@article {pmid41929479,
year = {2026},
author = {Pan, Y and Li, B and Liu, L and Wang, Z and Liu, X},
title = {Gut dysbiosis induces the development of asthenozoospermia through butanoate metabolism.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1760881},
pmid = {41929479},
issn = {1664-3224},
mesh = {Male ; Humans ; *Asthenozoospermia/metabolism/etiology/microbiology ; *Dysbiosis/complications/metabolism/microbiology ; Animals ; Mice ; *Gastrointestinal Microbiome ; *Butyrates/metabolism ; Adult ; Fecal Microbiota Transplantation ; Case-Control Studies ; Sperm Motility ; Metabolomics ; Spermatozoa ; },
abstract = {BACKGROUND: Asthenozoospermia is a leading cause of male infertility with a rising incidence. While gut dysbiosis is implicated in metabolic disease, its role in asthenozoospermia pathogenesis remains unclear.

MATERIALS AND METHODS: We conducted a case-control study comparing the fecal microbiomes of men with isolated asthenozoospermia (n=60) and healthy controls (n=60) using shotgun metagenomic sequencing. Causality was assessed by fecal microbiota transplantation (FMT) from patients or controls into germ-free male mice. Metabolic perturbations were profiled by untargeted serum metabolomics and targeted short-chain fatty acid (SCFA) quantification in humans, alongside untargeted testicular metabolomics and serum SCFAs in recipient mice.

RESULTS: Metagenomic analysis (LEfSe) identified species-level differences, with marked depletion of butyrate-producing taxa in asthenozoospermia, most notably the prototypical butyrate producer Faecalibacterium prausnitzii. The relative abundance of F. prausnitzii was significantly positively correlated with sperm motility and progressive motility, linking gut composition to sperm quality in asthenozoospermia. Untargeted serum metabolomics identified 39 differential metabolites; KEGG enrichment prioritized butanoate metabolism. Targeted SCFA profiling confirmed significantly lower serum butyrate in asthenozoospermia versus controls. In germ-free males, FMT with patient-derived microbiota reduced sperm motility and progressive motility and induced histopathological abnormalities, including decreased interstitial Leydig cells, loss and atrophy of select intratubular cells, and an increased proportion of abnormal seminiferous tubules. Following patient FMT, recipient mice exhibited significantly reduced serum butyrate; testicular metabolomics revealed distinct profiles with 140 key differential metabolites, again implicating butanoate metabolism. Mechanistically, reduced F. prausnitzii-derived butyrate might impair Leydig cell steroidogenesis via disrupted PPAR signaling.

CONCLUSIONS: Asthenozoospermia is associated with gut dysbiosis characterized by loss of butyrate-producing bacteria, systemic and testicular disturbances in butyrate metabolism, and microbiota-mediated transmission of impaired sperm quality. These findings implicate the gut-testis axis in asthenozoospermia pathogenesis and nominate butyrate metabolism as a potential therapeutic target.},
}

Male
Humans
*Asthenozoospermia/metabolism/etiology/microbiology
*Dysbiosis/complications/metabolism/microbiology
Animals
Mice
*Gastrointestinal Microbiome
*Butyrates/metabolism
Adult
Fecal Microbiota Transplantation
Case-Control Studies
Sperm Motility
Metabolomics
Spermatozoa

@article {pmid41929953,
year = {2026},
author = {Oso, TA and Okesanya, OJ and Adebayo, UO and Obadeyi, KB and Ayelaagbe, OB and Talabi, OA and Adewole, PD and Anorue, CO and Ahmed, MM and Talabi, OT and Ogaya, JB and Lucero-Prisno, DE},
title = {Microbiome alterations in Alzheimer's disease: A systematic review of current evidence and global perspectives.},
journal = {Journal of Alzheimer's disease reports},
volume = {10},
number = {},
pages = {25424823261436287},
pmid = {41929953},
issn = {2542-4823},
abstract = {BACKGROUND: Growing evidence implicates the gut-brain axis in Alzheimer's disease (AD), with gut microbiome dysbiosis proposed to modulate neuroinflammation, amyloid pathology, and cognitive decline.

OBJECTIVE: To systematically synthesize human studies (2021-2025) profiling gut microbiomes in AD; identify consistent taxonomic and functional signatures; map geographic study distribution; and highlight translational gaps.

METHODS: A PRISMA-compliant systematic review of human studies using 16S rRNA, metagenomics, metatranscriptomics, or fecal microbiota transplantation (FMT)/probiotic designs was conducted. Two reviewers screened studies and assessed quality using Joanna Briggs Institute tools. Owing to heterogeneity, findings were narratively synthesized across microbiome diversity, taxonomy, function, metabolism, oral-brain links, causality, interventions, and predictive analyses.

RESULTS: Thirty-seven studies, mainly from Asia with some from Europe, North America, and Africa, revealed consistent gut dysbiosis in AD. Findings show reduced alpha-diversity, loss of short-chain fatty acid-producing bacteria (e.g., Faecalibacterium prausnitzii, Bifidobacterium), and enrichment of pro-inflammatory taxa (Escherichia/Shigella, Proteobacteria). Functional analyses indicate reduced butyrate synthesis, disrupted lipid and tryptophan-kynurenine metabolism, and links with apolipoprotein epsilon (ε4) gene and cognition. Limited causal evidence arises from Mendelian randomization and small FMT trials, with randomized, longitudinal confirmation still needed.

CONCLUSIONS: Current evidence suggests a biologically plausible association between gut microbiota and AD pathogenesis, positioning microbiome-derived biomarkers and interventions as promising but still exploratory avenues. Harmonized, longitudinal, multi-omic, and geographically inclusive studies are urgently needed to clarify causal mechanisms and translate these correlational findings into validated diagnostics and therapeutics.},
}

@article {pmid41931118,
year = {2026},
author = {Ansari, S and Purohit, KJ and Shelke, AB and Shah, M and Nkhoma, IA and Navale, AM and Wakchaure, R},
title = {Microbiota-driven mechanisms in multisystem diseases: integrative evidence across cardiovascular, metabolic, neurological and autoimmune disorders.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {5},
pages = {},
pmid = {41931118},
issn = {1572-9699},
mesh = {Humans ; *Dysbiosis/microbiology ; *Autoimmune Diseases/microbiology ; *Cardiovascular Diseases/microbiology ; *Nervous System Diseases/microbiology ; *Gastrointestinal Microbiome ; *Metabolic Diseases/microbiology ; Animals ; },
abstract = {The human microbiota represents one of the body's most influential biological systems, engaging in constant metabolic, immunological, and neuroendocrine communication with the host. Disruption of this intricate ecosystem, or dysbiosis, has emerged as a fundamental determinant in the onset and progression of numerous chronic diseases. This review consolidates contemporary evidence on how alterations in microbial composition, metabolite production, and barrier integrity contribute to pathophysiological changes across multiple organ systems. Gut-derived metabolites-including short-chain fatty acids, bile acid derivatives, trimethylamine-N-oxide, and lipopolysaccharide-serve as key mediators linking microbial imbalance to systemic inflammation, metabolic dysfunction, autoimmunity, and neurodegeneration. We outline the mechanistic pathways through which dysbiosis promotes hypertension, atherosclerosis, obesity, type 2 diabetes, Parkinson's disease, Alzheimer's disease, rheumatoid arthritis, inflammatory bowel disease, asthma, chronic obstructive pulmonary disease, urinary tract infections, and chronic kidney disease. Particular emphasis is placed on the gut-brain, gut-lung, and gut-kidney axes, which facilitate bidirectional immune and metabolic signalling between the intestine and distant tissues. Additionally, the review highlights emerging therapeutic interventions aimed at restoring microbial homeostasis, including targeted dietary strategies, probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and microbiome-directed pharmacological approaches. Collectively, the evidence positions the microbiota as a central regulator of human health and disease, offering a compelling platform for next-generation diagnostic and therapeutic innovation. Advancing mechanistic understanding of host-microbe interactions will be essential to developing personalized microbiome-based strategies capable of preventing, mitigating, or reversing disease across diverse clinical contexts.},
}

Humans
*Dysbiosis/microbiology
*Autoimmune Diseases/microbiology
*Cardiovascular Diseases/microbiology
*Nervous System Diseases/microbiology
*Gastrointestinal Microbiome
*Metabolic Diseases/microbiology
Animals

