Journal of the Pediatric Infectious Diseases Society},
volume = {},
number = {},
pages = {},
doi = {10.1093/jpids/piag004},
pmid = {41553256},
issn = {2048-7207},
abstract = {We queried pediatric infectious diseases physicians via the Emerging Infections Network regarding management preferences for Clostridioides difficile infection (CDI). We explored use of vancomycin, fidaxomicin, bezlotoxumab and fecal microbiota transplantation and found that physicians are increasingly considering newer and adjunctive therapies for pediatric CDI, highlighting the need for updated guidelines.},
}

@article {pmid41550945,
year = {2025},
author = {Bibbò, S and De Maio, F and Capone, F and Quaranta, G and Rondinella, D and Rosato, R and Minelli, M and De Lorenzis, D and Sanguinetti, M and Cammarota, G and Di Lazzaro, V and Masucci, L},
title = {Correction: Case Report: Fecal microbiota transplantation via capsules ameliorated clinical outcomes in a patient with multiple sclerosis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1768227},
doi = {10.3389/fimmu.2025.1768227},
pmid = {41550945},
issn = {1664-3224},
abstract = {[This corrects the article DOI: 10.3389/fimmu.2025.1678759.].},
}

@article {pmid41548987,
year = {2026},
author = {Wang, A and Miao, Z and Huang, B and Zeng, J and Yuan, M and Yan, D},
title = {Baicalin Restores the Hypoglycemic Effect of Metformin by Regulating the Microbial Imidazole Propionate and Short-Chain Fatty Acids.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.70186},
pmid = {41548987},
issn = {1099-1573},
support = {82204699//National Natural Science Foundation of China/ ; 82130112//National Natural Science Foundation of China/ ; U24A20789//National Natural Science Foundation of China/ ; 2022-4-20218//Capital's Funds for Health Improvement and Research/ ; 2022-051//Youth Beijing Scholar/ ; 320.6750.2023-03-16//Clinical Research Project of Wu Jieping Medical Foundation/ ; },
abstract = {Gut microbiota dysbiosis is implicated in metformin non-response. This study aimed to investigate whether baicalin, a microbiota-modulating flavonoid derived from Radix Scutellariae, could restore metformin sensitivity and explored the underlying mechanisms. Fecal samples from metformin-treated responders and non-responders were collected and used to establish mouse models via fecal microbiota transplantation (FMT). The hypoglycemic efficacy of baicalin in combination with metformin was then evaluated. Serum levels of imidazole propionate (ImP) and the expression of downstream signaling proteins were assessed. Gut microbiota analysis identified ImP-producing bacteria modulated by baicalin, which was further validated in vitro. The roles of these bacteria and short-chain fatty acids (SCFAs) in metformin responsiveness were also examined. In vitro experiments were conducted to investigate the mechanism of SCFAs affect the production of ImP. Metformin responder and non-responder mouse models were successfully established. Baicalin co-administration significantly ameliorated insulin resistance in non-responder mice, reduced serum ImP levels, suppressed p38γ/Akt/AMPK (S485) signaling, and restored AMPK (T172) phosphorylation. Baicalin markedly suppressed key ImP-producing bacteria-Staphylococcus epidermidis and Streptococcus mutans. Notably, colonization with S. epidermidis induced metformin non-response in previously responsive mice. Furthermore, baicalin increased the abundance of SCFA-producing bacteria and elevated colonic SCFAs levels. SCFAs reduced ImP production by inhibiting the growth of ImP-producing bacteria, thereby enhancing metformin responsiveness. These findings indicate that baicalin restores metformin sensitivity by enriching SCFAs, suppressing ImP-producing bacteria, and lowering serum ImP, thereby reinstating metformin's hypoglycemic action. This study supports the potential of baicalin as an adjunct therapy for overcoming metformin non-response.},
}

@article {pmid41547475,
year = {2026},
author = {González, CA and Suárez, BG and Moreno, MB and Puig-Asensio, M and Alonso, VR and Marín, GS and Martí, CS and Ramón Santos, J and Alonso, LR},
title = {Clostridioides difficile infection: Position paper of the Catalan Society of Gastroenterology.},
journal = {Gastroenterologia y hepatologia},
volume = {},
number = {},
pages = {502634},
doi = {10.1016/j.gastrohep.2025.502634},
pmid = {41547475},
issn = {0210-5705},
abstract = {INTRODUCTION: Clostridioides difficile infection (CDI) is the leading cause of healthcare-associated infectious diarrhea and is associated with significant morbidity and mortality, primarily due to its high recurrence rate. For this reason, the Catalan Society of Gastroenterology commissioned the development of a position paper aimed at providing practical recommendations, grounded in scientific evidence and expert consensus, on the diagnosis and management of CDI.

METHODS: This position paper was developed by specialists in Gastroenterology, Infectious Diseases and Microbiology. It was based on a non-systematic review of the scientific evidence. Recommendations were formulated through expert consensus.

RESULTS: The document presents a structured approach to the diagnosis and treatment of CDI, emphasizing individualized management and strategies to reduce recurrence rates. Key components include the role of fecal microbiota transplantation and a therapeutic algorithm informed by disease severity and by whether the episode is initial or recurrent.

CONCLUSIONS: This position paper aims to serve as a practical, evidence-based guide for healthcare professionals involved in the clinical management of CDI, promoting the implementation of optimal therapeutic strategies and addressing the main challenges associated with this infection.},
}

@article {pmid41547302,
year = {2026},
author = {Zhang, W and Zhang, K and Xu, W and Sun, X and Xue, Y},
title = {Microbiota-targeted modulation of the gut-kidney axis in diabetic kidney disease: Therapeutic advances and future perspectives.},
journal = {Biochemical and biophysical research communications},
volume = {800},
number = {},
pages = {153294},
doi = {10.1016/j.bbrc.2026.153294},
pmid = {41547302},
issn = {1090-2104},
abstract = {Diabetic kidney disease (DKD) is increasingly recognized as a systemic disorder driven by immune-metabolic dysfunction, in which the gut microbiota plays a pivotal role. Dysbiosis of the intestinal microbiota disrupts epithelial barrier integrity, promotes endotoxemia, and triggers chronic low-grade inflammation, contributing to renal injury and fibrosis. Conversely, declining kidney function exacerbates gut microbial imbalance and uremic toxin accumulation, forming a bidirectional pathological loop. Beyond the classical gut-kidney axis, recent findings highlight the existence of a multi-organ signaling network-encompassing immune, metabolic, and hematopoietic pathways-that mediates cross-talk between the gut and kidneys. Microbial metabolites such as short-chain fatty acids, indoxyl sulfate, and bile acids act as endocrine-like regulators modulating renal inflammation, fibrosis, and metabolic stress. This review outlines the mechanistic underpinnings of gut-derived renal injury, including gut-immune-kidney, gut-metabolism-kidney, and gut-bone marrow-kidney axes. We also discuss emerging microbiota-targeted therapies, including probiotics, engineered bacteria, fecal microbiota transplantation, and AI-based personalized interventions. Together, these insights support a systems-level redefinition of DKD and underscore the therapeutic potential of restoring gut microbial homeostasis.},
}

@article {pmid41547071,
year = {2026},
author = {Xu, X and Fang, H and Liu, F and Zhou, Y and Wen, Y and Wang, X and Du, D and Lu, L and Yin, J and Sun, T and He, F and He, J and Zhou, M},
title = {Akebia saponin D attenuates ulcerative colitis via targeting EGFR and remodeling gut microbiota homeostasis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {151},
number = {},
pages = {157829},
doi = {10.1016/j.phymed.2026.157829},
pmid = {41547071},
issn = {1618-095X},
abstract = {BACKGROUND: Ulcerative colitis (UC), a refractory subtype of inflammatory bowel disease (IBD), is clinically characterized by chronic abdominal pain and bloody hematochezia. Although therapeutic interventions have advanced significantly in recent years, existing treatment modalities remain limited. Akebia saponin D (ASD), a bioactive triterpenoid saponin extracted from the traditional medicinal herb Dipsacus asper, has been demonstrated potent multimodal bioactivity.

PURPOSE: This study systematically evaluates the therapeutic potential of ASD in UC treatment and elucidates its underlying molecular mechanisms.

METHODS: A dextran sulfate sodium (DSS)-induced UC mouse model was established, and ASD treatment was administered to observe its effects on colitis and organ toxicity. Inflammation was induced in NCM460 and HT29 cells using lipopolysaccharide (LPS), and ASD treatment was applied to evaluate its anti-inflammatory effects. To assess the involvement of the gut microbiota and metabolite landscape, fecal microbiota transplantation (FMT), 16S rRNA sequencing, and untargeted metabolomics were conducted. Single-cell RNA sequencing (scRNA-seq) was performed using the MGISEQ-2000 platform to characterize the ASD-induced cellular landscape of the colon. Additionally, network pharmacology approaches were employed to predict and validate potential molecular targets of ASD.

RESULTS: ASD demonstrated significant therapeutic efficacy in UC, as evidenced by attenuated body weight loss, restored colonic length, and improved mucosal barrier integrity. Treatment with ASD substantially remodeled the gut microbiota composition and metabolic profiles, notably elevating the abundance of Akkermansia muciniphila (A. muciniphila) and levels of indole-3-carbinol (I3C). Single-cell resolution analysis revealed that ASD promoted the expansion of Hmgb2[+] transit-amplifying cells (TACs) and Muc2[+] goblet cells (GCs) in colonic tissues. Mechanistically, we demonstrated that EGFR is a key molecular target of ASD upstream of the MEK/ERK/AP-1 signaling cascade.

CONCLUSION: Our study demonstrates that ASD, as a microbiota-modulating therapeutic agent, alleviates intestinal inflammation by inhibiting the mitogen-activated protein kinase (MAPK) signaling pathway.},
}

@article {pmid41546540,
year = {2026},
author = {Thelen, AC and Korten, NM and Blischke, L and Voelz, C and Beyer, C and Seitz, J and Trinh, S},
title = {Faecal Microbiota Transplantation in Anorexia Nervosa: A Systematic Review of Methodologies, Outcomes, and Challenges With Recommendations for Future Studies.},
journal = {European eating disorders review : the journal of the Eating Disorders Association},
volume = {},
number = {},
pages = {},
doi = {10.1002/erv.70080},
pmid = {41546540},
issn = {1099-0968},
support = {//Doktor Robert Pfleger-Stiftung/ ; START (101/23)//RWTH Aachen University/ ; START (16/22)//RWTH Aachen University/ ; },
abstract = {OBJECTIVE: Anorexia nervosa (AN) is a severe psychiatric disorder displaying an altered gut microbiome. Faecal microbiome transplantation (FMT) has emerged as a powerful research tool and potential treatment option in AN due to the microbiome-gut-brain axis. Current studies are limited and reveal variable FMT protocols. This leads to heterogeneous outcomes and complicates drawing definitive conclusions from existing literature. This review aims to compile and assess the different protocols and develop recommendations on ideal donors, handling of faeces, recipients, duration/frequency of FMT, and measuring transfer success for future FMT studies regarding AN.

METHODS: We systematically screened three databases (Pubmed, Embase, Web of Science), identifying 13 studies, including two human case reports, one human study protocol, and 10 animal studies.

RESULTS: While all studies demonstrated microbial alterations in the recipients, not all animal studies successfully induced an AN/underweight phenotype, suggesting that precise coordination of study protocol components to allow further refinement is essential.

CONCLUSION: Researchers should prioritise clear, comprehensive, and transparent documentation to ensure the interpretability and reproducibility of FMT procedures. Detailed reporting will enable more meaningful comparisons across studies, deepen our understanding of the microbiome's role in AN, and help identify methodological factors that influence outcomes. Ultimately, completeness of documentation in FMT studies in AN has substantial potential to support future clinical applications and improve patient care.},
}

@article {pmid41545905,
year = {2026},
author = {Ma, J and Liu, M and Xu, J and Liu, B and Cui, Y and Shi, Y},
title = {Fecal microbiota transplantation mitigates lipopolysaccharide-induced oxidative stress in weaned piglets by modulating gut microbiota and enhancing riboflavin metabolism.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {9},
pmid = {41545905},
issn = {1674-9782},
support = {CARS-34//Modern Agro-industry Technology Research System of China/ ; No. 244200510010//the Science and Technology Innovation Leading Talent in Central Plains/ ; No.30500636//the Outstanding Talents of Henan Agricultural University/ ; },
abstract = {BACKGROUND: During the weaning phase, piglets are exposed to significant physiological and environmental stressors, which disrupt the balance of their intestinal microbiota and often lead to severe diarrhea. Previous studies have demonstrated that alfalfa fiber, derived from the stems and leaves of alfalfa, can effectively alleviate diarrhea in piglets. Additionally, multiple studies have highlighted the potential of fecal microbiota transplantation (FMT) in mitigating diarrhea in various models of intestinal diseases in young animals. However, the specific mechanisms by which FMT from targeted sources alleviates diarrhea in weaned piglets remain to be fully elucidated.

RESULTS: In this study, FMT from donor piglets fed an alfalfa fiber-supplemented diet effectively alleviated diarrhea, improved intestinal morphology, and enhanced gut barrier function in weaned piglets. FMT further promoted the colonization of beneficial bacterial genera (including UCG-005, unclassified Lachnospiraceae, Lachnospiraceae AC2044 group, UCG-002, Candidatus Saccharimonas, and Lachnospiraceae ND3007 group) while inhibiting the detrimental genus Tyzzerella, consequently enhancing the production of short-chain fatty acids (SCFAs). Additionally, FMT upregulated riboflavin metabolism, leading to elevated flavin adenine dinucleotide (FAD) levels and increased glutathione reductase activity, thereby collectively attenuating lipopolysaccharide (LPS)-induced oxidative stress and contributing to intestinal health.