@article {pmid41931990,
year = {2026},
author = {Gao, J and Yi, Y and Ran, W and Cheng, Y and Deng, W and Duan, S and Shi, F and Wei, Y and Zhang, Y and Gong, Q},
title = {Targeting astrocytic Nrf2 by Trilobatin alleviates lipopolysaccharide-induced depressive-like behaviors and cognitive impairment in mice: Mechanistic insights into gut microbiota and metabolites modulation.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {155},
number = {},
pages = {158118},
doi = {10.1016/j.phymed.2026.158118},
pmid = {41931990},
issn = {1618-095X},
mesh = {Animals ; *NF-E2-Related Factor 2/metabolism ; *Gastrointestinal Microbiome/drug effects ; Mice ; Lipopolysaccharides ; Male ; *Cognitive Dysfunction/drug therapy/chemically induced ; Mice, Inbred C57BL ; *Astrocytes/drug effects/metabolism ; Neuroprotective Agents/pharmacology ; *Depression/drug therapy/chemically induced ; Disease Models, Animal ; Behavior, Animal/drug effects ; *Disulfides/pharmacology ; Alzheimer Disease/drug therapy ; Oxidative Stress/drug effects ; Major Depressive Disorder/drug therapy ; Flavonoids ; Polyphenols ; },
abstract = {BACKGROUND: Clinical and preclinical evidence links major depressive disorder (MDD) and Alzheimer's disease (AD), suggesting MDD treatment could prevent some AD. Dysfunction within the microbiota-gut-brain axis contributes to MDD and AD pathogenesis via dysregulated microbial metabolites. Trilobatin (TLB) functions as a neuroprotective agent modulating gut microbiota. However, its capacity to alleviate depressive-like behavior and cognitive deficits through restoration of gut microbial ecology and metabolite profiles requires clarification.

OBJECTIVE: The present research was designed to examine the impact of TLB on depressive-like behavior and cognitive impairments, and the role of the gut microbiota and metabolites.

METHODS: Neuroprotective effects of TLB on MDD and AD were evaluated using an LPS mouse model exhibiting depressive-like behavior and memory impairment. The principal molecular target of TLB was identified through a combination of single-cell sequencing, surface plasmon resonance, and gene knockout approaches. Mechanistic insights into gut microbiota and metabolites were gained through 16S rRNA sequencing and fecal microbiota transplantation (FMT).

RESULTS: TLB attenuated LPS-induced depressive-like behaviors manifested as lowered sucrose preference, extended immobility, and improved cognitive deficits as reflected by Y-maze and novel object recognition. Mechanistically, TLB directly bound Nrf2, enhanced Nrf2-ARE activity, and suppressed neuroinflammation and oxidative stress. TLB restored gut microbiota homeostasis, elevated Akkermansia muciniphila (AKK) abundance and short-chain fatty acids, and strengthened intestinal tight junction proteins. FMT from TLB-treated mice replicated these benefits in wild-type but not Nrf2-knockout mice. AKK supplementation similarly ameliorated behavioral and cognitive deficits via Nrf2 activation.

CONCLUSION: Our findings reveal that TLB mitigates neuropsychiatric deficits by activating Nrf2, remodeling restructuring gut microbiota and fortifying intestinal barrier function. The Nrf2-mediated microbiota-gut-brain axis is suggested as a potential therapeutic target for MDD and AD, positioning TLB as a promising natural Nrf2 activator.},
}

Animals
*NF-E2-Related Factor 2/metabolism
*Gastrointestinal Microbiome/drug effects
Mice
Lipopolysaccharides
Male
*Cognitive Dysfunction/drug therapy/chemically induced
Mice, Inbred C57BL
*Astrocytes/drug effects/metabolism
Neuroprotective Agents/pharmacology
*Depression/drug therapy/chemically induced
Disease Models, Animal
Behavior, Animal/drug effects
*Disulfides/pharmacology
Alzheimer Disease/drug therapy
Oxidative Stress/drug effects
Major Depressive Disorder/drug therapy
Flavonoids
Polyphenols

@article {pmid41932357,
year = {2026},
author = {Winston, JA and Jennings, R and Randolph, NK and Welton, M and Partridge, E and Schreeg, M and Yaxley, PE and Rudinsky, AJ},
title = {Fecal microbiota transplantation dosing regimen accelerates clinical resolution in canine parvovirus infection: a novel spectrum-of-care approach.},
journal = {Journal of the American Veterinary Medical Association},
volume = {264},
number = {8},
pages = {991-999},
doi = {10.2460/javma.25.11.0764},
pmid = {41932357},
issn = {1943-569X},
mesh = {Animals ; Dogs ; Female ; Male ; *Dog Diseases/therapy/virology ; Double-Blind Method ; *Fecal Microbiota Transplantation/veterinary ; Feces/virology ; *Parvoviridae Infections/veterinary/therapy ; *Parvovirus, Canine ; Prospective Studies ; },
abstract = {OBJECTIVE: To evaluate the efficacy of a novel spectrum-of-care fecal microbiota transplant (FMT) dosing regimen as an adjunctive therapy for canine parvovirus (CPV).

METHODS: 27 client-owned dogs naturally infected with CPV were enrolled from March to November 2023 in a prospective, double-blinded, placebo-controlled clinical trial. Patients were randomized into FMT-treated (n = 19) or placebo-treated (8) groups. Along with conventional treatments, CPV-infected dogs were administered FMT (single FMT enema, then 14 days of oral lyophilized FMT capsules) or placebo (single saline enema, then 14 days of oral placebo capsules) at admission. During hospitalization, dogs were monitored daily including fecal, clinical severity, and medication scores. Feces and serum were collected at admission, day 4, day 7, day 14, and day 21 for quantification of CPV viral shedding and immune response (bead-based multiplex of cytokines/chemokines). The primary outcome variable was length of hospitalization.

RESULTS: Interim analysis revealed that placebo-treated dogs had excessive study withdrawals due to worsening clinical status when compared to FMT-treated dogs (37.5% compared to 0%, respectively), leading to ethical discontinuation of the placebo arm. Fecal microbiota transplant-treated dogs had significantly reduced hospitalization length and medications required for treatment (maximum medication score) compared to placebo-treated dogs. Fecal microbiota transplant did not reduce fecal viral shedding or elicit a host immune response.

CONCLUSIONS: This novel FMT dosing regimen (single enema FMT followed by oral capsular FMT), designed to be feasible for inpatients or outpatients, accelerated clinical recovery from CPV.

CLINICAL RELEVANCE: In-house and commercially available FMT products were effective in CPV-infected dogs, thus broadening the spectrum of care available to these patients.},
}

Animals
Dogs
Female
Male
*Dog Diseases/therapy/virology
Double-Blind Method
*Fecal Microbiota Transplantation/veterinary
Feces/virology
*Parvoviridae Infections/veterinary/therapy
*Parvovirus, Canine
Prospective Studies

@article {pmid41932472,
year = {2026},
author = {Yan, Q and Yang, F and Li, Q and Wang, J and Wang, Y and Zeng, X and Shen, R and Yang, J and Peng, Y and Si, D and Diao, Y and Wei, L},
title = {Atractylodes macrocephala polysaccharide AMP1-1 ameliorates weightless-induced cognitive dysfunction via the microbiota-gut-brain axis.},
journal = {International journal of biological macromolecules},
volume = {358},
number = {},
pages = {151754},
doi = {10.1016/j.ijbiomac.2026.151754},
pmid = {41932472},
issn = {1879-0003},
mesh = {Animals ; *Polysaccharides/pharmacology/chemistry ; *Gastrointestinal Microbiome/drug effects ; *Cognitive Dysfunction/drug therapy/etiology/metabolism ; Rats ; *Atractylodes/chemistry ; Male ; NF-kappa B/metabolism ; Toll-Like Receptor 4/metabolism ; Hippocampus/drug effects/metabolism ; Rats, Sprague-Dawley ; *Brain/drug effects/metabolism ; Signal Transduction/drug effects ; Myeloid Differentiation Factor 88/metabolism ; Fecal Microbiota Transplantation ; },
abstract = {Atractylodes macrocephala Koidz., a traditional Chinese medicine known for "strengthening the spleen and replenishing qi", has been recognized for its gastrointestinal protective and immunomodulatory properties, suggesting a potential role in gut-brain axis regulation. This study investigated the protective effect and underlying mechanism of a purified inulin-type polysaccharide from Atractylodes macrocephala, AMP1-1, against weightlessness-induced cognitive impairment via the microbiota-gut-brain axis. Using a tail-suspension rat model to simulate microgravity, we assessed: (i) cognitive function through behavioral tests; (ii) neuroinflammation and barrier integrity through histological staining, ELISA, and Western blot; and (iii) gut microbiota composition through 16S rDNA sequencing and metabolomics analysis. Fecal microbiota transplantation (FMT) and butyrate supplementation were employed to validate the causal contributions of gut microbiota and their metabolites. AMP1-1 administration significantly improved cognitive performance, inhibited hippocampal neuroinflammation via the TLR4/MyD88/NF-κB pathway, and enhanced the integrity of both intestinal and blood-brain barriers in suspended rats. It also reshaped the gut microbiota structure, elevated fecal butyrate levels, and reduced systemic lipopolysaccharide (LPS). FMT from AMP1-1-treated donors replicated the cognitive and barrier-protective effects in recipient rats, and butyrate supplementation similarly alleviated neuroinflammation and cognitive deficits. These findings demonstrate that AMP1-1 alleviates weightlessness-induced cognitive impairment by modulating the gut microbiota to promote butyrate production, thereby restoring gut and brain barriers, suppressing peripheral and central inflammation, and inhibiting the hippocampal TLR4/MyD88/NF-κB pathway. AMP1-1 emerges as a promising prebiotic-like agent for preventing neuroinflammation-related cognitive decline under microgravity conditions.},
}

Animals
*Polysaccharides/pharmacology/chemistry
*Gastrointestinal Microbiome/drug effects
*Cognitive Dysfunction/drug therapy/etiology/metabolism
Rats
*Atractylodes/chemistry
Male
NF-kappa B/metabolism
Toll-Like Receptor 4/metabolism
Hippocampus/drug effects/metabolism
Rats, Sprague-Dawley
*Brain/drug effects/metabolism
Signal Transduction/drug effects
Myeloid Differentiation Factor 88/metabolism
Fecal Microbiota Transplantation

@article {pmid41932647,
year = {2026},
author = {Wang, DY and Wang, YW and Yu, KC and Yang, X and Ma, J and Li, BH and Peng, YL and Deng, XY and Chen, ZX and Wang, L},
title = {Probiotic potential of Parabacteroides johnsonii in mitigating age-related ovarian functional decline.},
journal = {Journal of genetics and genomics = Yi chuan xue bao},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jgg.2026.03.023},
pmid = {41932647},
issn = {1673-8527},
abstract = {The gut microbiota is increasingly recognized as a regulator of reproductive health, yet its role in ovarian aging remains unclear. Here, we combine Mendelian randomization (MR) analysis with experimental validation to investigate the causal relationship between gut microbiota and ovarian aging. MR analysis identifies four microbial taxa significantly associated with age at natural menopause. In mouse models, germ-free mice exhibit accelerated ovarian functional decline, including reduced ovarian reserve and impaired folliculogenesis. Fecal microbiota transplantation (FMT) from young donors alleviates ovarian aging phenotypes, whereas FMT from aged donors exacerbates functional decline. Metagenomic analysis reveals species-level differences between young and ovarian-aging mice, with Parabacteroides johnsonii (P. johnsonii) enriched in young mice. Administration of P. johnsonii to middle-aged mice improves ovarian reserve, reduces follicular atresia, enhances granulosa cell proliferation, and decreases systemic inflammation. These findings highlight a causal role of the gut microbiota in ovarian aging and support microbiota-targeted interventions as a potential strategy to preserve ovarian function.},
}

@article {pmid41932663,
year = {2026},
author = {Lu, S and Shengle, Q and Shiqing, L and Huihuang, D and Qiaolian, C and Ruifeng, C and Pei, F and Xiao, W and Conglin, L and Xiaoqian, S and Zhonghao, F and Xin, Z and Qian, G and Xiangying, A and Weiqi, P and Yutao, W and Luping, L and Zifeng, Y},
title = {Sheng Jiangsan alleviated influenza-induced acute lung injury by regulating Lactobacillus murinus.},
journal = {Journal of ethnopharmacology},
volume = {367},
number = {},
pages = {121524},
doi = {10.1016/j.jep.2026.121524},
pmid = {41932663},
issn = {1872-7573},
mesh = {Animals ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; *Acute Lung Injury/drug therapy/virology/microbiology ; Gastrointestinal Microbiome/drug effects ; *Orthomyxoviridae Infections/drug therapy/complications/microbiology ; Mice ; Male ; Lung/drug effects/pathology/virology ; *Antiviral Agents/pharmacology/therapeutic use ; Mice, Inbred BALB C ; *Anti-Inflammatory Agents/pharmacology ; RNA, Ribosomal, 16S/genetics ; *Lactobacillus/drug effects ; Dogs ; STAT1 Transcription Factor/metabolism ; },
abstract = {Sheng Jiangsan (SJS) authorized by the Chinese Food and Drug Administration for treating wind-heat common cold, exhibits broad-spectrum antiviral activity. However, its specific antiviral and anti-inflammatory mechanisms require clarification. Gut microbiota and their metabolites play significant roles in lung disease progression and intervention, yet no research has explored whether the anti-influenza effect of SJS-derived Qingjie-Tuire (QT) Granule involves these pathways.

AIM OF THE STUDY: This study aimed to determine whether QT Granule exerts its anti-influenza effects through modulation of gut microbiota and metabolites, specifically investigating associated antiviral and anti-inflammatory mechanisms. An experimental study employing influenza-infected mice. Mechanistic analysis integrated 16S rRNA full-length sequencing, UHPLC-MS/MS metabolomics, fecal microbiota transplantation (FMT), and targeted probiotic intervention.

MATERIALS AND METHODS: Influenza-infected mice received QT Granule treatment. Gut microbiota composition was analyzed via full-length 16S rRNA sequencing. Metabolite profiles were assessed using UHPLC-MS/MS. Functional validation involved QT-treated mice FMT into infected mice and supplementing infected mice with Lactobacillus murinus and Lactobacillus reuteri (species enriched by QT). Outcomes included lung pathology, viral titers, survival, and lung/intestinal inflammation, and intestinal barrier integrity.

RESULTS: QT treatment significantly reduced lung pathological damage, lowered viral titers, restored pulmonary macrophage and T-cell proportions, decreased p-STAT1/p-STAT3/p-ERK expression, maintained intestinal barrier function, attenuated lung and intestinal inflammation, and prolonged survival time/survival rate in infected mice. QT intervention restored influenza-depleted UFAs, including docosahexaenoic acid (DHA) and arachidonic acid (AA), and enriched L. murinus and L. reuteri. Crucially, both FMT using QT-treated mouse feces and direct supplementation with L.murinus/L. reuteri replicated QT's core therapeutic effects.

CONCLUSIONS: QT Granule exerts potent anti-influenza and anti-inflammatory effects by modulating gut microbiota (specifically enriching L.murinus and L.reuteri) and restoring UFA metabolites. This gut-lung axis mechanism provides novel insight into traditional Chinese medicine intervention in viral lung diseases.},
}

Animals
*Drugs, Chinese Herbal/pharmacology/therapeutic use
*Acute Lung Injury/drug therapy/virology/microbiology
Gastrointestinal Microbiome/drug effects
*Orthomyxoviridae Infections/drug therapy/complications/microbiology
Mice
Male
Lung/drug effects/pathology/virology
*Antiviral Agents/pharmacology/therapeutic use
Mice, Inbred BALB C
*Anti-Inflammatory Agents/pharmacology
RNA, Ribosomal, 16S/genetics
*Lactobacillus/drug effects
Dogs
STAT1 Transcription Factor/metabolism

@article {pmid41933285,
year = {2026},
author = {Yu, Q and Chen, A and Yi, J and Iqbal, M and Tang, Z and Ge, H and Hu, Y and Liu, W and Zheng, L and Tang, J and Xiang, J},
title = {Gut microbiota-associated nutritional-immune status predicts prognosis in postoperative NSCLC patients.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2652460},
pmid = {41933285},
issn = {1949-0984},
mesh = {Humans ; *Carcinoma, Non-Small-Cell Lung/surgery/immunology/microbiology/diagnosis ; *Gastrointestinal Microbiome ; Animals ; *Lung Neoplasms/surgery/immunology/microbiology ; Prognosis ; Male ; Female ; *Nutritional Status ; Mice ; Fecal Microbiota Transplantation ; Middle Aged ; Retrospective Studies ; Aged ; Bacteria/classification/genetics/isolation & purification/metabolism ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; Prospective Studies ; Fatty Acids, Volatile/metabolism ; Postoperative Period ; },
abstract = {BACKGROUND: Surgical resection is the primary treatment for non-small cell lung cancer (NSCLC) patients with stages I and II; however, the postoperative prognosis varies among individuals. The prognostic nutritional index (PNI) reflects the nutritional-immune status of patients, but its microbial determinants remain unclear.