CONCLUSIONS: We found that FMT modulates the structure of the gut microbiota, enhances microbial diversity and composition, increases the production of SCFAs, and upregulates riboflavin metabolism to elevate FAD levels. These changes collectively enhance immune and antioxidant capacities, thereby alleviating diarrhea.},
}

@article {pmid41545303,
year = {2026},
author = {Huang, JJ and YousefiAsl, M and Singh, N and Grivas, P and Bhatia, S},
title = {Steroid-sparing strategies for managing immune-related adverse events.},
journal = {Journal for immunotherapy of cancer},
volume = {14},
number = {1},
pages = {},
doi = {10.1136/jitc-2025-013776},
pmid = {41545303},
issn = {2051-1426},
mesh = {Humans ; *Neoplasms/drug therapy/immunology ; *Immune Checkpoint Inhibitors/adverse effects ; *Drug-Related Side Effects and Adverse Reactions/drug therapy/etiology ; *Steroids/therapeutic use ; *Immunotherapy/adverse effects/methods ; },
abstract = {Although immune checkpoint inhibitors (ICI) have greatly improved outcomes in several cancer types, their use is also associated with immune-related adverse events (irAEs) that can impact any organ system and lead to significant morbidity and even mortality. Current approaches to treatment of irAEs largely rely on the use of systemic corticosteroids, which can compromise antitumor immune responses and oncologic outcomes. Prolonged use of systemic corticosteroids is also associated with its own set of toxicities. Thus, there is a critical need for steroid-sparing treatment approaches for irAEs.In this article, we review the literature for alternative therapeutic approaches for irAEs, which include targeted delivery (alternate routes of administration) of steroids (eg, budesonide) as well as systemic non-steroidal strategies using other mechanisms of action, such as integrin/cytokine blockade, antibody depletion, disease-modifying antirheumatic drugs and fecal microbiota transplant, among others. Many of these approaches have shown significant promise in their ability to induce a clinical response and improve symptoms, even in the setting of steroid-refractory or steroid-dependent irAEs. These approaches are being increasingly used as primary and secondary prophylaxis in patients at high risk of irAEs. Importantly, these strategies may mitigate steroid-associated toxicities, preserve antitumor immune responses and allow continuation of ICI after development of irAEs, hence enabling the full potential of ICI against cancer.},
}

Humans
*Neoplasms/drug therapy/immunology
*Immune Checkpoint Inhibitors/adverse effects
*Drug-Related Side Effects and Adverse Reactions/drug therapy/etiology
*Steroids/therapeutic use
*Immunotherapy/adverse effects/methods

@article {pmid41544875,
year = {2026},
author = {Zuo, G and Chang, F and Yuan, X and Shen, Y and Guo, X and Tang, B and Huang, JA and Liu, Z and Lin, Y},
title = {Differential toll-like receptor 2 activation by Akkermansia muciniphila and Bacteroides thetaiotaomicron mediates the beneficial effects of Fu brick tea polysaccharide against colitis.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {108100},
doi = {10.1016/j.phrs.2026.108100},
pmid = {41544875},
issn = {1096-1186},
abstract = {Fu Brick Tea Polysaccharide (FBTP) ameliorates dextran sulfate sodium (DSS)-induced colitis in mice. However, the key intestinal bacterial strains and downstream molecular mechanisms mediating these protective effects remain unclear. In this study, FBTP ameliorated colitis and concurrent liver injury in a microbiota-dependent manner, primarily by enriching Akkermansia muciniphila (A. muciniphila) and depleting Bacteroides thetaiotaomicron (B. thetaiotaomicron). The essential role of the microbiota was confirmed through fecal microbiota transplantation. Mechanistically, A. muciniphila synergistically employed both its microbe-associated molecular patterns (MAMPs) and metabolic activity to activate the toll-like receptor 2 (TLR2)-Akt anti-inflammatory signaling pathway, favorably modulating Treg/Th17 immune homeostasis. However, challenging its established status as a beneficial commensal, B. thetaiotaomicron was found to activate the TLR2-NF-κB pro-inflammatory pathway driven primarily by its MAMPs, significantly exacerbating colitis, bacterial translocation, and liver injury. The pivotal role of TLR2 in mediating these divergent bacterial outcomes was confirmed through gene knockdown experiments. In conclusion, this study reveals that FBTP restores immune homeostasis by orchestrating a complex, TLR2-dependent interplay between beneficial (A. muciniphila) and pathobiontic (B. thetaiotaomicron) bacteria. This discovery not only clarifies the therapeutic mechanism of FBTP but also highlights the context-dependent risk of key commensals, offering critical insights for developing more precise microbiota-targeted interventions.},
}

@article {pmid41543761,
year = {2026},
author = {Munira, MS and Stevens, JE and Shahin, W and Wang, K and Franks, AE and Perez, ARJ and Scott, JW and Hill-Yardin, EL},
title = {Towards treatments targeting the gut to improve behavioural outcomes in autism spectrum disorder.},
journal = {Journal of neural transmission (Vienna, Austria : 1996)},
volume = {},
number = {},
pages = {},
pmid = {41543761},
issn = {1435-1463},
support = {APP2003848//National Health and Medical Research Council/ ; },
abstract = {Autism spectrum disorder (ASD; autism) is a prevalent and heterogeneous neurodevelopmental disorder characterised by social communication difficulties, repetitive behaviour, and restricted interests. For individuals with autism, in particular those who require substantial care-giver support, irritability, heightened sensitivity and aggressive behaviours in response to sensory, social, or environmental triggers can limit access to health, education and community services and impact quality of life. Although gastrointestinal (GI) symptom severity is associated with irritable behaviours in autism, there are few approved medications to address challenging behaviour or comorbid psychiatric disorders, or gut dysfunction in autism. Here, we review the mode of action of drugs undergoing clinical trials for treating irritable behaviour and improving social communication as well as potentially gastrointestinal symptoms in individuals with autism. Repurposed medications such as pimavanserin (an atypical antipsychotic) and the antiparasitic suramin are being trialled for treating irritable behaviours and impaired social interaction, respectively, in autism. NTI164 is a medicinal cannabis-derived biopharmaceutical undergoing clinical safety and efficacy trials for improving social communication and similarly, ML-004 is an investigational drug being assessed for treating social communication deficits. Two other repurposed medications previously utilised for schizophrenia; brexpiprazole and lumateperone, as well as AB-2004, a microbial metabolite sequestering agent (with proposed actions on gut function), are undergoing clinical trials to assess impacts on irritability associated with autism. We also outline emerging findings from clinical studies on the use of gut-targeted small molecules and bacteriophage therapy, prebiotics, probiotic supplementation and faecal microbiota transplantation (FMT), and their potential impact on behavioural symptoms in autism.},
}

@article {pmid41543263,
year = {2026},
author = {Baral, B and Parajuli, M and Pinilla, J and Muniz, J and Baral, B and Cançado, GGL},
title = {Safety and efficacy of oral microbiome therapy for the treatment of recurrent Clostridioides difficile infection: a systematic review and meta-analysis of randomized controlled trials.},
journal = {Scandinavian journal of gastroenterology},
volume = {},
number = {},
pages = {1-9},
doi = {10.1080/00365521.2026.2616310},
pmid = {41543263},
issn = {1502-7708},
abstract = {INTRODUCTION: This systematic review and meta-analysis aimed to assess the safety and efficacy of oral microbiome therapy (OMT) for the treatment of recurrent Clostridioides difficile infection (CDI).

METHODS: A comprehensive search was performed in PubMed, Cochrane library, Scopus and Embase. All randomized controlled trials (RCTs) meeting predefined inclusion criteria were included. Statistical analysis was performed using R software.

RESULTS: Three RCTs comprising 469 patients were analyzed, of whom 250 (53%) received OMT and 219 (47%) received placebo. OMT significantly reduced CDI recurrence at week 8 compared to placebo (risk ratio [RR] 0.57; 95% confidence interval [CI] 0.33-0.99; p = 0.04). In exploratory efficacy analyses, no significant differences in recurrence were observed between groups when stratified by prior fidaxomicin use (RR 0.36; 95% CI 0.03-4.01; p = 0.40) or vancomycin use (RR 0.68; 95% CI 0.30-1.55; p = 0.35). Similarly, Firmicutes engraftment at week 1 (mean difference [MD] 41.78; 95% CI -10.55 to 94.11; p = 0.12) and week 8 (MD 34.06; 95% CI -2.49 to 70.61; p = 0.07) did not show statistically significant between-group differences. Safety outcomes and adverse events were comparable between OMT and placebo.

CONCLUSION: OMT seems to reduce CDI recurrence at week 8 compared with placebo while demonstrating a comparable safety profile, supporting its role as an effective, well-tolerated therapy for recurrent CDI. New studies are necessary to confirm these findings.

REGISTRATION: The study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO) under registration number CRD420251022230.},
}

@article {pmid41541603,
year = {2026},
author = {Cheung, SLY and Kenway, LC},
title = {Pathophysiological Mechanisms and Nonpharmacological Interventions in Irritable Bowel Syndrome: Current Insights and Future Directions.},
journal = {Journal of nutrition and metabolism},
volume = {2026},
number = {},
pages = {4520019},
pmid = {41541603},
issn = {2090-0724},
abstract = {Irritable bowel syndrome, diagnosed using the ROME IV diagnostic criteria, is one of the most common dysfunctional disorders of the gastrointestinal system with a high global prevalence. Although symptom presentation is diverse, symptoms primarily manifest as abdominal pain, bloating, and alterations to bowel habits, negatively impacting quality of life but without an associated increase in mortality risk. Disruptions to the gut-brain axis, the bidirectional communication system between the central nervous system and the enteric nervous system, are hypothesised to be at the core of irritable bowel syndrome. Dysfunction may also be associated with stress and anxiety, as well as dietary factors, among other aspects related to physical and social environment, genetic predisposition and medical history. Patients with irritable bowel syndrome have also demonstrated increased vulnerability to neurotransmitter imbalances, with abnormalities associated with changes in gastrointestinal motility, low-grade inflammation and visceral pain. Moreover, chronic stress and anxiety may significantly exacerbate symptoms through the upregulation of cortisol secretion, disrupting the gut microbiome and elevating visceral sensitivity. While the gut microbiome maintains the integrity of the gut-brain axis and intestinal barrier, decreases in its diversity heighten susceptibility to intestinal inflammation. Although there is currently no known cure for irritable bowel syndrome, research supports stress management and behavioural therapies, a low fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) diet, and probiotic supplementation as key interventions to alleviate symptoms. Additionally, faecal microbiota transplantation emerges as a promising intervention that addresses some of the limitations in current interventions. This literature review explores the pathophysiological mechanisms relating to irritable bowel syndrome, with insight into current interventions and future directions to directly address the underlying factors driving symptomology.},
}

@article {pmid41540689,
year = {2026},
author = {Zhang, Y and Duan, Y and Zhang, C and Yu, L and Liu, Y and Xing, L and Wang, L and Yu, N and Peng, D and Chen, W and Wang, Y},
title = {[Poria cocos polysaccharide alleviates cyclophosphamide-induced intestinal barrier dysfunction and inflammation in mice by modulating gut flora].},
journal = {Nan fang yi ke da xue xue bao = Journal of Southern Medical University},
volume = {46},
number = {1},
pages = {34-46},
doi = {10.12122/j.issn.1673-4254.2026.01.04},
pmid = {41540689},
issn = {1673-4254},
support = {82505171 and 82204748//Natural Science Foundation for the Youth (NSFY) of China/ ; },
mesh = {Animals ; Cyclophosphamide/adverse effects ; *Gastrointestinal Microbiome/drug effects ; Mice, Inbred BALB C ; Mice ; *Intestinal Mucosa/drug effects/microbiology ; *Polysaccharides/pharmacology ; Inflammation ; *Poria/chemistry ; Wolfiporia/chemistry ; Male ; },
abstract = {OBJECTIVES: To investigate the protective effects of Poria cocos polysaccharide (PCP) against cyclophosphamide (CTX)-induced intestinal mucosal injury and its impact on gut flora and their metabolites in mice.

METHODS: Adult BALB/C mice were randomized into normal control group, CTX model group, glutamine (positive control) group, and low-, medium- and high-dose PCP treatment groups. In all but the normal control group, the mice were subjected to modeling of CTX-induced intestinal mucosal injury by intraperitoneal CTX injections for 3 days, followed by treatment with gavage of normal saline, glutamine (300 mg/kg), or PCP at 75, 150, or 300 mg/kg for 7 consecutive days. The colonic expressions of tight junction proteins (occludin and ZO-1), serum endotoxin, D-lactate, and DAO levels, intestinal permeability, colon injury, and colonic cytokine levels (IL-4, IL-22, IL-17A, and IFN-γ mRNA) were assessed. Gut microbiota, short-chain fatty acids (SCFAs; mainly acetates and propionates) and colonic GPR41 expression were analyzed using 16S rRNA sequencing, GC-MS, and Western blotting, respectively. Fecal microbiota transplantation (FMT) experiment was conducted to validate the role of gut microbes in PCP-mediated repair of intestinal injuries.

RESULTS: Compared with those in the model group, the mice treated with PCP showed significantly increased colonic occludin and ZO-1 expressions, reduced serum endotoxin, D-lactate and DAO levels, and lowered intestinal permeability with increased colonic expressions of IL-4, IL-22, IL-17A, and IFN-γ mRNA. PCP treatment obviously increased the abundance of Muribaculaceae, decreased Lactobacillus and Bacteroides, increased the contents of acetate and propionate in the colon, and upregulated colonic GPR41 expression. The results of FMT experiment confirmed the crucial role of gut microbes in PCP-mediated repair of CTX-induced intestinal injuries in mice.

CONCLUSIONS: PCP can protect against CTX-induced intestinal mucosal injury in mice possibly by modulating gut flora and SCFAs metabolism to enhance intestinal defense capacity.},
}

Animals
Cyclophosphamide/adverse effects
*Gastrointestinal Microbiome/drug effects
Mice, Inbred BALB C
Mice
*Intestinal Mucosa/drug effects/microbiology
*Polysaccharides/pharmacology
Inflammation
*Poria/chemistry
Wolfiporia/chemistry
Male

@article {pmid41539854,
year = {2026},
author = {Choi, S and Kwon, H and Kim, WK and Ko, G},
title = {Attenuation of Clostridioides difficile Infection by Clostridium hylemonae.},
journal = {Journal of microbiology and biotechnology},
volume = {36},
number = {},
pages = {e2510017},
doi = {10.4014/jmb.2510.10017},
pmid = {41539854},
issn = {1738-8872},
mesh = {*Clostridium Infections/microbiology/therapy/prevention & control ; Animals ; *Clostridium/physiology/genetics ; Gastrointestinal Microbiome ; Mice ; *Clostridioides difficile ; Disease Models, Animal ; Feces/microbiology ; Metagenomics ; },
abstract = {Clostridioides difficile infection (CDI) is a bacterial infection of the colon that can cause diarrhea and colitis. The use of antimicrobials disrupts the intestinal microbiota, weakening colonization resistance and creating an environment in which C. difficile can establish infection. It is, therefore, necessary to identify specific bacteria that are helpful for the recovery of the intestinal microbiota in individuals with CDI. Previous studies have identified several strains that showed a negative correlation with C. difficile. Among these strains, C. hylemonae DSM 15053, which possesses the bai operon similar to Clostridium scindens, was selected. To test this hypothesis, we utilized a CDI mouse model and evaluated the inhibitory effect of C. hylemonae DSM 15053. Furthermore, to gain insights into the underlying mechanisms, we performed gut microbiota analysis. Contrary to our expectations, C. hylemonae DSM 15053 did not significantly produce SBAs. Interestingly, however, microbial diversity and richness were significantly higher in the C. hylemonae DSM 15053-treated group compared with the PBS control group. In addition, we observed a higher abundance of the genera Phocaeicola, Akkermansia, and Parabacteroides in the C. hylemonae DSM 15053 group. Moreover, metagenomic and metabolomic analyses revealed that C. hylemonae DSM 15053 mitigates CDI through a mechanism distinct from that of C. scindens KCTC 5591, which primarily functions as a regulator of bile acid metabolism.},
}

*Clostridium Infections/microbiology/therapy/prevention & control
Animals
*Clostridium/physiology/genetics
Gastrointestinal Microbiome
Mice
*Clostridioides difficile
Disease Models, Animal
Feces/microbiology
Metagenomics