METHODS: PNI was analyzed in a cohort of 372 retrospective and 139 prospective NSCLC patients. This analysis integrated gut microbiota signatures using 16S rRNA sequencing, fecal metabolomics, and murine fecal microbiota transplantation (FMT) models.

RESULTS: A PNI value of ≥46.2 stratified postoperative NSCLC patients with improved 5-y survival (HR = 0.3889, 95% CI 0.2840-0.5356, p < 0.001). Patients with a high PNI showed enrichment of short-chain fatty acid (SCFA)-producing taxa, such as Akkermansia and Eubacterium hallii, and elevated butyrate/isovalerate levels, correlating with increased infiltration of CD8[+] T cells (Pearson r = 0.51, p = 0.02). FMT from high-PNI patients reduced lung tumor growth in mice compared with FMT from low-PNI patients (7.2 vs 18 nodules, p = 0.01). Oral administration of A. muciniphila or/and E. hallii or butyrate suppressed tumor growth and enhanced CD8[+] tumor-infiltrating lymphocytes (TILs) (p < 0.001).

CONCLUSION: PNI and its linked gut microbiota‒SCFA axis are clinically prognostic biomarkers and potential immunomodulatory targets for early-stage NSCLC. Targeting this axis may serve as a promising coadjuvant strategy for NSCLC patients undergoing surgical resection.},
}

Humans
*Carcinoma, Non-Small-Cell Lung/surgery/immunology/microbiology/diagnosis
*Gastrointestinal Microbiome
Animals
*Lung Neoplasms/surgery/immunology/microbiology
Prognosis
Male
Female
*Nutritional Status
Mice
Fecal Microbiota Transplantation
Middle Aged
Retrospective Studies
Aged
Bacteria/classification/genetics/isolation & purification/metabolism
Feces/microbiology
RNA, Ribosomal, 16S/genetics
Prospective Studies
Fatty Acids, Volatile/metabolism
Postoperative Period

@article {pmid41938830,
year = {2026},
author = {Wu, T and Xing, H and Wu, T and Xie, X and Ji, L and Wang, W and Zhang, X and Zhang, Y and Jiang, C and Bao, T},
title = {Imbalance of the Brain-Gut-Microbiota Axis in Major Depressive Disorder: From Pathogenesis to Clinical Translation.},
journal = {Neuropsychiatric disease and treatment},
volume = {22},
number = {},
pages = {591429},
pmid = {41938830},
issn = {1176-6328},
abstract = {Major depressive disorder (MDD) is one of the most common psychiatric conditions, characterized by complex pathogenesis and marked inter-individual variability in treatment response, leading to persistent impairment of physical and mental health as well as social functioning. In recent years, the brain-gut-microbiota axis (BGMA) has emerged as a key biological pathway linking the gut microbiota with the central nervous system, and its role in MDD has become a major research focus. Although substantial progress has been made in elucidating the association between MDD and the BGMA, the precise mechanisms, critical pathways, and their integrated clinical applications remain to be fully clarified. On the basis of a comprehensive overview of the physiological functions, structural components, and disease associations of the BGMA, this review systematically summarizes the bidirectional interactions between MDD and the BGMA. Integrating the latest findings from preclinical and clinical studies, we further dissect the key regulatory pathways of this axis in MDD and highlight the therapeutic potential of BGMA-based interventions, including pharmacotherapy, fecal microbiota transplantation, dietary modulation, and physical therapies. This work aims to provide a theoretical foundation for developing novel treatment strategies for patients with MDD and for improving their prognosis and quality of life.},
}

@article {pmid41939435,
year = {2026},
author = {Yan, D and Li, Q and Wang, M and Nie, Y and Sun, X and Na, L and Wang, H},
title = {Platelet-Rich Plasma Attenuates Knee Osteoarthritis in Rats via Modulation of Gut Microbiota.},
journal = {Drug design, development and therapy},
volume = {20},
number = {},
pages = {574392},
pmid = {41939435},
issn = {1177-8881},
mesh = {Animals ; *Platelet-Rich Plasma ; Rats ; *Osteoarthritis, Knee/therapy/drug therapy/pathology ; Male ; *Gastrointestinal Microbiome/drug effects ; Rats, Sprague-Dawley ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Injections, Intra-Articular ; },
abstract = {BACKGROUND: Platelet-rich plasma (PRP), a platelet and plasma concentrate extracted from whole blood via centrifugation, has multiple bioactive properties. However, its role in the progression of knee osteoarthritis (KOA) and the underlying mechanisms of action remain unclear. In this study, we investigated the therapeutic effects of PRP extracted from rat whole blood on the progression of KOA and assessed whether its mechanism involves modulation of the gut microbiota (GM).

METHODS: Knee osteoarthritis (KOA) rat models were established by intra-articular injection of 1 mg of sodium monoiodoacetate (MIA) into the knee joints. The rats were administered intra-articular injections of 60 μL of PRP on days 15, 17, and 19 post-modeling. Moreover, we established pseudo-germ-free (pGF) KOA rat models and performed fecal microbiota transplantation (FMT) experiments to investigate whether the GM mediates the therapeutic effects of PRP on KOA. Therapeutic efficacy was assessed by conducting gait analysis, joint swelling measurement, and micro-CT scanning. The pathological changes were evaluated via Safranin O-Fast Green and hematoxylin-eosin (HE) staining, as well as immunohistochemistry (IHC). The alterations in the GM were evaluated by 16S rRNA gene sequencing.

RESULTS: We found that PRP effectively improved abnormal gait patterns, reduced inflammation levels, alleviated subchondral bone loss, repaired the damaged articular surface, and mitigated cartilage destruction in KOA rats. Concurrently, PRP intervention restored intestinal barrier function and positively modulated the dysregulated composition of the GM. The pGF condition reversed the improvements induced by PRP in KOA rats, whereas transplanting GM from PRP-treated KOA rats to recipient KOA rats promoted recovery in the latter.

CONCLUSION: This study demonstrated that PRP ameliorates KOA progression, at least partially, by modulating GM diversity (notably Ligilactobacillus murinus), enhancing intestinal barrier integrity, and reducing systemic inflammation.},
}

Animals
*Platelet-Rich Plasma
Rats
*Osteoarthritis, Knee/therapy/drug therapy/pathology
Male
*Gastrointestinal Microbiome/drug effects
Rats, Sprague-Dawley
Disease Models, Animal
Fecal Microbiota Transplantation
Injections, Intra-Articular

@article {pmid41939708,
year = {2026},
author = {Luo, X and Feng, J and Sun, Y and Tan, Z and Wang, L and Bao, Y and Lu, J and He, J and Lu, B},
title = {Synergistic effects of fecal microbiota transplantation and andrographolide on gut microbiota modulation in dextran sulfate sodium-induced colitis in mice.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1762107},
pmid = {41939708},
issn = {1664-302X},
abstract = {BACKGROUND: Andrographolide (Andro) and fecal microbiota transplantation (FMT) are emerging treatments for colitis. However, whether their combined administration provides superior efficacy has not been established.

METHODS: This study attempted to clarify the reparative effects of FMT, Andro, and their combination on colitis in mice. Research subjects were allocated to: (1) the Control (CTRL) group, (2) the dextran sulfate sodium (DSS) group, (3) the FMT group, (4) the Andro group, and (5) the Andro combined with FMT group. The experiment lasted 15 days, during which weight, colon length, and hematochezia were monitored. Colon tissues were histologically analyzed via HE staining to assess inflammatory infiltration. The concentrations of key serum inflammatory factors were measured using ELISA. WB and IHC were employed to quantify inflammatory factor levels in intestinal tissues. Finally, the taxonomic composition of colonic microbiota was examined with 16S rRNA gene sequencing.

RESULTS: All three treatments mitigated colitis, as indicated by lowered pathological body weight wasting, colon shortening, hematochezia, and inflammation. Serum and intestinal cytokine levels were significantly decreased following treatment. Mechanistic analysis indicated that Andro attenuated inflammatory responses primarily through inhibition of NF-κB. Moreover, 16S rRNA sequencing revealed a beneficial modulation of the gut microbiota by all three treatments compared with the DSS group. Integrated analysis demonstrated that Andro combined with FMT therapy produced superior therapeutic outcomes relative to either intervention alone.

CONCLUSION: The combined administration of Andro and FMT provides enhanced protection against DSS-induced colitis in mice, highlighting a potential synergistic therapeutic strategy.},
}

@article {pmid41939897,
year = {2026},
author = {Sun, X and Bai, X},
title = {Immune dysregulation in pediatric tic disorders: mechanisms, biomarkers, and therapeutic frontiers.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1708940},
pmid = {41939897},
issn = {1664-3224},
mesh = {Humans ; Biomarkers ; *Tic Disorders/immunology/therapy/etiology/diagnosis ; Child ; Animals ; Autoimmune Diseases/immunology/therapy ; Streptococcal Infections/immunology ; Gastrointestinal Microbiome/immunology ; Autoantibodies/immunology ; Cytokines/metabolism ; Obsessive-Compulsive Disorder ; },
abstract = {Tic Disorders (TDs) are common neurodevelopmental disorders characterized by complex pathophysiological mechanisms. A growing body of evidence in recent years suggests that immune system dysregulation plays a critical role in the pathogenesis and clinical course of TDs in a subset of pediatric patients. This review aims to systematically summarize the current understanding of the core mechanisms of immune dysregulation in pediatric TDs, potential biomarkers, and related therapeutic frontiers. We detail three core pathophysiological pathways, Post infectious autoimmunity, represented by the Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal Infections (PANDAS) and Pediatric Acute-onset Neuropsychiatric Syndrome (PANS) models. Its core mechanism involves the production of autoantibodies induced by molecular mimicry, which target basal ganglia neurons, such as cholinergic interneurons and dopamine receptors. Neuroinflammation is another critical pathway. This process involves T helper 17 (Th17) cell-mediated disruption of the blood-brain barrier and microglial activation. It is further characterized by elevated pro-inflammatory cytokines, such as Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-12 (IL-12). Microbiota-gut-brain axis dysregulation, wherein gut dysbiosis and compromised intestinal barrier function influence central nervous system (CNS) function through the neuro immune endocrine network. Building upon this framework, we evaluate potential biomarkers across various dimensions, including the findings and limitations in serology (cytokines), cerebrospinal fluid analysis (oligoclonal bands, MCP-1), neuroimaging (volumetric changes in the basal ganglia and PET imaging of neuroinflammation), and genetics (variations in the IL-1RN gene). Finally, we discuss the evolution from conventional treatments to emerging immune-targeted therapies. This encompasses core immunomodulatory therapies (Intravenous Immunoglobulin (IVIG) and plasmapheresis) and promising future strategies, such as fecal microbiota transplantation (FMT), targeted B-cell therapies, and small-molecule anti-inflammatory drugs. In conclusion, a deeper understanding of the immunological basis of TDs is paving the way for the development of more precise diagnostic tools and novel, individualized immunomodulatory interventions.},
}

Humans
Biomarkers
*Tic Disorders/immunology/therapy/etiology/diagnosis
Child
Animals
Autoimmune Diseases/immunology/therapy
Streptococcal Infections/immunology
Gastrointestinal Microbiome/immunology
Autoantibodies/immunology
Cytokines/metabolism
Obsessive-Compulsive Disorder

@article {pmid41940048,
year = {2026},
author = {Okita, A and Watanabe, T and Nakagawa, M and Ogino, K and Hashida, S and Tsukuda, K and Yokoyama, N},
title = {Full-Thickness Skin Transplantation Combined with Negative-Pressure Wound Therapy for a Refractory Peristomal Large Skin Ulcer Caused by Mucocutaneous Separation: A Case Report.},
journal = {Surgical case reports},
volume = {12},
number = {1},
pages = {},
pmid = {41940048},
issn = {2198-7793},
abstract = {INTRODUCTION: Stomal mucocutaneous separation is a frequent complication of colostomy, which may complicate wound care due to contamination from fecal leakage, resulting in delayed wound healing. In addition, systemic factors may further influence postoperative wound healing. We report successful combination treatment, involving full-thickness skin graft transplantation and negative-pressure wound therapy (NPWT) in a patient with a large peristomal ulcer that developed progressively in the postoperative course following complete circumferential mucocutaneous separation and infection, which occurred after neoadjuvant chemotherapy followed by laparoscopic abdominoperineal resection.

CASE PRESENTATION: A 75-year-old male, who had been diagnosed with advanced low rectal cancer, received 4 cycles of mFOLFOX6 chemotherapy (oxaliplatin, leucovorin, and fluorouracil) plus bevacizumab, followed by laparoscopic abdominoperineal resection with lymph node dissection. Approximately 4 weeks later, partial mucocutaneous separation developed, accompanied by subcutaneous abscess formation. Subsequently, this led to complete circumferential mucocutaneous separation, which evolved into a giant peristomal ulceration with a significant tissue loss. Conservative local wound care, including frequent debridement, was continued, and granulation tissue gradually filled the peristomal skin defect. Three months after the operation, full-thickness skin graft transplantation combined with NPWT was performed. At 6 years after the operation, the patient remained recurrence-free, and there were no postoperative complications or issues with the colostomy or skin graft.

CONCLUSIONS: This combination therapy successfully treated a giant peristomal ulcer that progressively developed after mucocutaneous separation with infection, which occurred later than typical postoperative wound complications following neoadjuvant chemotherapy (mFOLFOX6 + bevacizumab) and laparoscopic surgery. Delayed wound healing, potentially related to bevacizumab, may have contributed to both the late onset and unusually extensive progression of the ulcer. The therapy proved compatible with long-term stoma care.},
}

@article {pmid41940919,
year = {2026},
author = {Lapauw, L and Vermeiren, L and Vercauteren, L and Amini, N and Peeters, L and Dalle, S and Koppo, K and Derrien, M and Dupont, J and Raes, J and Gielen, E},
title = {An exploratory multi-biomarker panel including fecal calprotectin, Brain-Derived Neurotrophic Factor, Fibroblast-Growth Factor-21 and irisin shows poor diagnostic accuracy for detecting probable sarcopenia in community-dwelling older persons.},
journal = {Aging clinical and experimental research},
volume = {38},
number = {1},
pages = {},
pmid = {41940919},
issn = {1720-8319},
support = {G099721N//Fonds Wetenschappelijk Onderzoek/ ; },
mesh = {Humans ; Female ; Aged ; Male ; *Brain-Derived Neurotrophic Factor/analysis/metabolism ; Biomarkers/analysis/metabolism ; *Sarcopenia/diagnosis/metabolism ; *Leukocyte L1 Antigen Complex/analysis ; *Fibronectins/analysis/metabolism ; Cross-Sectional Studies ; *Feces/chemistry ; *Fibroblast Growth Factors/analysis/metabolism ; Independent Living ; Aged, 80 and over ; Myokines ; },
abstract = {BACKGROUNDS: Serum and fecal biological markers that reflect underlying drivers of sarcopenia, may aid in novel predictive or diagnostic tools for sarcopenia. AIMS: To explore the potential of five specific myokines and fecal calprotectin (fCPT) as biomarkers for diagnosing the presence of at least probable sarcopenia in community-dwelling individuals aged ≥ 65 years. METHODS: This cross-sectional, exploratory study included 156 participants (median age 73y), of whom 59 (20♂, 39♀) had at least probable sarcopenia per EWGSOP2 criteria, and 97 (33♂, 64♀) controls. Myostatin, irisin, Brain-Derived Neurotrophic Factor (BDNF), Insulin-like Growth Factor-1 (IGF-1), Fibroblast Growth Factor-21 (FGF-21), and fCPT were measured using Enzyme-Linked ImmunoSorbent Assay (ELISA). Muscle mass and function were assessed via appendicular lean mass (ALM), hand grip strength (HGS), 5-time chair stand test (CST), gait speed, and the Short Physical Performance Battery (SPPB). Linear and logistic regressions analyses were performed. Diagnostic accuracy was evaluated using Area’s Under the Curve (AUC). RESULTS: Participants with fCPT < 50 µg/g walked faster than those with fCPT ≥ 200 µg/g. Higher fCPT associated with slower gait speed (β: -0.003; 95% CI [-0.001; -0.00002]), while IGF-1 associated with higher HGS (β: 0.077; 95% CI [0.039; 0.116]). BDNF alone diagnosed at least having probable sarcopenia (AUC: 0.63; sensitivity 53%, specificity 71%). A multi-biomarker panel comprising BDNF, irisin, FGF-21 and fCPT modestly improved accuracy (AUC: 0.71; sensitivity 64%, specificity 77%), but this improvement was not statistically significant compared with the single biomarkers BDNF (p = 0.330) and fCPT (p = 0.180). DISCUSSION: The multi-biomarker panel significantly diagnosed at least having probable sarcopenia, but with high false negative (36%) and positive (23%) rates, respectively. CONCLUSION: The clinical relevance of this specific multi-biomarker panel may be limited due to moderate diagnostic accuracy. Validation in larger cohorts is needed.},
}