@article {pmid41539785,
year = {2026},
author = {Huang, F and Guo, A and Liu, S and Liu, H and Zhang, Z and Lin, T and Xiao, S and Luo, K and Kong, J and Wu, L and Yan, H},
title = {Gut microbiota-derived propionate alleviate traumatic painful neuroma through inhibiting the RIG-I-NF-κB-mediated neuroinflammation.},
journal = {Food research international (Ottawa, Ont.)},
volume = {226},
number = {},
pages = {118087},
doi = {10.1016/j.foodres.2025.118087},
pmid = {41539785},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology/drug effects ; *NF-kappa B/metabolism ; Mice ; *Propionates/pharmacology/metabolism ; Fecal Microbiota Transplantation ; Male ; *DEAD Box Protein 58/metabolism ; *Neuroma/drug therapy ; Signal Transduction/drug effects ; Mice, Inbred C57BL ; Disease Models, Animal ; *Neuroinflammatory Diseases ; Sciatic Nerve/injuries ; },
abstract = {Traumatic painful neuroma (TPN) is a debilitating condition that frequently develops after peripheral nerve injury, yet its pathogenesis remains poorly elucidated. Growing evidence implicates the gut microbiota in the regulation of pain and inflammatory processes, but its specific role in TPN has not been investigated. This study examines the contribution of the gut microbiota and its metabolite propionate to TPN development via modulation of the RIG-I-NF-κB signaling pathway. In a murine model of sciatic nerve transection, we identified distinct gut microbial communities between TPN-susceptible and non-susceptible mice, characterized by a reduction in beneficial bacteria and decreased fecal propionate levels in TPN-prone mice. Depletion of gut microbiota through antibiotic treatment aggravated neuroma formation and pain-like behaviors, effects that were reversible by fecal microbiota transplantation (FMT). Administration of propionate dose-dependently ameliorated neuroinflammation, fibrotic progression, and pain responses. Mechanistic studies revealed that propionate suppressed the RIG-I-NF-κB pathway activation, downregulated pro-inflammatory cytokines, and enhanced intestinal barrier integrity. Notably, FMT from propionate-treated mice replicated these protective outcomes. Our results indicate that gut microbiota-derived propionate mitigates TPN by inhibiting RIG-I-NF-κB-driven neuroinflammation and preserving gut barrier function, underscoring the gut-brain-nerve axis as a promising target for TPN therapy.},
}

Animals
*Gastrointestinal Microbiome/physiology/drug effects
*NF-kappa B/metabolism
Mice
*Propionates/pharmacology/metabolism
Fecal Microbiota Transplantation
Male
*DEAD Box Protein 58/metabolism
*Neuroma/drug therapy
Signal Transduction/drug effects
Mice, Inbred C57BL
Disease Models, Animal
*Neuroinflammatory Diseases
Sciatic Nerve/injuries

@article {pmid41539758,
year = {2026},
author = {Zhang, T and Liu, H and Yuan, J and Xie, B},
title = {Auricularia auricula polysaccharides intervention in vivo: inhibition of endogenous malodorous gas compounds through gut regulation and enhanced liver metabolism.},
journal = {Food research international (Ottawa, Ont.)},
volume = {226},
number = {},
pages = {118122},
doi = {10.1016/j.foodres.2025.118122},
pmid = {41539758},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Polysaccharides/pharmacology ; *Liver/metabolism/drug effects ; Rats ; Male ; Prebiotics/administration & dosage ; *Auricularia/chemistry ; Rats, Sprague-Dawley ; Diet, High-Fat/adverse effects ; Feces/chemistry ; Fermentation ; Fecal Microbiota Transplantation ; *Gases/metabolism ; },
abstract = {High-fat and high-protein diets increase susceptibility to endogenous malodorous gas compounds (EMGCs), particularly in long-term enclosed environments with limited nutrients. Auricularia auricula polysaccharides (AAP) are proposed to mitigate protein residues fermentation by gut microbiota, thereby reducing EMGCs accumulation and benefiting both health and environmental quality. This study elucidated the prebiotic mechanisms of AAP via rat interventions, fecal microbiota transplantation in pseudo-sterile rats, and in vitro fermentation with AAP-derived functional components and specific bacterial strains. Results demonstrated that AAP intervention effectively reduced EMGCs levels in feces and adipose tissue induced by high-fat and high-protein diets. The degradation products of AAP, including mannitol, lactose, and lyxose, along with reshaped gut microbiota, especially the functional strain Bacteroides xylanisolvens, all exhibited independent EMGCs-inhibiting activities. Mechanistically, AAP or its degradation products enhanced hepatic CYP450 expression through bile acid-mediated enterohepatic circulation, forming a gut-liver axis for EMGCs suppression. Additionally, gut metabolites lactose and maltose promoted colonic carbohydrate absorption, hepatic Col5a3 and Col1a1 enhanced hepatic protein absorption. Upregulated gut metabolites (histidine, choline bitartrate, lactose, maltose) and hepatic genes (Abcg8, Abcb9) enriched the ABC transporter pathway, expediting hepatic EMGCs excretion. This study supports AAP as a dietary supplement to inhibit EMGCs, ensuring environmental livability and health.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Polysaccharides/pharmacology
*Liver/metabolism/drug effects
Rats
Male
Prebiotics/administration & dosage
*Auricularia/chemistry
Rats, Sprague-Dawley
Diet, High-Fat/adverse effects
Feces/chemistry
Fermentation
Fecal Microbiota Transplantation
*Gases/metabolism

@article {pmid41539609,
year = {2026},
author = {Yang, D and Ren, D and Zhang, Y and Hao, Y and Yue, Y and Li, Q and Fan, Q and Sun, C and Cui, M and Zhang, M},
title = {The Gut Microbiota Dysbiosis in Geriatric Multimorbidity: Pharmacotherapeutic Implications, Pathophysiological Mechanisms, and Precision Modulation Strategies.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103023},
doi = {10.1016/j.arr.2026.103023},
pmid = {41539609},
issn = {1872-9649},
abstract = {Aging around the world is accelerating. With that comes the intersection of geriatric multimorbidity and polypharmacy, creating a large uncertainty about the pharmacological efficacy and therapeutic consequences of medications used when multiple concurrent health issues exist. The gut microbiota coordinates the way drugs work through multiple pathways: through the way drugs are metabolised, the way they maintain immune homeostasis, and the way they regulate the epithelial barrier. For these reasons, the gut microbiota is becoming an important therapeutic target for optimizing precision medicine strategies in treating patients with geriatric multimorbidities. In this narrative review, we systematically synthesize the evidence regarding how gut dysbiosis leads to decreased efficacy of multi-drug regimens through the interplay between metabolism, immune response, and barrier function in aging patients with multimorbidities, and we evaluate targeted interventions. Furthermore, we demonstrate that current interventions (e.g., probiotics, prebiotics, fecal microbiota transplants (FMT), phage therapy, and dietary modulation) have unique benefits but are limited by inter-individual variability, safety concerns, and a lack of proven long-term efficacy. Thus, many areas of microbiota-drug interactions in older adults with multimorbidity should be explored through future research. Key areas to address are: the establishment of large, multicenter longitudinal cohorts of older adults with multimorbidity that would allow for repeated collection of microbiota profiles, medication use, and health outcomes to identify the evolving interaction between multimorbidity, microbiota, and polypharmacy; the urgent need for standardized and integrated databases of microbiome-drug interactions that harmonize data formats, provide metabolic annotations and medication identifiers in order to support reproducible cross-study validation; and the further validation and application of artificial intelligence (AI) and machine learning (ML) in clinical trials. High-dimensional data collected from cohorts and databases will enable the development of predictive algorithms to identify individual drug responses and how effective microbiota-targeted interventions will be; these algorithms must then be prospectively validated. Ultimately, these initiatives are necessary to move toward the personalized management of microbiota-drug interactions in older adults with multimorbidity, providing greater safety of polypharmacy and promoting healthy aging.},
}

@article {pmid41539110,
year = {2026},
author = {Shrivastav, K and Pandey, M and Gor, H and Nema, V},
title = {Gut virome plays an extended role with bacteriome in neurological health and disease.},
journal = {Journal of the neurological sciences},
volume = {481},
number = {},
pages = {125754},
doi = {10.1016/j.jns.2026.125754},
pmid = {41539110},
issn = {1878-5883},
abstract = {The gut-brain axis (GBA) is a complex two-way communication system that links the gastrointestinal tract and the central nervous system (CNS) through neural, immune, hormonal, and microbial pathways. The microbiota-gut-brain axis (MGBA), a more specific concept, focuses on how gut microorganisms, including bacteria, viruses, and other microbes, modulate this communication and influence neurological health. This comprehensive review examines the intricate mechanisms through which gut microorganisms modulate neural function and contribute to neurological health and disease pathogenesis. The gut microbiota, comprising bacteria, viruses, fungi, and bacteriophages, produces essential neuroactive compounds including neurotransmitters- Gamma-Aminobutyric Acid (GABA), serotonin (5-HT), dopamine (DA), short-chain fatty acids (SCFAs), and metabolites that directly influence brain physiology through vagal, hormonal, and immunological pathways. Dysbiosis of the gut microbiota has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, autism spectrum disorders, and schizophrenia. In healthy conditions, beneficial bacterial strains such as Lactobacillus species synthesize GABA and regulate mood, while SCFA-producing bacteria like Fecalibacterium prausnitzii maintain blood-brain barrier integrity and exert neuroprotective effects. Conversely, pathological states demonstrate altered microbial compositions, reduced bacterial diversity, and compromised production of beneficial metabolites. Emerging evidence highlights the previously underexplored role of the gut virome, particularly bacteriophages, in regulating bacterial populations and influencing neurodevelopment. Viral dysbiosis correlates with cognitive impairment and neurodegenerative processes through modulation of bacterial metabolism and inflammatory responses. Understanding these complex host-microbiome-virome interactions provides novel therapeutic opportunities for neurological disorders through targeted interventions including probiotics, fecal microbiota transplantation, and phage-based therapies, representing a paradigm shift toward microbiome-centered approaches in neurological medicine.},
}

@article {pmid41539104,
year = {2026},
author = {Gong, Z and Xia, Y and Jiang, Y and Zhang, Y and Xu, C and Zhao, L and Zhang, R and Cai, W and Wen, Y and Ma, J and Yang, S and Gao, S},
title = {Xin-Ji-Er-Kang alleviates heart failure induced by myocardial ischemia-reperfusion injury through reshaping gut microbiota and metabolites.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {151},
number = {},
pages = {157800},
doi = {10.1016/j.phymed.2026.157800},
pmid = {41539104},
issn = {1618-095X},
abstract = {BACKGROUND: The relationship between the gut-heart axis and heart failure has attracted growing interest, making the gut microbiota a potential target for new treatments. Previously, we have reported the beneficial effects of the traditional Chinese medicine Xin-Ji-Er-Kang (XJEK) on heart failure (HF), but the influence of the intestinal microbiota on XJEK's protection of the heart remains to be confirmed.

PURPOSE: This study investigates the role of gut microbiota in XJEK's therapeutic impact on HF and elucidates its potential mechanism.

STUDY DESIGN: MIR-induced HF model mice were established and different concentrations of XJEK were administered by gavage. The pharmacological effects of XJEK were evaluated by multiple pharmacodynamic methods. Subsequently, fecal microbiota transplantation (FMT) and antibiotic-induced microbiota inhibition were used to explore the effect of XJEK on HF. We next employed 16S rRNA sequencing combined with fecal metabolomics to investigate alterations in gut microbiota and metabolic profiles, and further investigated the effects of mono-colonization with D. piger in mice.

RESULTS: XJEK administration dose-dependently enhanced cardiac function and reduced myocardial damage in MIR-induced HF mice, as evidenced by reduced cardiomyocyte hypertrophy, diminished myocardial fibrosis, and a decline in serum levels of NT-proBNP and cTnI. FMT from XJEK-treated mice to recipient mice revealed that the therapeutic effects of XJEK on heart failure partially depend on the gut microbiota. XJEK reshaped the gut microbiota, leading to elevated abundance of probiotics Faecalibacterium, Limosilactobacillus and Bifidobacterium, while pathogenic bacteria Staphylococcus was depleted. Additionally, XJEK elevated the levels of beneficial metabolites, including deoxycholic acid and β-MCA. Notably, XJEK led to a rise in the relative abundance of D. fairfieldensis, and through the study of D. piger of the same genus, it was found that Desulfovibrio may produce beneficial effects in HF mice.

CONCLUSION: XJEK effectively improved cardiac function, mitigated myocardial injury, and suppressed the progression of heart failure. XJEK improved gut microbiota composition and related metabolism, alleviating heart failure.},
}

@article {pmid41539094,
year = {2026},
author = {Wang, L and Xiong, Z and Chen, J and Liu, J and Liu, M and Yan, X and Fang, Z},
title = {Synergistic gut microbiome-host lipid axis underlies the antihypertensive effect of Qianyang Yuyin formula.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {151},
number = {},
pages = {157804},
doi = {10.1016/j.phymed.2026.157804},
pmid = {41539094},
issn = {1618-095X},
abstract = {BACKGROUND: Prehypertension (Pre-HTN) is highly prevalent and substantially increases the risk of developing hypertension and cardiovascular disease. Gut microbiota (GM) dysbiosis and altered lipid metabolism are increasingly recognized as critical regulators of blood pressure (BP). Traditional Chinese Medicine (TCM) formulas, such as Qianyang Yuyin Granules (QYYY), offer multi-target interventions, yet their preventive mechanisms in Pre-HTN remain unclear.

PURPOSE: This study aimed to investigate the antihypertensive effects of QYYY and elucidate its underlying mechanisms in a prehypertensive rat model.

METHODS: Prehypertensive spontaneously hypertensive rats (SHRs) were treated with QYYY for four weeks. Multi-omics analyses, including metagenomics, plasma metabolomics, and transcriptomics, were conducted. Causal involvement of GM was tested using antibiotic-induced pseudo-germ-free SHRs with fecal microbiota transplantation (FMT) from QYYY-treated donors, administered alone or in combination with QYYY. Gut barrier integrity, systemic inflammation, and vascular function were evaluated by histology, immunofluorescence, transmission electron microscopy, and ELISA.

RESULTS: QYYY significantly lowered SBP and DBP, reversed GM dysbiosis, normalized the Firmicutes/Bacteroidetes ratio, and modulated differential bacteria including Frisingicoccus and Blautia. These microbial shifts correlated with restoration of lysophosphatidylethanolamines (LPEs), inversely associated with BP, revealing a GM-lipid-BP axis. FMT alone was insufficient, whereas the combination of FMT+QYYY produced the strongest antihypertensive effect, restoring intestinal barrier integrity, enhancing ZO-1 expression, and normalizing Ang-II and NO levels. Transcriptomic analyses suggested PPAR and ROS signaling pathways as potential mechanisms mediating the antihypertensive effect of QYYY.

CONCLUSION: QYYY prevents BP elevation in Pre-HTN via synergistic microbiota-dependent and independent mechanisms, offering a comprehensive strategy for early hypertension prevention.},
}

@article {pmid41539089,
year = {2026},
author = {Ou, G and Wu, J and Wang, S and Bi, W and Peng, R and Liu, P and Jiang, Y and Chen, Y and Xu, H and Deng, L and Zhao, H and Chen, X and Xu, L},
title = {Plantago asiatica L. extract alleviates hyperuricemia-associated renal injury by modulating gut microbiota to inhibit NLRP3 inflammasome activation.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {151},
number = {},
pages = {157771},
doi = {10.1016/j.phymed.2026.157771},
pmid = {41539089},
issn = {1618-095X},
abstract = {BACKGROUND: Plantago asiatica L. (PTGA) is a widely used herbal medicine for the treatment of gout and hyperuricemia (HUA). Emerging evidence highlights the pivotal role of the gut microbiota in the pathogenesis of gout and HUA. However, existing research has failed to identify and verify the key mediator strains of PTGA that exert its role in lowering uric acid.

METHODS: A hyperuricemia mouse model was established by intraperitoneal co-administration of hypoxanthine (100 mg/kg) combined with potassium oxonate (50 mg/kg) daily for 10 consecutive days. Serum uric acid (sUA) levels and renal function parameters were assessed using biochemical assay kits. 16S rRNA sequencing combined with non-targeted metabolomics was employed to characterize alterations in gut microbiota and intestinal metabolites. Western blotting was performed to examine the expression of intestinal and renal uric acid transporters, intestinal tight junction proteins, and NLRP3 inflammasome-related proteins. Finally, the mediate role of gut microbiota was verified through fecal microbiota transplantation (FMT) and oral supplementation with Lachnospiraceae bacterium.