Humans
Female
Aged
Male
*Brain-Derived Neurotrophic Factor/analysis/metabolism
Biomarkers/analysis/metabolism
*Sarcopenia/diagnosis/metabolism
*Leukocyte L1 Antigen Complex/analysis
*Fibronectins/analysis/metabolism
Cross-Sectional Studies
*Feces/chemistry
*Fibroblast Growth Factors/analysis/metabolism
Independent Living
Aged, 80 and over
Myokines

@article {pmid41942347,
year = {2026},
author = {Joshi, M and Sharma, S and Thakur, B and Kaur, S and Mouafo, HT},
title = {Combatting multidrug resistance in Klebsiella pneumoniae: mechanisms, global trends, and innovative therapeutic strategies.},
journal = {Future microbiology},
volume = {21},
number = {3},
pages = {329-348},
pmid = {41942347},
issn = {1746-0921},
mesh = {Humans ; *Drug Resistance, Multiple, Bacterial/genetics ; *Anti-Bacterial Agents/pharmacology/therapeutic use ; *Klebsiella pneumoniae/drug effects/genetics/pathogenicity ; *Klebsiella Infections/microbiology/epidemiology/drug therapy/therapy ; Cross Infection/microbiology/epidemiology ; beta-Lactamases/metabolism/genetics ; Virulence ; },
abstract = {Emergence of drug-resistant bacterial infections, particularly those caused by Klebsiella pneumoniae, represents a growing public health issue. K. pneumoniae is the leading cause of nosocomial infections, associated with diverse diseases and high mortality rates. Its ability to develop multiple resistance mechanisms, including biofilm formation, efflux pump activity, β-lactamase production, enzymatic modification, and porin loss, contributes to its resistance to conventional antibiotics. These challenges urge the ned for novel therapeutics and alternative therapies. While resistance rates remain lower in developed countries, regions in Africa, South Asia, and Middle East report rates exceeding 80%, often due to antibiotic misuse and inadequate regulations. Particularly concerning are novel hypervirulent carbapenem-resistant strains linked to bloodstream infections and high mortality, especially in low- and middle-income countries. Emerging approaches, including fecal microbiota transplantation, might help gut dysbiosis and enhance host immunity against carbapenemase-producing Enterobacterales. Additionally, molecular studies identified cytoplasmic response regulators that promote resistance gene expression and plasmid-mediated transfer, offering prospective therapeutic targets. This review summarizes current knowledge regarding the genetic, molecular, and epidemiological mechanisms of multidrug resistance and virulence in K. pneumoniae, and discusses emerging therapeutic strategies including new β-lactamase inhibitors, bacteriophage and host-directed therapies, in silico therapeutic strategies, and vaccine development.},
}

Humans
*Drug Resistance, Multiple, Bacterial/genetics
*Anti-Bacterial Agents/pharmacology/therapeutic use
*Klebsiella pneumoniae/drug effects/genetics/pathogenicity
*Klebsiella Infections/microbiology/epidemiology/drug therapy/therapy
Cross Infection/microbiology/epidemiology
beta-Lactamases/metabolism/genetics
Virulence

@article {pmid41943291,
year = {2026},
author = {Yin, W and Yan, Z and Wang, Z and Zhou, Z},
title = {Structural characterization of a polysaccharide isolated from Allium macrostemon Bunge bulbus and its mechanism in ameliorating DSS-induced ulcerative colitis in mice.},
journal = {Carbohydrate polymers},
volume = {381},
number = {},
pages = {125174},
doi = {10.1016/j.carbpol.2026.125174},
pmid = {41943291},
issn = {1879-1344},
mesh = {Animals ; *Colitis, Ulcerative/chemically induced/drug therapy/metabolism/microbiology ; *Polysaccharides/chemistry/pharmacology/isolation & purification/therapeutic use ; Mice ; Dextran Sulfate ; Gastrointestinal Microbiome/drug effects ; Male ; *Allium/chemistry ; Fatty Acids, Volatile/metabolism ; Fecal Microbiota Transplantation ; Colon/drug effects/metabolism ; Mice, Inbred C57BL ; Chive ; },
abstract = {A polysaccharide (AMP) was isolated and purified from the bulbus of Allium macrostemon Bunge (AMB) and structurally characterized. AMP, with the weight-average molecular weight of 9.007 kDa, is a branched polysaccharide with a main chain composed of →1)-β-D-Fruf-(2→ and →1,6)-β-D-Fruf-(2→ linkages, with short side chains formed by β-D-Fruf-(2 → 6)-β-D-Fruf-(2→. AMP administration effectively mitigated DSS-induced ulcerative colitis (UC) in mice by reinforcing the integrity of the intestinal barrier, balancing gut microbiota, replenishing short-chain fatty acids (SCFAs) levels, and restoring normal metabolic activity in the colon. AMP treatment decreased the harmful bacterial, including Bacteroides, Escherichia-Shigella, Parabacteroides, and the Clostridia vadinBB60 cluster, while increasing beneficial SCFAs-producing such as Ruminococcus and the Christensenellaceae R-7 group. Fecal microbiota transplantation experiments further demonstrated that AMP exerted its anti-colitis effect through a microbiota-dependent manner. In addition, in vitro fermentation experiment showed that AMP can be translated to SCFAs by gut microbiota. Meanwhile, AMP regulated metabolic pathways such as the glycerophospholipid, arachidonic acid, and linoleic acid metabolism in colon tissue. The acute toxicity test showed AMP possesses a wide safety margin. Collectively, our data highlight AMP as a promising functional food component for the prevention of UC, and provide a scientific basis for developing AMP-derived bioactive products.},
}

Animals
*Colitis, Ulcerative/chemically induced/drug therapy/metabolism/microbiology
*Polysaccharides/chemistry/pharmacology/isolation & purification/therapeutic use
Mice
Dextran Sulfate
Gastrointestinal Microbiome/drug effects
Male
*Allium/chemistry
Fatty Acids, Volatile/metabolism
Fecal Microbiota Transplantation
Colon/drug effects/metabolism
Mice, Inbred C57BL
Chive

@article {pmid41943367,
year = {2026},
author = {Gao, X and Huang, H and Hu, L and Ding, W and Hou, Z and Xu, R and Du, G and Kang, Z},
title = {High-molecular weight hyaluronic acid protects against colitis by remodeling microbiota and restoring barrier function.},
journal = {Carbohydrate polymers},
volume = {381},
number = {},
pages = {125145},
doi = {10.1016/j.carbpol.2026.125145},
pmid = {41943367},
issn = {1879-1344},
mesh = {Animals ; *Hyaluronic Acid/pharmacology/chemistry/therapeutic use ; Molecular Weight ; Intestinal Barrier Function/drug effects ; Dextran Sulfate ; *Colitis/chemically induced/drug therapy/metabolism ; Mice ; *Gastrointestinal Microbiome/drug effects ; Male ; *Colitis, Ulcerative/drug therapy/chemically induced ; Mice, Inbred C57BL ; Colon/drug effects/pathology ; },
abstract = {Hyaluronic acid (HA) is a promising therapeutic candidate for ulcerative colitis (UC), yet how its molecular weight (Mw) governs efficacy and the associated microbiota-linked mechanisms remain insufficiently defined. Here, we systematically evaluated biotechnologically produced HA with distinct Mws (LHA, 2 kDa; MHA, 300 kDa; HHA, 3000 kDa) in a dextran sulfate sodium (DSS)-induced murine colitis model. A Mw-associated protective trend was observed, with HHA showing the most consistent beneficial profile in alleviating clinical manifestations, preserving colonic architecture, and restoring epithelial barrier integrity (Occludin, ZO-1, and mucin). Mechanistically, HHA attenuated systemic inflammation (TNF-α, IL-1β, and LPS) and was associated with modulation of the NF-κB/PPARγ signaling axis. Integrated 16S rRNA sequencing and untargeted metabolomics further revealed that HHA reshaped the gut ecosystem by enriching beneficial genera, including Bifidobacterium and Lactobacillus, and promoted metabolic homeostasis, characterized by increased vitamin B6-related metabolites (pyridoxal) and fatty acids, together with reduced purine metabolism. Molecular dynamics simulations suggested a putative interaction in which microbiota-associated pyridoxal may bind TNF-α, providing a structural hypothesis for the observed attenuation of inflammatory signaling. Moreover, fecal microbiota transplantation (FMT) demonstrated that the HHA-conditioned microbiota was sufficient to confer protection against DSS colitis. Collectively, these findings identify HHA as a bioactive polymer that ameliorates colitis via a coordinated microbiota-metabolism-immunity axis.},
}

Animals
*Hyaluronic Acid/pharmacology/chemistry/therapeutic use
Molecular Weight
Intestinal Barrier Function/drug effects
Dextran Sulfate
*Colitis/chemically induced/drug therapy/metabolism
Mice
*Gastrointestinal Microbiome/drug effects
Male
*Colitis, Ulcerative/drug therapy/chemically induced
Mice, Inbred C57BL
Colon/drug effects/pathology

@article {pmid41944837,
year = {2026},
author = {Weirauch, T and Vehreschild, MJGT},
title = {[Modulation of the gut microbiome for the eradication of multidrug-resistant pathogens: current approaches and perspectives].},
journal = {Bundesgesundheitsblatt, Gesundheitsforschung, Gesundheitsschutz},
volume = {69},
number = {5},
pages = {590-596},
pmid = {41944837},
issn = {1437-1588},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; *Drug Resistance, Multiple, Bacterial ; *Gastrointestinal Microbiome/drug effects ; *Probiotics/therapeutic use ; Evidence-Based Medicine ; *Bacterial Infections/microbiology/therapy ; Treatment Outcome ; *Cross Infection/microbiology/prevention & control ; },
abstract = {The global rise in antibiotic resistance represents one of the greatest threats facing modern medicine. Colonization of the gastrointestinal tract with multidrug-resistant organisms is considered a critical risk factor for nosocomial infections across various patient populations. In this context, targeted decolonization strategies are moving into the focus of clinical research. For a long time, non-absorbable antibiotics were considered a promising approach for local eradication; however, the evidence generated on this question does not suggest sufficient clinical efficacy of this approach. Alternative strategies, such as fecal microbiota transplantation, have shown encouraging results in case reports and small-scale studies for the decolonization of multidrug-resistant organisms. Live biotherapeutic products and certain probiotics are also being explored as potential options for microbiome modulation and reduction of antimicrobial resistance. However, the current evidence base remains heterogeneous, and robust randomized controlled trials are largely lacking. This article aims to provide an overview on the current understanding of gastrointestinal colonization with multidrug-resistant organisms and to discuss the clinical relevance of non-absorbable antibiotics as well as the potential role of microbiome-based therapies in the context of the global antibiotic resistance crisis.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Anti-Bacterial Agents/therapeutic use/administration & dosage
*Drug Resistance, Multiple, Bacterial
*Gastrointestinal Microbiome/drug effects
*Probiotics/therapeutic use
Evidence-Based Medicine
*Bacterial Infections/microbiology/therapy
Treatment Outcome
*Cross Infection/microbiology/prevention & control

@article {pmid41945234,
year = {2026},
author = {Huang, B and An, H and Qiu, Y and Ye, T and Huang, Y and Zheng, M and Shi, D and Su, Y and Wang, R},
title = {Comparative Effectiveness and Safety of Fecal Microbiota Transplantation in Ulcerative Colitis: An Updated Systematic Review and Meta-Analysis.},
journal = {Advances in therapy},
volume = {43},
number = {6},
pages = {2645-2667},
pmid = {41945234},
issn = {1865-8652},
support = {82204925//National Natural Science Foundation of China/ ; 82474290//National Natural Science Foundation of China/ ; CACM-2024-QNRC2-B39//Young Talent Supporting Program of the China Association of Chinese Medicine (CACM)/ ; X2024004//Financial Project of Fujian Province/ ; 2024J01782//Natural Science Foundation of Fujian Province, China/ ; 2025QNGGA002//Fujian Provincial Science and Technology Project in Traditional Chinese Medicine/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Colitis, Ulcerative/therapy ; Randomized Controlled Trials as Topic ; Enema ; Remission Induction ; Treatment Outcome ; Colonoscopy ; },
abstract = {INTRODUCTION: Fecal microbiota transplantation (FMT) is a potential therapy for ulcerative colitis (UC). Evidence has expanded, but the impact of delivery route on efficacy and safety remains uncertain.

METHODS: We systematically searched PubMed, Embase, Cochrane Library, Web of Science and China National Knowledge Infrastructure (CNKI) from inception to October 2025 for randomized controlled trials (RCTs) comparing donor-derived FMT with placebo/sham or autologous FMT in patients with UC. Primary outcomes were clinical and endoscopic remission at induction (8-12 weeks). Adverse events (AEs) were secondary. Random effect models generated risk ratios (RRs) with 95% CIs. Pre-specified subgroup analyses compared delivery routes (colonoscopy, rectal enema, combined colonoscopy + enema, nasoduodenal infusion, oral capsules).

RESULTS: Sixteen RCTs were included. Overall, FMT improved clinical remission (RR = 1.81, 95% CI: 1.41-2.31; I[2] = 0%) and endoscopic remission (RR = 1.74, 95% CI: 1.00-3.01; I[2] = 45.5%). By route, significant effects were seen for colonoscopy (RR = 1.58, 95% CI 1.05-2.37), rectal enema (RR = 1.62, 95% CI 1.04-2.54) and combined colonoscopy + enema (RR = 2.39, 95% CI 1.47-3.89) for clinical remission; nasoduodenal and oral capsule results were imprecise. For endoscopic remission, the combined route showed the most consistent benefit (RR = 2.19, 95% CI 1.04-4.62). AEs did not differ from control (RR = 1.03, 95% CI 0.90-1.18; I[2] = 11.2%).

CONCLUSIONS: FMT improves induction-phase clinical and endoscopic remission in patients with UC without increasing AEs. Efficacy appears route-dependent, with colonoscopy + enema demonstrating the largest effect. Head-to-head trials optimizing route and dosing with longer follow-up are warranted.},
}

Humans
*Fecal Microbiota Transplantation/methods/adverse effects
*Colitis, Ulcerative/therapy
Randomized Controlled Trials as Topic
Enema
Remission Induction
Treatment Outcome
Colonoscopy

@article {pmid41945453,
year = {2026},
author = {Kraeuter, AK and Sarnyai, Z},
title = {Ketogenic diet-derived faecal microbiota transplantation improved sensorimotor gating deficits in an acute NMDA-receptor antagonist model of schizophrenia in mice.},
journal = {Food & function},
volume = {17},
number = {8},
pages = {3529-3536},
doi = {10.1039/d6fo00213g},
pmid = {41945453},
issn = {2042-650X},
mesh = {Animals ; *Schizophrenia/therapy/chemically induced/physiopathology/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; *Fecal Microbiota Transplantation ; *Sensory Gating ; *Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors ; *Diet, Ketogenic ; Disease Models, Animal ; Dizocilpine Maleate ; Gastrointestinal Microbiome ; Feces/microbiology ; },
abstract = {Ketogenic diets (KDs) show promise as a novel treatment for schizophrenia, although its mechanisms of action are still unclear. KDs have been shown to modify the gut microbiota and may exert some of their brain-directed effects through that. We hypothesised that KD-induced changes in the gut microbiota mediate some of the therapeutic effects of KDs in a preclinical model of schizophrenia. To test this hypothesis, we transplanted the gut microbiota through faecal matter obtained from mice maintained on a KD to standard diet-fed mice (faecal microbiota transplantation; FMT) and assessed its effect on a translationally validated endophenotype of psychotic disorders, the sensorimotor gating deficit induced by the NMDA-receptor antagonist MK-801, in mice. Faecal samples were collected from male C57BL/6 mice fed a KD for 4 months and prepared into a liquid for inoculation. Ten-week-old male C57BL/6 mice maintained on a standard diet (SD) received 3 inoculations every second day. One week after the last inoculation, animals received 0.2 mg kg[-1] MK-801 (dizocilpine) to induce a schizophrenia-like sensorimotor gating deficit as measured by the pre-pulse inhibition (PPI) of startle. MK-801 reduced PPI, which was attenuated by the faecal microbial transplant derived from mice fed with a KD. We showed for the first time that FMT through inoculation with KD faeces improved a highly translatable behavioural endophenotype of schizophrenia. Our novel findings confirm that some of the beneficial effects of KDs in schizophrenia are mediated by the gut microbiota.},
}

Animals
*Schizophrenia/therapy/chemically induced/physiopathology/microbiology
Male
Mice
Mice, Inbred C57BL
*Fecal Microbiota Transplantation
*Sensory Gating
*Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors
*Diet, Ketogenic
Disease Models, Animal
Dizocilpine Maleate
Gastrointestinal Microbiome
Feces/microbiology