RESULTS: In the HUA model, elevated sUA levels (p < 0.01), activation of the renal NLRP3 inflammasome (p < 0.05), renal edema, and impaired renal function were accompanied by gut microbiota dysbiosis. PTGA extract markedly reduced sUA levels by approximately 70 % compared to the model group (p < 0.01), regulated uric acid transporter expression in both the intestine and kidney (p < 0.05), and reshaped gut microbiota composition. Moreover, PTGA enhanced intestinal uric acid catabolism of uric acid in the intestine. FMT and Lachnospiraceae bacterium supplementation experiments further confirmed the regulation of the gut microbiota is a key mediator of PTGA's therapeutic efficacy.

CONCLUSION: This study demonstrates that PTGA exerts hypouricemic and renoprotective effects through modulation of the gut-kidney axis by enriching Lachnospiraceae, promoting intestinal uric acid catabolism, and suppressing renal NLRP3 inflammasome activation. These findings provide novel mechanistic insights into the gut microbiota-dependent therapeutic action of herbal medicine, distinguishing this work from previous studies focused solely on direct organ-level effects.},
}

@article {pmid41538937,
year = {2026},
author = {Yan, H and Wang, C and Wang, H and Liu, J and Zhou, H and Zhong, W and Wang, X and Chen, Y and Ju, Z and Tong, H and Zhang, Y},
title = {Perfluorooctane sulfonates drives colitis via a gut microbiota-bile acid-endoplasmic reticulum stress axis in mice: Mechanistic validation and targeted interventions.},
journal = {Journal of hazardous materials},
volume = {503},
number = {},
pages = {141122},
doi = {10.1016/j.jhazmat.2026.141122},
pmid = {41538937},
issn = {1873-3336},
abstract = {Perfluorooctane sulfonate (PFOS), a widespread environmental pollutant, is implicated in systemic toxicity, yet its role in colitis remains unclear. This study aimed to investigate whether PFOS exacerbates colitis via the gut microbiota-bile acid-endoplasmic reticulum stress (ERS) axis and to explore potential interventions. Following 15-week oral PFOS exposure (0.1 or 0.3 mg/kg/d), mice developed dose-dependent colitis, featuring weight loss, colon shortening, barrier dysfunction, and elevated inflammation. High-dose PFOS disturbed bile acid homeostasis, depleting conjugated species like tauroursodeoxycholic acid (TUDCA) while accumulating deconjugated bile acids such as deoxycholic acid (DCA), thereby activating ERS pathways (PERK/eIF2α, IRE1/XBP1, ATF6). Gut microbiota analysis revealed reduced diversity, a lower Firmicutes/Bacteroidetes ratio, increased bacteria with bile salt hydrolase (BSH) activity (e.g., Lachnospira), and decreased potential bacteria (e.g., Akkermansia). Interventions with TUDCA, a BSH inhibitor, or fecal microbiota transplantation from healthy donors alleviated colitis, restored conjugated bile acids, and suppressed ERS. These findings demonstrate that PFOS triggers colitis via BSH-mediated bile acid deconjugation and ERS activation, highlighting the therapeutic potential of targeting this axis.},
}

@article {pmid41538653,
year = {2026},
author = {Zhang, H and Sun, J and Zheng, X and Yang, H and Xie, A and Ding, Y and Mei, Y and Li, J and Hu, Y and Ren, M and Liu, Y and Liang, Y},
title = {Fermented Lacticaseibacillus Paracasei Cultures Ameliorate Colitis by Modulating Microbiota-Derived Tryptophan Metabolism and Macrophage Polarization.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e13920},
doi = {10.1002/advs.202513920},
pmid = {41538653},
issn = {2198-3844},
support = {HBNYHXGG2024-10//Hubei Provincial Agricultural Science and Technology Research Project/ ; 2024AFB698//Natural Science Foundation of Hubei Province, China/ ; 2022BCE006//Key Research and Development Program of Hubei Province/ ; 2662025SKPY011//Fundamental Research Funds for the Central Universities/ ; },
abstract = {High-density solid-state fermented probiotic products, combining live bacteria with microbial and substrate-derived bioactives, offer a potential solution to address dysregulation of gut microbiota-immune homeostasis associated with inflammatory bowel disease (IBD). However, their synergistic efficacy against IBD remains elusive. Here, we discuss our high-density solid-state fermented Lacticaseibacillus paracasei culture (PYW) and its effects on dextran sulfate sodium (DSS)-induced colitis. Comparison of the effects of PYW, enriched with viable cells and bioactive metabolites-obtained via fermentation with wheat bran-with those of its thermally inactivated postbiotic (SPYW) shows superior efficacy of PYW than SPYW, with a viable bacterial load of ≥ 5 × 10[10] CFU g[-1] being indispensable. PYW effectively restores microbiota structure, restructures the gut tryptophan metabolic network, enriching indole-3-lactic acid (ILA) and indole-3-acetic acid (IAA), which activate the aryl hydrocarbon receptor (AhR) signaling pathway, suppress pro-inflammatory mediators, and strengthen mucosal barriers. Antibiotic depletion abolishes the effects of PYW, while fecal microbiota transplantation from PYW-treated donors and exogenous ILA/IAA supplementation replicate its anti-colitic benefits. These findings suggest that PYW alleviates colitis via microbiota-dependent enrichment of ILA/IAA and subsequent AhR pathway activation, highlighting its potential as a probiotic therapeutic targeting the microbiota-metabolism-immunity regulatory axis in IBD.},
}

@article {pmid41536244,
year = {2026},
author = {Girdhar, K and Dedrick, S and Rhodes, L and Kim, D and Powis, A and Mahon, C and Chapdelaine, H and Obaid, L and McNamara, M and Altindis, E},
title = {Diet, gut microbiome, and type 1 diabetes: from risk to translational opportunity.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2614039},
doi = {10.1080/19490976.2026.2614039},
pmid = {41536244},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Diabetes Mellitus, Type 1/microbiology/therapy/etiology/immunology ; Animals ; *Diet ; Prebiotics/administration & dosage ; Probiotics/administration & dosage ; Fecal Microbiota Transplantation ; },
abstract = {The incidence of type 1 diabetes (T1D) has risen sharply in recent decades, implicating the role of environmental factors in disease pathogenesis. Diet, a primary driver of gut microbiome development and composition, along with other environmental exposures, has emerged as a potential modulator of T1D risk and progression. While nutrients, such as certain vitamins, may exert protective effects, the roles of other dietary factors (e.g., early exposure to dietary antigens) remain unclear. Importantly, diet shapes the gut microbiome, which produces immunomodulatory metabolites, including secondary bile acids, short-chain fatty acids (SCFAs), and others that directly influence immune responses. This review presents evidence on how specific dietary factors, including macronutrients (fats, carbohydrates, proteins, such as gluten and milk proteins), fibers, and breastfeeding, affect the gut microbiome and T1D. We also discuss the effects of microbiome-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, on T1D and their potential as future therapeutic strategies. Although animal studies provide compelling mechanistic insights, the results from human trials remain inconsistent, underscoring the urgent need for longitudinal and interventional studies to establish causality. Understanding the complex interplay between diet, the gut microbiome, and immune homeostasis is essential for developing personalized strategies to prevent and treat T1D and delay-related complications.},
}

Humans
*Gastrointestinal Microbiome
*Diabetes Mellitus, Type 1/microbiology/therapy/etiology/immunology
Animals
*Diet
Prebiotics/administration & dosage
Probiotics/administration & dosage
Fecal Microbiota Transplantation

@article {pmid41535719,
year = {2026},
author = {Almonte, AA and Thomas, S and Iebba, V and Kroemer, G and Derosa, L and Zitvogel, L},
title = {Gut dysbiosis in oncology: a risk factor for immunoresistance.},
journal = {Cell research},
volume = {},
number = {},
pages = {},
pmid = {41535719},
issn = {1748-7838},
support = {INCA_16698//CNIB (INCA)/ ; 955575//EC | Horizon 2020 Framework Programme (EU Framework Programme for Research and Innovation H2020)/ ; },
abstract = {The gut microbiome is recognized as a determinant of response to immune checkpoint inhibitor (ICI) therapies in cancer. However, the clinical translation of microbiome science has been hampered by inconsistent definitions of dysbiosis, inadequate biomarker frameworks, and limited mechanistic understanding. In this review, we synthesize the current state of knowledge on how gut microbial composition and function influence ICI efficacy, highlighting both correlative and causal evidence. We discuss computational approaches based on α-diversity or taxonomic abundance and argue for more functionally and clinically informative models, such as the topological score (TOPOSCORE) and other dysbiosis indices derived from machine learning. Using retrospective analyses of metagenomic datasets from thousands of patients and healthy controls, we examine microbial patterns that distinguish responders from non-responders. We also explore how dysbiosis perturbs immunoregulatory pathways, including bile acid metabolism, gut permeability, and mucosal immunomodulation. Finally, we assess emerging therapeutic strategies aimed at correcting microbiome dysfunction - including dietary modification, bacterial consortia, and fecal microbiota transplantation - and describe how they are being deployed in multiple clinical trials. We conclude with a brief discussion of the ONCOBIOME initiative, which works with international partners to incorporate microbiome science into oncology workflows. By refining our understanding of gut-immune interactions and translating it into action, microbiome-informed oncology may unlock new therapeutic potential for patients previously resistant to immunotherapy.},
}

@article {pmid41535683,
year = {2026},
author = {Chen, S and Yuan, Y and Wang, Y and Peng, Y and Tun, HM and Jiang, Z and Miao, Y and Lee, S and Yin, X and Shen, X and DeLeon, O and Chang, EB and Chan, FKL and Sun, Y and Ng, SC and Su, Q},
title = {Identification of antimicrobial peptides from ancient gut microbiomes.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-68495-0},
pmid = {41535683},
issn = {2041-1723},
support = {2025 Youth Science and Technology Talent Development Program//China Association for Science and Technology (China Association for Science & Technology)/ ; },
abstract = {Fecal coprolites preserve ancient microbiomes and are a potential source of extinct but highly efficacious antimicrobial peptides (AMPs). Here, we develop AMPLiT (AMP Lightweight Identification Tool), an efficient tool deployable to portable hardware for AMP screening in metagenomic datasets. AMPLiT demonstrates AUPRC performances of 0.9486 ± 0.0003 and reasonable overall training time of 3200 ± 53 s. By computationally utilizing AMPLiT, we analyze seven ancient human coprolite metagenomes, identifying 160 AMP candidates. Of 40 representative peptides synthesized, 36 (90%) peptides demonstrate measurable antimicrobial activity at 100 μM or less in vitro. Strikingly, approximately two-thirds of these peptides are sourced from Segatella copri, a dominant ancient gut commensal that is conspicuously underrepresented in modern populations, particularly those with Westernized lifestyles. Representative S. copri-derived AMPs exhibit disruptions against membranes of pathogenic bacteria, coupled with low cytotoxicity and hemolytic risk. In vivo, lead peptides demonstrate potent antibacterial and wound-healing efficacy comparable to traditional antibiotics, especially in combating gram-positive pathogens. Our findings highlight the ancient gut microbiomes as sources of novel AMPs, offering valuable insights into the historical role of S. copri in human health and its decline in contemporary populations.},
}

@article {pmid41535300,
year = {2026},
author = {Wong, OWH and Xu, Z and Chan, SSM and Mo, FYM and Shea, CKS and Su, Q and Wan, MYT and Cheung, CP and Ching, JYL and Tang, W and Tun, HM and Chan, FKL and Ng, SC},
title = {A novel synbiotic (SCM06) for anxiety and sensory hyperresponsiveness in children with autism spectrum disorder: an open-label pilot study.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-025-00902-8},
pmid = {41535300},
issn = {2055-5008},
support = {NCI202346//New Cornerstone Science Foundation/ ; },
abstract = {Anxiety and sensory hyperresponsiveness are common in children with autism spectrum disorder (ASD), but effective treatments are lacking. Targeting the microbiota-gut-brain axis is a promising strategy. This open-label pilot study evaluated SCM06, a novel synbiotic designed to target anxiety and sensory hyperresponsiveness, in 30 children with ASD (mean age 8.2 years, 22 males). We assessed symptom improvement, compliance, and safety, and collected stool samples for metagenomics and metabolomic analysis over 12 weeks. SCM06 was safe and well-tolerated, and significant improvements were observed in anxiety, sensory hyperresponsiveness, and abdominal pain. Following SCM06 treatment, increase in Bifidobacterium pseudocatenulatum was associated with improved functional abdominal pain (p = 0.0011, p_adj = 0.054), while the abundances of valeric acid and butyric acid increased (p_adj = 0.004 and p_adj = 0.072). Key microbial species, Coprococcus comes and Veillonella dispar, were candidate mediators of symptom improvements. Further randomised controlled trials are warranted to confirm its clinical efficacy.},
}

@article {pmid41447757,
year = {2026},
author = {Mandala, A and Undi, RB and Janssen, RC and Sugino, KY and Zhao, W and Nelson, BN and Teague, AM and Patil, NY and Zemsky Berry, K and Varshney, R and Bergman, BC and Rudolph, MC and Joshi, AD and Rajala, RVS and Jonscher, KR and Friedman, JE},
title = {Reprogramming offspring liver health: maternal indole supplementation as a preventive strategy against MASLD.},
journal = {EBioMedicine},
volume = {123},
number = {},
pages = {106098},
pmid = {41447757},
issn = {2352-3964},
mesh = {Animals ; Female ; *Indoles/administration & dosage/pharmacology ; Mice ; Humans ; Pregnancy ; Male ; Gastrointestinal Microbiome/drug effects ; *Liver/metabolism/pathology/drug effects ; *Dietary Supplements ; *Fatty Liver/prevention & control/etiology/metabolism/pathology ; Disease Models, Animal ; Prenatal Exposure Delayed Effects ; Receptors, Aryl Hydrocarbon/metabolism ; Diet, Western/adverse effects ; Maternal Exposure ; Ceramides/metabolism ; Fecal Microbiota Transplantation ; Hepatic Stellate Cells/metabolism/drug effects ; Indoleacetic Acids ; },
abstract = {BACKGROUND: Disruptions in early-life gut microbiota and metabolites associated with maternal Western-style diet (WD) during critical windows of development are linked to metabolic and inflammatory diseases in offspring, including metabolic dysfunction-associated steatotic liver disease (MASLD) in later life. These disturbances can alter microbial metabolite production, such as tryptophan derivatives, which are crucial for immune and metabolic regulation. However, the specific effects of maternal supplementation with tryptophan metabolites on offspring gut microbiome maturation and MASLD risk remain unexplored.

METHODS: WD-fed mouse dams were supplemented with microbial metabolites indole (Ind) or indole-3-acetic acid (I3A) during gestation and lactation; male offspring were weaned to chow diet for 9 weeks, followed by a 4-week WD challenge. Fecal microbiota transfer (FMT) was performed from offspring to naïve recipients, followed by a 4-week WD challenge. Human LX-2 stellate cells were used to study mechanisms for indole and very long-chain (VLC) ceramide effects on TGF-β-induced fibrosis.

FINDINGS: Maternal supplementation with Ind or I3A had long-term protective effects in adult WD-challenged offspring against excess weight gain, steatosis, stellate cell activation, and fibrosis. Perinatal exposure to Ind or I3A activated offspring aryl hydrocarbon receptor (AHR) signalling in gut and liver, which trans-repressed known and new target genes, including ceramidases Asah2 and Acer3, leading to increased VLC ceramides. FMT from offspring with perinatal exposure to Ind protected recipients from WD-induced fibrogenesis and increased beneficial VLC ceramides in recipient livers. In vitro, LX-2 stellate cells cultured with Ind or VLC ceramides demonstrated an anti-fibrotic effect, which was abolished by AHR inhibition.

INTERPRETATION: Maternal indole supplementation, through sustained activation of AHR in offspring gut and liver and an increase in hepatic VLC ceramides, prevents diet-induced MASLD and fibrosis in offspring, offering a novel therapeutic pathway for prevention of paediatric MASLD.

FUNDING: See Acknowledgements.},
}

Animals
Female
*Indoles/administration & dosage/pharmacology
Mice
Humans
Pregnancy
Male
Gastrointestinal Microbiome/drug effects
*Liver/metabolism/pathology/drug effects
*Dietary Supplements
*Fatty Liver/prevention & control/etiology/metabolism/pathology
Disease Models, Animal
Prenatal Exposure Delayed Effects
Receptors, Aryl Hydrocarbon/metabolism
Diet, Western/adverse effects
Maternal Exposure
Ceramides/metabolism
Fecal Microbiota Transplantation
Hepatic Stellate Cells/metabolism/drug effects
Indoleacetic Acids

@article {pmid41392089,
year = {2025},
author = {Wilson, BC and Tweedie-Cullen, RY and Albert, BB and Derraik, JGB and Ho, D and Depczynski, M and Creagh, C and Edwards, T and Gali, S and Thabrew, H and Cutfield, WS and O'Sullivan, JM},
title = {Encapsulated faecal microbiota transfer in young women with anorexia nervosa: an open-label feasibility pilot trial.},
journal = {Nature communications},
volume = {17},
number = {1},
pages = {571},
pmid = {41392089},
issn = {2041-1723},
mesh = {Humans ; *Anorexia Nervosa/therapy/microbiology ; Female ; Pilot Projects ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Gastrointestinal Microbiome/physiology ; Feasibility Studies ; Young Adult ; Adult ; Adolescent ; Treatment Outcome ; Feces/microbiology ; },
abstract = {Perturbations of the gut microbiome have been associated with anorexia nervosa (AN) suggesting microbiome-modulation treatments, like faecal microbiota transfer (FMT), may offer therapeutic benefits. This open-label feasibility pilot trial evaluated the tolerability and microbiological impact of encapsulated, multi-donor FMT in 18 young women with AN (Registration: ACTRN12621001504808). Participants completed clinical and microbiome assessments at enrolment (3 weeks pre-treatment), baseline, and 3, 6, and 12 weeks post-treatment. Fifteen participants completed FMT, and 11 completed the final follow-up. The primary outcome was the change in gut microbiome composition from baseline to 3 weeks compared with natural variation between enrolment and baseline. FMT produced a significantly greater shift post-treatment (mean ± SD Bray-Curtis dissimilarity 0.36 ± 0.11; p = 0.0007), with participants gaining 38 ± 16 new species. Donor-derived strains comprised 41 ± 12% of the microbiome at 3 weeks, with engraftment persisting at 6 and 12 weeks. FMT was generally well tolerated; adverse events were mostly mild to moderate and overlapped with typical AN symptomatology. Monitoring of clinical outcomes supported the safety profile and suggested potential improvements in anxiety and metabolic parameters; however, the small sample and absence of a control arm preclude safety and efficacy inference. Overall, these findings warrant further investigation through randomised controlled trials in AN.},
}

Humans
*Anorexia Nervosa/therapy/microbiology
Female
Pilot Projects
*Fecal Microbiota Transplantation/methods/adverse effects
*Gastrointestinal Microbiome/physiology
Feasibility Studies
Young Adult
Adult
Adolescent
Treatment Outcome
Feces/microbiology

@article {pmid41535289,
year = {2026},
author = {Panah, FM and Støving, RK and Sjögren, M and Micali, N and Maschek, S and Reis, KD and Mirsepasi-Lauridsen, HC and Petersen, AM and Nielsen, DS and Helms, M and Rasmussen, MA and Barfod, KK},
title = {Impact of a single fecal microbiome transplantation in adult women with anorexia nervosa: an open-label feasibility pilot trial.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-68455-8},
pmid = {41535289},
issn = {2041-1723},
support = {R370-2021-863//Lundbeckfonden (Lundbeck Foundation)/ ; },
abstract = {Anorexia nervosa (AN) is a severe mental disorder characterized by restrictive eating and disturbance in the way one's body weight or shape is experienced, often accompanied by depression and anxiety. Current evidence-based treatments for AN have limited efficacy, with less than half of the patients achieving full recovery in long-term follow-up studies. Recent findings have identified gut microbiota (GM) dysbiosis as a potential contributor to AN pathology through the gut-brain axis. This open-label, non-randomized, feasibility trial (Clinicaltrials.gov Identifier: NCT05834010) evaluated the feasibility of utilizing fecal microbiota transplantation (FMT) to modify the GM and GM-associated signaling in females with AN and to examine biological effects following a single FMT procedure. Adult female participants diagnosed with AN were recruited. FMT was administered either orally via capsules or as rectal enema. Stool and blood samples were collected pre- and one week post-FMT to assess GM composition, hormonal changes, and biomarkers. Primary endpoints: Feasibility of FMT in individuals with AN and preferred route of FMT. Secondary endpoints: A single FMT treatment can alter GM composition in individuals with AN short term and relevant gut brain signaling in serum. 18/22 participants (81%) completed FMT and sampling and 19/22 participants chose oral capsules, with no serious adverse effects reported. GM analysis showed significant shifts toward donor composition 1-week post-FMT, with improved stool consistency. No significant changes were observed in psychopathology measures or appetite-related biomarkers. Oral FMT is a feasible intervention for adult women with AN, leading to changes in GM profile. Future studies should focus on placebo-controlled trials to assess the efficacy of repeated oral treatments and explore long-term effects on GM, appetite, body weight, sex hormones, disorder-specific symptoms, and overall well-being.},
}

@article {pmid41532069,
year = {2026},
author = {Mu, S and Chang, M and Shen, Y and Wu, X and Han, Y and Xiang, H and Luo, Y and Chen, Y and Zheng, H and Song, Z and Tong, C},
title = {Gut microbiota metabolite butyric acid alleviated Klebsiella Pneumoniae induced lung injury by regulating CX3CR1[+]NK via PI3K/AKT pathway.},
journal = {Burns & trauma},
volume = {14},
number = {},
pages = {tkaf069},
doi = {10.1093/burnst/tkaf069},
pmid = {41532069},
issn = {2321-3868},
abstract = {BACKGROUND: The expression of CX3CR1 is regulated by the gut microbiota and is correlated with the prognosis of sepsis in patients. However, the underlying mechanism has remained uncertain. This study aims to explore the role of gut microbiota components in regulating CX3CR1 expression and its impact on pneumonia-induced lung injury during sepsis.

METHODS: Mice were fed a mixture of antibiotics to establish a pseudogerm-free mouse model and then infected with Klebsiella pneumoniae. Fecal microbiota transplantation (FMT) was performed on microbiota-depleted mice, and 16S rRNA gene sequencing and targeted metabolomics were used to identify the key metabolites. Flow cytometry was employed to analyze the phenotypes of natural killer (NK) cells. Butyric acid was added as a supplement for rescue. Next, NK92 cells were pretreated with butyric acid to explore the potential signaling pathways involved.

RESULTS: In the animal study, we revealed that the expression of CX3CR1 on NK cells depended on the intestinal microbiota and its metabolites, which were related to the survival rates of gut microbiota-depleted mice after K. pneumoniae infection. FMT increased the percentage of CX3CR1[+] NK cells in the lungs of these mice, restored the disordered microbiota and metabolites, and alleviated the lung injury induced by infection. Among the metabolites, butyric acid was identified as the key metabolite and was shown to increase the proportion of CX3CR1[+] NK cells and interferon (IFN)-γ secretion, reduce bacterial loads, increase lung tissue damage, and increase survival rates. In vitro, butyric acid activated the PI3K/AKT pathway in NK92 cells, promoted CX3CR1 expression, and enhanced NK cell activity and migration ability.

CONCLUSIONS: We concluded that butyric acid alleviated K. pneumoniae-induced lung injury by regulating CX3CR1[+] NK cells via the PI3K/AKT pathway.},
}

@article {pmid41530748,
year = {2026},
author = {Zhang, Y and Sun, C and Wang, Y and Zhang, H and Fan, Y and Zhao, H and Li, P},
title = {Targeting gut-liver-kidney axis: microbiota-derived metabolites and therapeutic implications.},
journal = {Cell communication and signaling : CCS},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12964-025-02625-x},
pmid = {41530748},
issn = {1478-811X},
support = {82174296//National Natural Science Foundation of China/ ; },
abstract = {The gut-liver-kidney axis has emerged as a central regulatory network orchestrating metabolic, immune, and inflammatory homeostasis across organ systems. At its core lies the dynamic interplay between gut microbiota and host metabolism. Dysbiosis and impaired intestinal barrier integrity facilitate the systemic translocation of microbial metabolites-such as short-chain fatty acids (SCFAs), bile acids (BAs), trimethylamine-N-oxide (TMAO), and tryptophan derivatives-which profoundly influence hepatic lipid metabolism, renal immune responses, and overall metabolic balance. This review examines the molecular mechanisms through which gut-derived metabolites contribute to liver and kidney pathology, emphasizing inter-organ signaling and the pathological cascade of the "leaky gut-hepatic injury-renal dysfunction" loop. We critically evaluate emerging therapeutic strategies targeting this axis, including probiotic supplementation, fecal microbiota transplantation (FMT), dietary modulation (low-protein, high-fiber regimens), and pharmacological detoxification (e.g., AST‑120, molecular adsorbent recirculating systems [MARS]). Finally, we propose a conceptual "diet-microbiota-drug" triad to guide precision interventions, and discuss current challenges such as interindividual variability, the lack of standardized assessment tools, and the need for integrative multi‑omics and clinical validation. A deeper mechanistic understanding of gut-organ crosstalk may pave the way for innovative therapies to restore systemic metabolic homeostasis.},
}

@article {pmid41530607,
year = {2026},
author = {Miller, CB and Bader, GA and Kay, CL},
title = {Fecal Microbiota Transplantation in 2025: Two Steps Forward, One Step Back.},
journal = {Current gastroenterology reports},
volume = {28},
number = {1},
pages = {5},
pmid = {41530607},
issn = {1534-312X},
mesh = {*Fecal Microbiota Transplantation/trends/methods ; Humans ; *Irritable Bowel Syndrome/therapy ; *Clostridium Infections/therapy ; *Inflammatory Bowel Diseases/therapy ; },
abstract = {PURPOSE OF REVIEW: This review summarizes the history and current landscape of fecal microbiota transplantation (FMT), with an emphasis on use of the therapy for Clostridioides difficile infection (CDI), inflammatory bowel disease (IBD), and irritable bowel syndrome (IBS). We clarify indications, evidence, and current recommendations for FMT-highlighting major advances and minor setbacks that have led to the state of FMT in 2025.

RECENT FINDINGS: After decades of steady progress, the U.S. Food and Drug Administration (FDA) approved the first FMT-based therapies: fecal microbiota, live-jslm and fecal microbiota spores, live-brpk-in 2022 and 2023, respectively. The 2024 American Gastroenterological Association (AGA) Practice Guideline on Fecal Microbiota-Based Therapies for Select Gastrointestinal Diseases made specific recommendations for conventional FMT and these FDA-approved therapies for multiple CDI presentations, as well as for IBD and IBS. Conventional FMT remains an option for CDI; however, OpenBiome's halt of shipped, frozen FMT preparations on December 31, 2024, has made access more challenging in 2025. Although first reported almost seventy years ago, extensive efforts over the last two decades have placed FMT in routine algorithms for many patients with CDI. While understanding of the intestinal microbiome's role in other gastrointestinal conditions is expanding, and FMT may modulate these pathways, additional evidence is needed before FMT becomes routine outside CDI.},
}

*Fecal Microbiota Transplantation/trends/methods
Humans
*Irritable Bowel Syndrome/therapy
*Clostridium Infections/therapy
*Inflammatory Bowel Diseases/therapy

@article {pmid41530574,
year = {2026},
author = {Deng, YH and Liu, Q and Luo, XQ},
title = {The gut-kidney axis in pediatric acute kidney injury: a review of pathophysiological mechanisms and therapeutic frontiers.},
journal = {Pediatric nephrology (Berlin, Germany)},
volume = {},
number = {},
pages = {},
pmid = {41530574},
issn = {1432-198X},
support = {2024JJ6595//Natural Science Foundation of Hunan Province/ ; },
abstract = {Acute kidney injury (AKI) is a frequent and severe condition in hospitalized children, leading to significant morbidity, mortality, and long-term risk of chronic kidney disease. This review explores the gut-kidney axis, a concept describing the bidirectional relationship between the gut microbiome and kidney function, as a critical driver of pediatric AKI. In critically ill children, interventions such as broad-spectrum antibiotics and necessary nutritional support strategies (e.g., parenteral nutrition or fasting) can cause profound gut microbial imbalance (dysbiosis). This dysbiosis initiates a deleterious feedback loop, exacerbating kidney injury. Key mechanisms include the disruption of the intestinal barrier (leaky gut), which allows bacterial endotoxins to enter the bloodstream, triggering renal inflammation via Toll-like receptor 4 signaling. Concurrently, the dysbiotic gut increases production of directly nephrotoxic gut-derived uremic toxins, such as indoxyl sulfate and p-cresyl sulfate, while failing to produce protective anti-inflammatory metabolites like short-chain fatty acids. While therapies targeting the microbiome, such as probiotics, prebiotics, and fecal microbiota transplantation, are theoretically promising, their clinical use in pediatric AKI is unsupported by evidence and carries substantial risks, particularly iatrogenic infection. A significant knowledge gap exists due to a relative lack of pediatric-specific clinical research. The conclusion emphasizes an urgent need for longitudinal, multi-omics studies in children to understand this axis, identify functional biomarkers, and develop safe, targeted therapies to improve outcomes.},
}

@article {pmid41529466,
year = {2026},
author = {Wang, Z and Yu, Y and Shao, W and Zhao, Y and Li, Z and Han, J and Wen, J and Meng, Y and Lin, Y and Wang, S},
title = {Puerarin ameliorates alcoholic liver disease by regulating intestinal flora and MAPK/Nrf2 signalling pathways.},
journal = {Ecotoxicology and environmental safety},
volume = {309},
number = {},
pages = {119699},
doi = {10.1016/j.ecoenv.2026.119699},
pmid = {41529466},
issn = {1090-2414},
abstract = {Puerarin is a natural flavonoid glycoside extracted from the traditional Chinese medicine Puerariae Lobatae Radix or Pueraria lobata (Willd), known for its hepatoprotective properties. While prior studies indicate that PR can mitigate ALD, the underlying mechanisms by which PR exerts its anti-ALD effects via intestinal flora remain poorly understood. This study aimed to investigate the metabolic differences of PR in normal and ALD model rats were analyzed using UHPLC-HRMS. Further validation of PR metabolic products in vivo through in vitro fecal fermentation. Additionally, the relationship between the anti-ALD properties of PR and intestinal flora was explored using 16S rRNA sequencing technology, with confirmation obtained from fecal microbiota transplantation (FMT) experiments and functional strain experiments. Finally, through non-targeted metabolomics and liver transcriptomics combined with in vitro cell pharmacological studies, the mechanism of action of PR and its in vitro fermentation metabolites against ALD was explored. In the PR metabolic test, 20 metabolites were identified in the serum, urine, and feces of normal and ALD model rats, primarily associated with reactions including deglycosylation, hydrogenation, aldehyde esterification, hydroxylation, and methylation. 6 metabolites were verified in vitro transformation system. Subsequently, we used FMT experiments and 16S rRNA sequencing to find that intestinal flora imbalance can lead to liver disease and PR can improve liver disease by regulating intestinal flora. Based on multi-omics analysis and in vitro pharmacological activity analysis, PR and its in vitro fermented metabolites inhibit MAPK and Nrf2 pathways, further reducing inflammation and oxidative stress. The results of this study show that PR can improve ALD, with its mechanism of action potentially involving regulation of the intestinal flora, suppression of inflammatory responses, and inhibition of oxidative stress.},
}

@article {pmid41527151,
year = {2026},
author = {Li, JY and Huang, HB and Shi, CW and Pan, TX and Li, MH and Wang, N and Shan, JJ and Jiang, YL and Yang, WT and Cao, X and Wang, JZ and Guan, JY and Yu, SY and Wang, CF and Yang, GL},
title = {Increased caecal Intestinimonas abundance inhibits E. tenella gametogenesis via EtGFAT regulation and alleviates infection through immunity.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-025-02302-8},
pmid = {41527151},
issn = {2049-2618},
support = {32072888, U21A20261, 32202819//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Chicken coccidiosis caused by Eimeria tenella (E. tenella) poses a major threat to global poultry production, with its tropism for the caecal microenvironment and dynamic interactions with the resident microbiota remaining incompletely understood. The caecal microbiota plays a critical role in host‒parasite interplay, yet the mechanisms through which microbial homeostasis influences E. tenella development and host resistance remain elusive. This study aimed to elucidate the causal relationship between caecal dysbiosis and E. tenella pathogenesis, with a focus on identifying microbiota-derived regulators of parasite development and host immunity.

RESULTS: Antibiotic-induced caecal dysbiosis (ABX) significantly impaired E. tenella macrogametogenesis, demonstrating microbiota-dependent regulation of parasitic development. Faecal microbiota transplantation (FMT) validated this causal link, revealing that microbial reconstitution restored parasite maturation. Notably, Intestinimonas spp. were identified as key inhibitors of E. tenella development through transcriptional regulation of the EtGFAT gene (Eimeria tenella glucosamine: fructose-6-phosphate aminotransferase), a critical mediator of macrogamete formation. Furthermore, the transplantation of Intestinimonas butyriciproducens (I. butyriciproducens) attenuated clinical manifestations of infection while increasing IFN-γ secretion from CD8[+] T lymphocytes, thereby enhancing host resistance to E. tenella.

CONCLUSIONS: This study revealed that caecal microbiota homeostasis is indispensable for E. tenella developmental progression and highlights Intestinimonas as a pivotal microbial regulator of parasite biology. The dual role of I. butyriciproducens in suppressing parasitic virulence and potentiating adaptive immune responses underscores the therapeutic potential of microbiota-targeted strategies. These findings provide a foundation for the development of novel anticoccidial interventions through targeted manipulation of caecal microbial communities. Video Abstract.},
}

@article {pmid41461024,
year = {2026},
author = {Ng, DZW and Koh, M and Low, A and Liu, L and Jumat, NHB and Zhang, Z and Koh, XQ and Zhu, M and Muthiah, M and Dan, YY and Lee, JWJ and Chan, ECY},
title = {Robust Workflow for Multiclass Host-Gut Microbial Cometabolite Quantitation in Human Stool via 3-Nitrophenylhydrazine Derivatization and LC-MS/MS: A Validated Analytical Platform for Translational Studies.},
journal = {Analytical chemistry},
volume = {98},
number = {1},
pages = {555-570},
doi = {10.1021/acs.analchem.5c05360},
pmid = {41461024},
issn = {1520-6882},
mesh = {Humans ; Tandem Mass Spectrometry/methods ; *Gastrointestinal Microbiome ; *Feces/chemistry/microbiology ; Chromatography, Liquid ; *Phenylhydrazines/chemistry ; *Fatty Acids, Volatile/analysis/metabolism ; *Bile Acids and Salts/analysis/metabolism ; Workflow ; Amino Acids, Branched-Chain/analysis/metabolism ; Tryptophan/analysis/metabolism ; Liquid Chromatography-Mass Spectrometry ; },
abstract = {Host-gut microbial co-metabolites, including short-chain fatty acids (SCFA), bile acids (BA), tryptophan metabolites, and branched-chain amino acids (BCAA), have key immune-metabolic functions affecting human health. Dysbiosis-induced alterations in their levels are implicated in the pathogenesis of diseases such as metabolic dysfunction-associated steatotic liver disease (MASLD). However, simultaneous quantitation of these chemically diverse analytes in stool remains analytically challenging due to their diverse physicochemical properties and wide concentration ranges. Here, we developed and rigorously validated a derivatization and targeted liquid chromatography tandem mass spectrometry workflow for the simultaneous quantitation of host-gut microbial cometabolites in human stool. A 3-nitrophenylhydrazine derivatization protocol was optimized by systematically adjusting reagent concentrations and introducing postreaction quenching to suppress in-line acetic acid derivatization. Chromatographic separation was enhanced by using a novel dual-additive mobile-phase strategy (formic acid and ammonium acetate in aqueous and organic phase, respectively) coupled to a mixed-mode C18-anion-exchange stationary phase, enabling improved resolution and sensitivity across chemically diverse metabolite classes. Our optimized analytical method achieved accurate, sensitive, and efficient quantitation of 38 metabolites (15 SCFA, 16 BA, 4 tryptophan metabolites, 3 BCAA) within 23 min, demonstrating excellent linearity (r[2] > 0.99) and precision (CV < 15%), with short- (autosampler, 4 °C) and long-term (freezer, -20 °C) stability. Comparative analysis of healthy controls and MASLD stools revealed distinct metabolic signatures, including reduced SCFA and C6-oxidized BA, and elevated conjugated and secondary BA derivatives in MASLD. Our study establishes an analytically rigorous platform for multiclass host-gut cometabolite quantitation in stool, with demonstrated utility for translational research into gut-liver axis disorders.},
}

Humans
Tandem Mass Spectrometry/methods
*Gastrointestinal Microbiome
*Feces/chemistry/microbiology
Chromatography, Liquid
*Phenylhydrazines/chemistry
*Fatty Acids, Volatile/analysis/metabolism
*Bile Acids and Salts/analysis/metabolism
Workflow
Amino Acids, Branched-Chain/analysis/metabolism
Tryptophan/analysis/metabolism
Liquid Chromatography-Mass Spectrometry

@article {pmid41527019,
year = {2026},
author = {Zhong, J and Zhu, B and Zou, Z and Li, Y and Feng, Y and Wu, K and Hou, X},
title = {Gut microbiota mediates the beneficial effects of exercise on autism-like behaviors.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-025-04632-x},
pmid = {41527019},
issn = {1471-2180},
support = {no. 2025A04J4356//the Guangzhou Municipal Science and Technology Bureau, Basic Research Program/ ; no. 2023B0303020001//the Key-Area Research and Development Program of Guangdong Province/ ; no. 2021ZDJS021//the Provincial Significant Scientific Research Projects for General Universities in Guangdong Province/ ; },
abstract = {BACKGROUND: The gut-brain axis plays a critical role in autism spectrum disorder (ASD), but the mechanisms through which exercise modulates gut microbiota, short-chain fatty acids (SCFAs), and central neurotransmitters to ameliorate ASD-like behaviors remain unclear. This study aimed to investigate the effects of exercise on ASD-like behaviors, gut microbiota, and metabolism in a valproic acid (VPA)-induced ASD rat model and to validate these findings via fecal microbiota transplantation (FMT).

METHODS: ASD rat models were established through prenatal exposure to VPA and divided into four groups: exercise (E_ASD), non-exercise (ASD), FMT, and sham FMT (sFMT). The E_ASD group underwent 6 weeks of voluntary wheel running, while the FMT group received fecal microbiota from the E_ASD group for 4 weeks. Behavioral assessments were conducted to evaluate cognitive and social functions. Fecal microbiota composition was analyzed via 16S rRNA sequencing, while SCFAs and neurotransmitters were measured using gas and liquid chromatography-mass spectrometry.

RESULTS: Six weeks of voluntary exercise significantly alleviated ASD-like behaviors, particularly improving social interactions. Exercise also altered gut microbiota composition, increasing Limosilactobacillus and Lactobacillus while decreasing Allobaculum. Additionally, SCFAs and neurotransmitter levels in the prefrontal cortex were modulated. Notably, FMT from the exercise group replicated these behavioral and metabolic improvements in ASD rats. Exercise improves ASD-like behaviors by modulating gut microbiota, SCFAs, and neurotransmitter levels, and FMT offers further validation of these effects.

CONCLUSION: These findings highlight exercise and FMT as promising strategies for alleviating ASD-related symptoms through gut-brain axis modulation.},
}

@article {pmid41526816,
year = {2026},
author = {Yang, Y and Wang, Y and Li, J and Gao, Y and Wu, Z and Tan, X and Feng, S and Cheng, W and Zhang, H and Gan, Q and Wei, H and Li, Q},
title = {Fecal microbiota transplantation from healthy piglets ameliorates intestinal inflammation in mice by modulating recipient metabolism.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-025-04590-4},
pmid = {41526816},
issn = {1471-2180},
support = {2025J01556//Fujian Provincial Natural Science Foundation of China/ ; },
}

@article {pmid41525948,
year = {2026},
author = {Valia, D and Karama, I and Ingelbeen, B and Garba, Z and Kleef, EV and Lompo, P and Tiendrebeogo, EW and Kaboré, B and Kiemdé, F and Yougbare, S and Tiendrebeogo, AL and Van Puyvelde, S and Prizzon, A and Vandenbroucke, AT and Argudín, MA and Kabamba, BM and Jacobs, J and Tinto, H and van der Sande, MAB and Robert, A and Rodriguez-Villalobos, H},
title = {Faecal colonisation with extended-spectrum β-lactamase-producing Escherichia coli and Klebsiella pneumoniae in rural Burkina Faso.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2026.01.001},
pmid = {41525948},
issn = {1469-0691},
abstract = {OBJECTIVES: The burden of extended-spectrum β-lactamase-producing Enterobacterales (ESBL-E) is rising globally and often linked to community-acquisition in low-resource settings. In sub-Saharan Africa (sSA), AMR occurrence in rural areas remains under-studied despite anticipated higher risks. We investigated the epidemiology and genetic characteristics of ESBL-E in rural Burkina Faso.

METHODS: In a community-based cross-sectional survey (May 2021-May 2022), participants were randomly selected in two health catchment areas and through face-to-face interviews, field workers collected data on hygiene, animal presence, household characteristics, and healthcare use. Stool samples were also collected for ESBL-E screening. Prevalence of ESBL-producing E. coli (ESBL-EC) and K. pneumoniae (ESBL-KP) was estimated, and associated factors assessed. Based on resistance profiles and PCR screening, selected isolates underwent whole-genome sequencing.

RESULTS: Among 1,482 participants, ESBL-E prevalence was 61.3% (58.8-63.7%): ESBL-EC 53.0% (50.5-55.5%) and ESBL-KP 22.3% (20.3-24.5%). Colonisation was more common in the rainy than dry season (70.2% vs 53.6%, p<0.001) and among individuals not washing hands with soap before meals (62.5% vs 49.0%, p<0.001). Ciprofloxacin-resistance exceeded 65% in both species. The predominant ESBL-gene was blaCTX-M-15 (47.3% in ESBL-EC, 19.9% in ESBL-KP), with one ESBL-EC isolate carrying blaNDM-5. IncF plasmids predominated, and plasmid-mediated quinolone-resistance genes (qnr, aac(6')-ib-cr, oqxAB) were frequently co-detected with ESBL genes.

CONCLUSION: ESBL-E prevalence was high and associated with poor hygiene and seasonal variation. Higher rainy season prevalence was not explained by reported antibiotic use and may reflect increased environmental exposure risks, which requires further exploration. Improving hygiene-standards and establishing community-level AMR surveillance can provide effective steps forward in mitigating AMR burden in rural sSA.},
}

@article {pmid41525005,
year = {2026},
author = {Mir, PA and Kumar, N and Bhutia, GT and Chaudhary, P and Kaur, G and Gupta, SK},
title = {The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.},
journal = {GeroScience},
volume = {},
number = {},
pages = {},
pmid = {41525005},
issn = {2509-2723},
abstract = {Alzheimer's disease (AD), the most common cause of dementia in the aging population, is marked by amyloid-beta (Aβ) plaques, tau tangles, and progressive neuronal degeneration, placing heavy clinical and socioeconomic burdens on healthcare worldwide. Aging remains the strongest risk factor, with chronic low-grade inflammation, oxidative stress, mitochondrial dysfunction, and impaired proteostasis creating a vulnerable brain environment that accelerates AD onset and progression. Recent evidence highlights the gut-glia-immune axis as a critical pathway linking age-related microbiome changes to glial dysfunction. Microbial metabolites, such as short-chain fatty acids and tryptophan derivatives, regulate microglial maturation, astrocytic activity, and neuroimmune signaling. However, age-associated dysbiosis disrupts glial homeostasis, amplifies neuroinflammation, and impairs amyloid clearance, thereby worsening neurodegeneration. Preclinical models including germ-free mice and fecal microbiota transplantation along with clinical studies of elderly AD patients, provide compelling evidence of microbiome-driven modulation of disease. From a therapeutic perspective, microbiome-targeted interventions including probiotics, prebiotics, synbiotics, and microbiota-directed small molecules offer promising strategies to restore glial balance, reduce inflammation, and protect cognitive function. This review highlights the therapeutic potential of probiotics, synbiotics, and fecal microbiota transplantation for mitigating neuroinflammation and cognitive decline in Alzheimer's disease. However, given the multifactorial nature of neurodegenerative disorders, these strategies are unlikely to be universally effective and must be tailored to individual patient profiles.},
}

@article {pmid41523758,
year = {2025},
author = {Khan, AS and Kamthan, M and Ali, A},
title = {Understanding the intricate interactions between microbiota and host.},
journal = {World journal of experimental medicine},
volume = {15},
number = {3},
pages = {101277},
pmid = {41523758},
issn = {2220-315X},
abstract = {The review examines the intricate relationship between the microbiota and its host, highlighting how these microbial communities influence various physiological functions beyond simple coexistence. The microbiota plays a crucial role in regulating the immune system, metabolism, and overall health. We explore the diverse microbial populations inhabiting different body regions and their essential contributions to maintaining balance within the host. Recent research has uncovered molecular mechanisms that govern microbiota-host interactions, offering new insights into how these microbes support health and, conversely, how imbalances known as dysbiosis can increase susceptibility to diseases. While much attention has been given to the gut microbiota, this review also explores the influence of microbes in other parts of the body, including their effects on various organs and tissues. Additionally, we discuss emerging evidence on the gut-brain axis, illustrating how the microbiota can impact brain function and behavior. Understanding this connection could open new possibilities for treating neurological and psychological disorders. Finally, we evaluate microbiota-based therapies such as probiotics and fecal microbiota transplantation, emphasizing the importance of personalized approaches. By integrating findings from multiple disciplines, this review provides a comprehensive perspective on the microbiota's vital role in human health and its potential as a therapeutic target.},
}

@article {pmid41523687,
year = {2026},
author = {Zhang, S and Cheng, X and Chen, L and Wang, Y},
title = {2'-Fucosyllactose (2'-FL) alleviates choline-deficient fat diet-induced nonalcoholic steatohepatitis (NASH) by remodeling intestinal flora.},
journal = {Food science and biotechnology},
volume = {35},
number = {1},
pages = {203-213},
pmid = {41523687},
issn = {2092-6456},
abstract = {UNLABELLED: Non-alcoholic steatohepatitis (NASH) is a progressive liver disease lacking effective treatment. This study investigated 2'-Fucosyllactose (2'-FL) for its therapeutic potential. In vitro, 2'-FL reduced lipid accumulation, oxidative stress, and inflammation in Hepa1-6 cells. In a NASH mouse model, 2'-FL alleviated key disease features: hepatic steatosis, inflammation, and oxidative stress. Furthermore, 2'-FL intervention reversed NASH-associated gut microbiota dysbiosis, specifically by increasing Bacteroidota and decreasing Firmicutes at the phylum level. Fecal microbiota transplantation (FMT) validated the role of gut microbiota in these effects. The findings indicate that 2'-FL ameliorates NASH by remodeling the gut microbiota, thereby reducing endotoxemia and improving lipid metabolism. This suggests 2'-FL as a promising dietary intervention for metabolic liver diseases.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s10068-025-02034-3.},
}

@article {pmid41522487,
year = {2026},
author = {Al Qassab, M and Chaarani, N and Hamou, A and Harb, R and Jradi, A and Zeineddine, M and Ghadieh, HE and Khattar, ZA and Azar, S and Kanaan, A and Harb, F},
title = {The Gut Microbiota-Insulin Resistance Axis: Mechanisms, Clinical Implications, and Therapeutic Potential.},
journal = {FASEB bioAdvances},
volume = {8},
number = {1},
pages = {e70080},
pmid = {41522487},
issn = {2573-9832},
abstract = {Emerging evidence highlights the pivotal role of the gut microbiota (GM) in regulating host metabolism and contributing to the development of insulin resistance (IR). Gut dysbiosis alters the production of critical metabolites, including short-chain fatty acids (SCFAs), bile acids, indole derivatives, and trimethylamine N-oxide (TMAO), which influence intestinal barrier integrity, inflammatory pathways, and glucose homeostasis. Recent clinical and translational studies indicate that SCFAs can improve fasting insulin and HOMA-IR, although the magnitude of benefit varies substantially across individuals, highlighting ongoing controversy surrounding their metabolic effects. Altered microbial regulation of bile-acid metabolism has also been implicated in impaired lipid and glucose signaling, reinforcing the relevance of FXR- and TGR5-mediated pathways in IR. Elevated TMAO levels have further been associated with adverse metabolic outcomes, though debate persists regarding its causal role versus its function as a diet-dependent biomarker. Microbiota-targeted strategies, including dietary fiber, probiotics, and fecal microbiota transplantation (FMT), show potential to modulate these metabolic pathways, yet clinical results remain inconsistent. This narrative review synthesizes recent mechanistic discoveries and clinical findings on microbiota-derived metabolites in IR, highlights key controversies, and outlines future priorities for translating microbiome science into effective and personalized interventions for metabolic disease prevention and management.},
}

@article {pmid41522358,
year = {2026},
author = {Jin, Y and Zhang, SJ and Zhuang, S and Li, P and Miao, H and Zhao, YY},
title = {Microbiota-gut-kidney axis in health and renal disease.},
journal = {International journal of biological sciences},
volume = {22},
number = {2},
pages = {750-770},
pmid = {41522358},
issn = {1449-2288},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Kidney/metabolism ; Animals ; *Renal Insufficiency, Chronic/microbiology/metabolism ; *Kidney Diseases/microbiology/metabolism ; Dysbiosis ; Acute Kidney Injury/microbiology/metabolism ; },
abstract = {Gut microbiota plays a central role in programming host metabolic function and immune modulation in both health and disease. Microbial dysbiosis leads to an increase in opportunistic pathogens and a reduction in beneficial bacteria, which collectively result in the excessive production of detrimental metabolites, particularly uremic toxins such as indoxyl sulfate and trimethylamine-N-oxide, while concurrently decreasing beneficial metabolites, such as short-chain fatty acids and tryptophan catabolites, including indole-3-aldehyde. The accumulation of harmful metabolites and depletion of protective metabolites contribute to fibrosis progression through various mediators, including the renin-angiotensin system, reactive oxygen species, Toll-like receptor 4, aryl hydrocarbon receptor, inhibitor of kappa B/nuclear factor kappa B, and Kelch-like ECH-associated protein 1/nuclear factor erythroid 2-related factor 2 pathways. This review highlights the pathogenic link between gut microbiota and kidney damage via the gut-kidney axis, encompassing acute kidney injury (AKI) and chronic kidney disease (CKD). Innovative therapeutic strategies, including microbial therapeutics (such as probiotics, prebiotics, and synbiotics), natural products (such as neohesperidin, isoquercitrin, and polysaccharides), and fecal microbiota transplantation, have been proposed to restore microbial balance and improve kidney function. Targeted modulation of the gut microbiota offers a promising strategy for developing novel treatments in AKI, CKD, and the transition from AKI-to-CKD. This approach has the potential to prevent or mitigate these conditions and their complications.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Kidney/metabolism
Animals
*Renal Insufficiency, Chronic/microbiology/metabolism
*Kidney Diseases/microbiology/metabolism
Dysbiosis
Acute Kidney Injury/microbiology/metabolism

@article {pmid41521300,
year = {2026},
author = {Deng, W and Chen, D and Wei, Y and Chen, W and Chen, K and Zhong, H and He, X},
title = {Washed microbiota transplantation relieves atopic dermatitis via gut-skin microbiome rebalancing.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04717-1},
pmid = {41521300},
issn = {1471-2180},
support = {2022B1111070006//Key-Area Research and Development Program of Guangdong Province/ ; 82300440//National Natural Science Foundation of China Youth Program/ ; },
abstract = {BACKGROUND: Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease in which dysbiosis of gut and skin microbiota contributes to pathogenesis and severity. Washed microbiota transplantation (WMT)-an improved form of fecal microbiota transplantation with enhanced safety and microbiota quality control-has shown efficacy in a single reported adolescent case. However, clinical data on WMT in AD and its effects on the skin and gut microbiota remain limited.

METHODS: Twenty-three patients with moderate-to-severe AD received at least two courses of WMT between January 2022 and December 2023. Disease activity was evaluated using the SCORing Atopic Dermatitis (SCORAD) index, the Eczema Area and Severity Index (EASI), the Numeric Rating Scale (NRS) for itch, and the Dermatology Life Quality Index (DLQI). Peripheral blood counts, cytokine profiles, lymphocyte subsets, and gut and skin microbiota were assessed before and after treatment.

RESULTS: WMT was well tolerated (58 sessions; 5.2% mild adverse events) and significantly improved SCORAD, EASI, DLQI, and NRS scores, with greater EASI reductions in adults than in children. Absolute basophil counts decreased significantly after treatment, whereas other hematologic and cytokine parameters remained stable. Gut microbiota showed an increased Gut Microbiome Health Index, a decreased Microbial Dysbiosis Index, and enrichment of short-chain fatty acid-producing taxa, including the Eubacterium coprostanoligenes group, Lachnospiraceae, and Coprococcus. Skin microbiota shifted from Staphylococcus dominance to higher abundances of Acinetobacter, Perlucidibaca, and other potentially protective genera, inversely correlating with disease severity and systemic inflammation.

CONCLUSIONS: WMT appears safe and effective in alleviating clinical manifestations of AD while reshaping both gut and skin microbiota. These parallel microbial shifts support the gut-skin axis as a therapeutic target and highlight WMT as a promising microbiota-centered intervention for immune-mediated skin diseases.},
}

@article {pmid41520913,
year = {2026},
author = {Yang, X and Liu, Y and Miao, K},
title = {Microbiome-Modulated Immunotherapy in Oncology: Current Applications and Future Prospects.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2026.01.001},
pmid = {41520913},
issn = {1096-3650},
abstract = {Cancer immunotherapy has transformed oncology, yet therapeutic efficacy remains heterogeneous and frequently limited by primary or acquired resistance. Increasing evidence demonstrates that both intra- and extratumoral microbiota critically modulate antitumor immunity, influencing clinical responses of immunotherapy and immune-related adverse events (irAEs). Microbial communities regulate the tumor immune microenvironment through multiple mechanisms, including microbe-associated molecular patterns, microbial metabolites, and outer membrane vesicles, acting on tumor or immune cells. These insights have fostered the development of microbiome-based applications in oncology, ranging from predictive biomarkers to therapeutic interventions such as engineered bacteria, fecal microbiota transplantation, probiotics, prebiotics, outer membrane vesicles, bacteriophages, and dietary modulation. Early-phase clinical studies indicate that microbiota-targeted strategies can enhance immunotherapy efficacy or mitigate irAEs, although strain specificity, interindividual variability, and safety remain significant challenges. Future progress will require mechanistic elucidation, integration of multi-omics analyses, standardization of methodologies, and personalized intervention frameworks to translate microbiome modulation into clinically actionable, precision immunotherapy.},
}

@article {pmid41520280,
year = {2026},
author = {van de Guchte, M and Mondot, S and Cadiou, J and Raghuvanshi, R and Rous, C and Doré, J},
title = {Improving ulcerative colitis prospects through fecal microbiota transfer: atypical donor microbiota can boost success rate.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2609457},
doi = {10.1080/19490976.2025.2609457},
pmid = {41520280},
issn = {1949-0984},
mesh = {*Fecal Microbiota Transplantation/methods ; *Colitis, Ulcerative/therapy/microbiology ; Animals ; Rats ; *Gastrointestinal Microbiome ; Humans ; Disease Models, Animal ; *Feces/microbiology ; Dysbiosis/therapy ; Treatment Outcome ; },
abstract = {Fecal microbiota transfer (FMT) has been used with variable success in the experimental treatment of ulcerative colitis (UC), and efforts to improve its efficacy very much remain a matter of trial and error. We recently predicted that atypical donor microbiota could improve results. Here, we provide experimental support for this prediction in a rat model where we induced a transition of the intestinal ecosystem to an alternative state characterized by chronic low-grade inflammation and dysbiosis. While autologous FMT did barely or not enhance the restoration of a healthy microbiota compared to a control group without FMT, the atypical allogenic microbiota from one of two donor rat strains proved remarkably successful in the restoration of a healthy microbiota, in some cases accompanied by a healthy distal colon histology. These results allow the rationalization of research efforts towards improvement of FMT efficacy in humans, and indicate that (initial) success of FMT should be monitored at the microbiota level as much as at the level of clinical symptoms. More importantly, they provide further support for our earlier published, clinical-data-based, conceptual model of the intestinal ecosystem which suggests promising opportunities for therapeutic innovation in UC treatment. This model notably predicts that, and explains why, symbio-therapy, acting on both microbiota and inflammation, may be more efficient than conventional inflammation-directed therapies, and can be used to guide and monitor treatments.},
}

*Fecal Microbiota Transplantation/methods
*Colitis, Ulcerative/therapy/microbiology
Animals
Rats
*Gastrointestinal Microbiome
Humans
Disease Models, Animal
*Feces/microbiology
Dysbiosis/therapy
Treatment Outcome

@article {pmid41519323,
year = {2026},
author = {Wang, L and Lu, C and Li, S and Wu, T and Ren, X and Song, S and Ai, C},
title = {Laminaria japonica fucoidan ameliorates D-galactose-induced cognitive impairment via the regulation of tryptophan metabolism along the gut-brain axis.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {150151},
doi = {10.1016/j.ijbiomac.2026.150151},
pmid = {41519323},
issn = {1879-0003},
abstract = {Aging is a multifactorial biological process in which chronic inflammation and oxidative stress are central to the development of age-related disorders, including neurodegenerative decline. Fucoidan, a sulfated polysaccharide extracted from brown algae, has well-documented anti-inflammatory and antioxidant effects, and therefore has the potential to be a neuroprotective agent against cognitive impairment associated with aging. In the present study, the major fucoidan fraction (LJF-2) isolated from Laminaria japonica was examined for its neuroprotective properties in a D-galactose induced aging mouse model. Oral administration of LJF-2 for 8 weeks significantly improved spatial learning and memory and suppressed neuroinflammatory responses and oxidative stress while significantly reducing the activation of astrocytes and microglia. These neuroprotective effects were linked to the regulation of key proteins involved in neuronal protection and synaptic function, such as neprilysin and synapsin, by cAMP response element-binding protein signaling. Furthermore, LJF-2 significantly remodeled the gut microbiota through a reduction in the abundance of the Bacteroidota, Proteobacteria, and several putative pathogenic genera, which enhanced the intestinal barrier integrity and modified the microbial metabolite profiles, especially those associated with tryptophan metabolism. Fecal microbiota transplantation experiments further confirmed the role of the gut microbiota modulated by LJF-2 in mediating its neuroprotective effects through reduction of oxidative stress and inflammation. Collectively, these findings suggest that LJF-2 may be a promising therapeutic approach to address the aging-related cognitive decline by modulating the gut-brain axis.},
}

@article {pmid41519109,
year = {2026},
author = {Hoedt, EC and Talley, NJ},
title = {Toward a personalized diet-microbiome strategy in inflammatory bowel disease: Matching donor, diet, and patient.},
journal = {Med (New York, N.Y.)},
volume = {7},
number = {1},
pages = {100918},
doi = {10.1016/j.medj.2025.100918},
pmid = {41519109},
issn = {2666-6340},
mesh = {Humans ; *Inflammatory Bowel Diseases/microbiology/therapy/diet therapy ; *Fecal Microbiota Transplantation/methods ; *Precision Medicine/methods ; *Gastrointestinal Microbiome ; *Diet ; },
abstract = {Fecal microbiota transplant plus dietary change to restore the imbalance of an individual's microbiome to relieve disorders such as inflammatory bowel disease has not been established but has promise. In this commentary, we suggest the need to embrace a more nuanced, personalized approach, one that considers microbial functionality, dietary context, and host compatibility.},
}

Humans
*Inflammatory Bowel Diseases/microbiology/therapy/diet therapy
*Fecal Microbiota Transplantation/methods
*Precision Medicine/methods
*Gastrointestinal Microbiome
*Diet

@article {pmid41518808,
year = {2026},
author = {Qu, J and Jiang, X and Ma, Y and Sheng, X and Pi, C and Wang, Y and Xu, Q and Li, R and Wang, P and Qian, D and Wang, J and Yi, Z and Yi, J and Wen, L and Liu, S},
title = {Unveiling the gut-brain axis: How chronic exposure to arsenic-induced microglial pyroptosis drives Alzheimer's disease-like pathology.},
journal = {Journal of hazardous materials},
volume = {503},
number = {},
pages = {141087},
doi = {10.1016/j.jhazmat.2026.141087},
pmid = {41518808},
issn = {1873-3336},
abstract = {Arsenic, a pervasive environmental contaminant in groundwater, poses a severe global threat to public health. Chronic arsenic exposure has been linked to neurological impairment, however, its specific pathogenic mechanism and whether the gut-brain axis plays a key role remain unclear. This study investigated the role of gut microbiota and its metabolite indoxyl sulfate (IS) in mediating chronic exposure to arsenic-induced cognitive impairment and Alzheimer's disease (AD)-like pathology, with a specific focus on microglial pyroptosis. We found that chronic arsenic exposure induced cognitive dysfunction and intestinal barrier injury, disrupted gut microbiota composition, promoted IS accumulation in serum and brain, and activated the AhR/NF-κB/NLRP3 signaling pathway, triggering microglial pyroptosis and elevating AD-like pathological markers in mice. Meanwhile, fecal microbiota transplantation (FMT) from arsenic-exposed mice recapitulated cognitive impairment, elevated IS levels, and neuroinflammation in recipient mice. Furthermore, arsenic upregulated hepatic IS-synthesis genes (CYP2E1, Sult1d1) and downregulated renal IS-excretion gene (ABCG2). In vitro, arsenic and IS co-exposure promoted M1 polarization and enhanced pyroptosis by activating the AhR/NF-κB/NLRP3 signaling pathway, while suppressing phagocytosis-related proteins (TREM2, SYK and CD36). Furthermore, SiAhR treatment could alleviated microglial inflammatory injury and enhancing the microglia's phagocytic capacity induced by arsenic and IS co-exposure in BV2 cells through inhibiting the AhR/NF-κB/NLRP3-mediated pyroptosis signaling pathway. In conclusion, chronic arsenic exposure induced cognitive impairment and AD-like pathological via the gut microbiota-AhR-pyroptosis cascade, where in IS accumulation served a key mediator. These findings provide new insights into preventing arsenic-related cognitive damage.},
}

@article {pmid41517132,
year = {2025},
author = {Lu, S and Gao, M and Kuttappan, D and Amalaradjou, MA},
title = {Low-Fat Cheddar Cheese Influences Gut Microbiota Composition and Diversity in Human Microbiota-Associated Mice.},
journal = {Foods (Basel, Switzerland)},
volume = {15},
number = {1},
pages = {},
pmid = {41517132},
issn = {2304-8158},
support = {430855//Foundation for Food and Agriculture Research New Innovator Award/ ; },
abstract = {Cheese is a complex fermented dairy food containing bioactive nutrients and microorganisms that can influence host physiology. However, most existing evidence of its health effects derives from observational studies or investigations of isolated components rather than the whole food matrix. The present study examined the impact of low-fat Cheddar cheese as a whole food on the gut microbiota using a human microbiota-associated (HMA) mouse model. Germ-free C57BL/6 mice were colonized with human fecal microbiota and randomly assigned to either a control diet or a diet supplemented with low-fat Cheddar cheese (7.5% w/w) for six weeks. Fecal samples were collected longitudinally and analyzed by 16S rRNA gene (V3-V4 region) amplicon sequencing. Human microbiota transplantation successfully established a stable, human-like gut microbial community in the mice. Cheese supplementation significantly increased alpha diversity (Shannon and Chao1 indices) and altered microbial composition, characterized by a higher relative abundance of Firmicutes and a reduction in Bacteroidetes (p < 0.001). At the genus level, Lactococcus and Streptococcus were enriched in cheese-fed mice, reflecting potential viable transfer of cheese-derived lactic acid bacteria. These findings provide experimental evidence that low-fat Cheddar cheese can beneficially influence the human-derived gut microbiota in an animal model and highlight the need for further clinical research to validate these effects in humans.},
}

@article {pmid41516340,
year = {2026},
author = {Liu, M and Wang, Y and Huang, H},
title = {Gut Microbiota-Derived Propionic Acid Mediates ApoA-I-Induced Amelioration of MASLD via Activation of GPR43-Ca[2+]-CAMKII-ATGL Hepatic Lipolysis.},
journal = {International journal of molecular sciences},
volume = {27},
number = {1},
pages = {},
pmid = {41516340},
issn = {1422-0067},
support = {5232004//Beijing Natural Science Foundation/ ; 32071130//National Natural Science Foundation of China/ ; },
mesh = {*Gastrointestinal Microbiome ; *Propionates/metabolism/pharmacology ; Animals ; *Receptors, G-Protein-Coupled/metabolism ; *Apolipoprotein A-I/metabolism/genetics ; *Lipolysis/drug effects ; Liver/metabolism ; Male ; Mice ; Humans ; Fecal Microbiota Transplantation ; Calcium/metabolism ; Mice, Inbred C57BL ; *Fatty Liver/metabolism ; *Non-alcoholic Fatty Liver Disease/metabolism ; },
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is a widespread hepatic condition characterised by hepatic lipid accumulation and inflammation. Emerging research highlights the contribution of the intestinal microbiota and its metabolic byproducts to the pathogenesis of MASLD through the gut-liver axis. Apolipoprotein A-I (apoA-I), the principal structural component of high-density lipoprotein (HDL), is linked to various metabolic disorders; however, its function in MASLD has not yet been clearly elucidated. This study sought to examine whether apoA-I protects against MASLD, with a focus on the possible role of the gut microbiota and propionic acid (PPA). The contribution of the gut microbiota was evaluated using faecal microbiota transplantation (FMT) and antibiotic cocktail (ABX)-mediated depletion. Microbial composition was assessed via 16S rRNA sequencing, and concentrations of short-chain fatty acids (SCFAs) were quantified. The effects of PPA on MASLD were examined using in vivo and in vitro models. The results showed that apoA-I overexpression alleviated MASLD in a gut microbiota-dependent manner, restored microbial homeostasis, and elevated PPA levels. PPA supplementation improved MASLD phenotypes. Mechanistically, PPA treatment was associated with the activation of the GPR43-Ca[2+]-CAMKII-ATGL pathway, suggesting that PPA plays a role in stimulating hepatic lipolysis and enhancing mitochondrial β-oxidation. These findings reveal a novel pathway through which apoA-I ameliorates MASLD by modulating the gut microbiota and increasing PPA levels, which activate a hepatic lipolysis cascade. The apoA-I-microbiota-PPA axis represents a promising therapeutic target for MASLD intervention.},
}

*Gastrointestinal Microbiome
*Propionates/metabolism/pharmacology
Animals
*Receptors, G-Protein-Coupled/metabolism
*Apolipoprotein A-I/metabolism/genetics
*Lipolysis/drug effects
Liver/metabolism
Male
Mice
Humans
Fecal Microbiota Transplantation
Calcium/metabolism
Mice, Inbred C57BL
*Fatty Liver/metabolism
*Non-alcoholic Fatty Liver Disease/metabolism

@article {pmid41516146,
year = {2025},
author = {Barbu, AC and Stoleru, S and Zugravu, A and Poenaru, E and Dragomir, A and Costescu, M and Aurelian, SM and Shhab, Y and Stoleru, CM and Coman, OA and Fulga, I},
title = {Dopamine and the Gut Microbiota: Interactions Within the Microbiota-Gut-Brain Axis and Therapeutic Perspectives.},
journal = {International journal of molecular sciences},
volume = {27},
number = {1},
pages = {},
doi = {10.3390/ijms27010271},
pmid = {41516146},
issn = {1422-0067},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Dopamine/metabolism ; *Brain/metabolism ; Animals ; Parkinson Disease/metabolism/microbiology/therapy ; *Brain-Gut Axis ; Gastrointestinal Tract/metabolism/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {The microbiota-gut-brain axis (MGBA) comprises a complex bidirectional communication network integrating neural, immune, metabolic, and endocrine pathways. Dopamine, traditionally viewed as a central neurotransmitter, also plays essential roles in the gastrointestinal (GI) tract, where it regulates motility, secretion, barrier homeostasis, and mucosal immunity. Growing evidence indicates that the gut microbiota significantly contributes to intestinal dopamine metabolism through specialized enzymatic pathways, particularly tyrosine decarboxylase in Enterococcus species and catechol dehydroxylase in Eggerthella species. These microbial reactions compete with host processes, alter dopaminergic tone, and degrade orally administered levodopa (L-DOPA), providing a mechanistic explanation for the variability in treatment response in Parkinson's disease (PD). Beyond PD, microbially mediated alterations in dopaminergic signaling have been implicated in mood disorders, neurodevelopmental conditions, metabolic dysfunction, and immune-mediated diseases. This review synthesizes current mechanistic and translational evidence on the dopamine-microbiota interface, outlines microbial pathways shaping dopaminergic activity, and highlights therapeutic opportunities including microbiota modulation, dietary strategies, fecal microbiota transplantation, and targeted inhibitors of microbial dopamine metabolism. Understanding this interface offers a foundation for developing personalized approaches in neurogastroenterology and neuromodulatory therapies.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Dopamine/metabolism
*Brain/metabolism
Animals
Parkinson Disease/metabolism/microbiology/therapy
*Brain-Gut Axis
Gastrointestinal Tract/metabolism/microbiology
Fecal Microbiota Transplantation

@article {pmid41515997,
year = {2025},
author = {Ahmed, I and Nijs, J and Vanroose, M and Vandeputte, D and Kindt, S and Elma, Ö and Hendrix, J and Huysmans, E and Lahousse, A},
title = {Oral and Gut Health, (Neuro) Inflammation, and Central Sensitization in Chronic Pain: A Narrative Review of Mechanisms, Treatment Opportunities, and Research Agenda.},
journal = {International journal of molecular sciences},
volume = {27},
number = {1},
pages = {},
doi = {10.3390/ijms27010114},
pmid = {41515997},
issn = {1422-0067},
mesh = {Humans ; *Chronic Pain/therapy/microbiology/etiology/metabolism ; Animals ; *Gastrointestinal Microbiome ; *Central Nervous System Sensitization ; *Oral Health ; *Neuroinflammatory Diseases ; Dysbiosis ; },
abstract = {Given the limited efficacy of current interventions and the complexity of chronic pain, identifying perpetuating factors is crucial for uncovering new mechanistic pathways and treatment targets. The oral and gut microbiome has emerged as a potential modulator of pain through immune, metabolic, and neural mechanisms. Contemporary evidence indicates that chronic pain populations exhibit altered oral and gut microbiota, characterized by reduced short-chain fatty acid (SCFA)-producing taxa and an overrepresentation of pro-inflammatory species. These compositional changes affect metabolites such as SCFAs, bile acids, and microbial cell wall components, which interact with host receptors to promote peripheral and central sensitization. Microbiota-derived metabolites modulate peripheral sensitization by altering nociceptive neuron excitability and stimulating immune cells to release pro-inflammatory cytokines that increase blood-brain barrier permeability, activate microglia, and amplify neuroinflammation. Activated microglia further disrupt the balance between excitatory and inhibitory neurotransmission by enhancing glutamatergic activity and weakening GABAergic signaling, thereby contributing to the induction and maintenance of central sensitization. While observational studies establish associations between dysbiosis and chronic pain, animal models and early human fecal microbiota transplantation studies suggest a potential causal role of dysbiosis in pain, although human evidence remains preliminary and influenced by diet, lifestyle, and comorbidities. Overall, microbiota appears to regulate pain via peripheral and central mechanisms, and targeting it through specific interventions, such as dietary modulation to enhance SCFA production, alongside broader lifestyle measures like sleep, physical activity, stress management, and oral hygiene, may represent a new therapeutic strategy for the management of chronic pain.},
}

Humans
*Chronic Pain/therapy/microbiology/etiology/metabolism
Animals
*Gastrointestinal Microbiome
*Central Nervous System Sensitization
*Oral Health
*Neuroinflammatory Diseases
Dysbiosis

@article {pmid41514614,
year = {2025},
author = {Peddireddi, RSS and Kuchana, SK and Kode, R and Khammammettu, S and Koppanatham, A and Mattigiri, S and Gobburi, H and Alahari, SK},
title = {Role of Gut Microbiome in Oncogenesis and Oncotherapies.},
journal = {Cancers},
volume = {18},
number = {1},
pages = {},
doi = {10.3390/cancers18010099},
pmid = {41514614},
issn = {2072-6694},
abstract = {The gut microbiome has emerged as a key regulator of human health, influencing not only metabolism and immunity but also the development and treatment of cancer. Mounting evidence suggests that microbial dysbiosis contributes to oncogenesis by driving chronic inflammation, producing genotoxic metabolites, altering bile acid metabolism, and disrupting epithelial barrier integrity. At the same time, the gut microbiome significantly modulates the host response to oncotherapies including chemotherapy, radiotherapy, and especially immunotherapy, where microbial diversity and specific taxa determine treatment efficacy and toxicity. This review synthesizes current evidence on the role of the gut microbiome in both oncogenesis and oncotherapies, focusing on thirteen cancers with the strongest and most clinically relevant microbiome associations, colorectal cancer, gastric cancer, hepatocellular carcinoma, gallbladder cancer, esophageal cancer, pancreatic cancer, oral squamous cell carcinoma, cervical cancer, prostate cancer, breast cancer, lung cancer, brain cancer, and melanoma. These cancers were selected based on robust mechanistic data linking microbial alterations to tumor initiation, progression, and therapy modulation, as well as their global health burden and translational potential. In addition, we have provided mechanistic insights or clinical correlations between the microbiome and cancer outcomes. Across cancers, common microbial mechanisms included pro-inflammatory signaling (e.g., NF-κB and STAT3 pathways), DNA damage from bacterial toxins (e.g., colibactin, nitrosating species), and metabolite-driven tumor promotion (e.g., secondary bile acids, trimethylamine N-oxide). Conversely, beneficial commensals such as Faecalibacterium prausnitzii and Akkermansia muciniphila supported antitumor immunity and improved responses to immune checkpoint inhibitors. In conclusion, the gut microbiome functions as both a driver of malignancy and a modifiable determinant of therapeutic success. Integrating microbiome profiling and modulation strategies such as dietary interventions, probiotics, and fecal microbiota transplantation into oncology practice may pave the way for personalized and more effective cancer care.},
}

@article {pmid41512666,
year = {2026},
author = {Liu, JB and Li, S and Sun, GZ and Lin, ZX and Miao, ZM},
title = {Gut microbiota modulation by novel synbiotic improves production performance and ovarian function in aged laying hens via gut-ovary axis.},
journal = {Poultry science},
volume = {105},
number = {3},
pages = {106394},
doi = {10.1016/j.psj.2026.106394},
pmid = {41512666},
issn = {1525-3171},
abstract = {The management of oxidative stress and ovarian dysfunction associated with aged laying hens, which is highly involved in gut microbiota, has been suggested as a feasible approach to improve production performance. Here, we investigated the effects of a novel synbiotic (Bacillus amyloliquefaciens + inulin, BAI), a gut microbiota regulator, on the improvement of production performance in aged laying hens, and dissected the underlying mechanisms using multi-omics analysis. Our findings showed that, compared to the control, high-dosage BAI supplementation significantly improved production performance; enhanced intestinal health, evidenced by the increase of villus height (p < 0.01), the expression of gut barrier-related genes (Claudin-1 and Claudin-2) (all p < 0.001), and immune levels (SIgA and IFN-γ) (all p < 0.01); meliorated ovarian function, confirmed by reduced oxidative stress (p < 0.001) and pathological lesions, as well as increased follicle numbers (p < 0.01 or p < 0.001), serum contents of reproductive hormone (estrogen, luteinizing hormone, and follicle-stimulating hormone) (p < 0.05 or p < 0.001), and the mRNA levels of yolk precursor synthesis-associated genes (APOVLDL-Ⅱ, VTG-Ⅱ, and VLDLR) (all p < 0.001). The 16S rRNA sequencing showed that BAI augmented the relative amount of Lactobacillus, Akkermansia, and Bacteroides and other short-chain fatty acids (SCFAs)-producers. Blood metabolome analysis demonstrated that the predominant metabolites changed by BAI were principally involved in SCFA metabolism, steroid hormone biosynthesis, steroid biosynthesis, and intestinal immune network for IgA production. Ovarian transcriptome analysis indicated that BAI significantly inhibited pathways of ferroptosis and peroxisome, confirmed by RT-qPCR. Furthermore, fecal microbiota transplantation (FMT) from BAI-treated aged hens improved production performance, ovarian function, and oxidative stress status in antibiotic-administrated hens. In sum, our study uncovers that BAI improves production performance and ovarian dysfunction via gut microbiota in aged laying hens. Thus, modulating gut microbiome is an effective approach to laying rate reduction of aged hens.},
}