@article {pmid41945864,
year = {2026},
author = {Jing, S and Lan, X and Liu, Y and Wang, J and Wang, Y and Guo, N},
title = {Rhodotorula dairenensis Affords Protection against Zearalenone-Induced Enterohepatic Toxicity by Regulating Gut Microbiota-Bile Acid-FXR Signaling Pathway.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {15},
pages = {12364-12383},
doi = {10.1021/acs.jafc.5c15173},
pmid = {41945864},
issn = {1520-5118},
mesh = {Animals ; *Receptors, Cytoplasmic and Nuclear/metabolism/genetics ; *Zearalenone/toxicity/metabolism ; Mice ; Receptor, Farnesoid X-Activated ; Signal Transduction/drug effects ; *Gastrointestinal Microbiome/drug effects ; Humans ; *Rhodotorula/metabolism ; *Bile Acids and Salts/metabolism ; Male ; Liver/metabolism/drug effects ; Mice, Inbred C57BL ; Bacteria/isolation & purification/classification/genetics/metabolism ; Intestines/microbiology/drug effects ; Probiotics/administration & dosage ; },
abstract = {Zearalenone (ZEN), a common mycotoxin contaminating crops, poses a threat to animal and human health, making efficient prevention and detoxification critical. A previous study from our group identified that Rhodotorula dairenensis ZDY342B (342B) removes ZEN via adsorption and degradation in vitro, but its in vivo protective effect and mechanism remain unclear. Using a mouse model, gavage with 342B and ZEN showed that 342B reduced ZEN accumulation in various organs, regulated gut microbiota composition and bile acid metabolism, and alleviated ZEN-induced intestinal barrier damage and hepatic inflammation. Antibiotic pretreatment and fecal microbiota transplantation confirmed gut microbiota-mediated 342B's protection, and 342B reduced ZEN's enterohepatic circulation. Inhibiting intestinal farnesoid X receptor (FXR) weakened 342B's protective effect, indicating FXR is the key target. In summary, 342B alleviates ZEN-induced intestinal and hepatic damage by regulating intestinal FXR signaling via the intestinal microbiota, providing a new approach for probiotic-based mycotoxin control.},
}

Animals
*Receptors, Cytoplasmic and Nuclear/metabolism/genetics
*Zearalenone/toxicity/metabolism
Mice
Receptor, Farnesoid X-Activated
Signal Transduction/drug effects
*Gastrointestinal Microbiome/drug effects
Humans
*Rhodotorula/metabolism
*Bile Acids and Salts/metabolism
Male
Liver/metabolism/drug effects
Mice, Inbred C57BL
Bacteria/isolation & purification/classification/genetics/metabolism
Intestines/microbiology/drug effects
Probiotics/administration & dosage

@article {pmid41946028,
year = {2026},
author = {Niu, L and Tan, Y and Cao, W and Wang, E and Qi, F},
title = {Lactobacillus casei serves as a primary functional strain in fecal microbiota-mediated neuroprotection against cerebral ischemia/reperfusion injury.},
journal = {Pathology, research and practice},
volume = {282},
number = {},
pages = {156441},
doi = {10.1016/j.prp.2026.156441},
pmid = {41946028},
issn = {1618-0631},
mesh = {Animals ; *Lacticaseibacillus casei/physiology ; *Reperfusion Injury/microbiology/pathology/prevention & control ; Mice ; Male ; *Brain Ischemia/microbiology/pathology ; *Fecal Microbiota Transplantation/methods ; Mice, Inbred C57BL ; *Neuroprotection/physiology ; *Gastrointestinal Microbiome/physiology ; Disease Models, Animal ; },
abstract = {OBJECTIVE: Cerebral ischemia/reperfusion (I/R) injury leads to neurological impairment, neuroinflammation, and neuronal death. Emerging evidence suggests gut microbiota influence neural function. This study explores the function of fecal microbiota transplantation (FMT) in cerebral I/R injury and explores the primary functional microbiota strain.

METHODS: Mouse models of cerebral I/R injury were generated using middle cerebral artery occlusion and reperfusion. Mice received FMT or L. casei administration, with or without the acetylcholine (ACh) receptor antagonist Benzethonium Chloride (BenC). Neurological function was evaluated using Longa scores, and MWM. Brain injury, neuronal death, and apoptosis were assessed via histological assessments. Neuroinflammation and cholinergic anti-inflammatory pathway (CAIP) activation were examined through ELISA, flow cytometry, immunofluorescence, immunohistochemistry, and western blot analyses. Microbiota composition was determined by 16S rRNA sequencing.

RESULTS: FMT substantially enhanced neurological function, reduced infarct size, ameliorated neuronal death, and restricted pro-inflammatory cytokine concentration and microglial activation. Lactobacillus casei (L. casei) was identified as the predominant strain enriched by FMT, positively correlating with ACh and α7nAChR levels. Both FMT and L. casei treatments restored serum ACh levels, upregulated α7nAChR expression, and increased anti-inflammatory immune cell infiltration, indicating CAIP activation. However, these neuroprotective effects were diminished by BenC, confirming dependence on cholinergic signaling.

CONCLUSION: This study suggests that FMT and L. casei attenuates I/R-induced neurological injury by activating the CAIP, suppressing neuroinflammation, and promoting neuronal survival. These findings highlight L. casei as a key microbiota-derived mediator of gut-brain axis-dependent neuroprotection.},
}

Animals
*Lacticaseibacillus casei/physiology
*Reperfusion Injury/microbiology/pathology/prevention & control
Mice
Male
*Brain Ischemia/microbiology/pathology
*Fecal Microbiota Transplantation/methods
Mice, Inbred C57BL
*Neuroprotection/physiology
*Gastrointestinal Microbiome/physiology
Disease Models, Animal

@article {pmid41946054,
year = {2026},
author = {Tang, S and Peng, Y and Li, Y and Li, Y and Sun, H and Piao, S and Liu, Z and Wu, Y and Hou, Z and Liu, Z and Liu, S and Wang, R},
title = {Congming decoction alleviates Alzheimer's Disease induced by Aβ25-35 in rats via the microbiota-metabolism-inflammation axis, demonstrating its formulation advantages.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {155},
number = {},
pages = {158139},
doi = {10.1016/j.phymed.2026.158139},
pmid = {41946054},
issn = {1618-095X},
mesh = {Animals ; *Alzheimer Disease/drug therapy/chemically induced/metabolism ; *Drugs, Chinese Herbal/pharmacology ; Male ; Rats ; Amyloid beta-Peptides ; *Gastrointestinal Microbiome/drug effects ; Rats, Sprague-Dawley ; Peptide Fragments ; Inflammation/drug therapy/metabolism ; Feces/chemistry ; Brain/drug effects/metabolism/pathology ; Disease Models, Animal ; Chromatography, High Pressure Liquid ; },
abstract = {BACKGROUND: Congming decoction (CMD) is a traditional Chinese herbal formulation traditionally employed for enhancing memory. Despite its historical use, the specific mechanisms and advantages of CMD in the context of Alzheimer's disease (AD) remain inadequately understood.

PURPOSE: This study seeks to elucidate the therapeutic effects of CMD on AD in rats induced by Aβ25-35 and to clarify its underlying process through a multi-perspective approach.

STUDY DESIGN AND METHODS: Cognitive function and pathological alterations were assessed using behavioral tests, hematoxylin and eosin (HE) staining, and immunohistochemistry. Fecal metabolomics analysis, conducted via ultra-high-performance liquid chromatography coupled with quadrupole Orbitrap mass spectrometry (UHPLC-Q-Orbitrap-MS), was utilized to investigate CMD's impact on metabolic disorders. The structure of the gut microbiota was analyzed through 16S rRNA sequencing. Short-chain fatty acids (SCFAs) and bile acids (BAs) in feces, serum, and brain tissue were quantified using gas chromatography-mass spectrometry (GC-MS) and ultra-high-performance liquid chromatography-tandem quadrupole mass spectrometry (UHPLC-TQ-MS). To establish causal relationships, experiments involving antibiotic-induced microbiota depletion (ABX) and fecal microbiota transplantation (FMT) were performed. Network pharmacology and molecular docking techniques were also employed to identify potential active components and targets. Inflammatory markers were evaluated using enzyme-linked immunosorbent assay (ELISA) kits, immunohistochemistry, and immunofluorescence in brain tissue.

RESULTS: CMD markedly enhanced learning and memory, mitigated pathological changes in the brain and colon, and reestablished gut microbiota equilibrium. It regulated 45 endogenous metabolites involved in BAs, α-linolenic acid, and linoleic acid metabolism. CMD also modulated the levels of SCFAs and BAs in fecal matter, serum, and brain tissue. Strong correlations were identified among gut microbiota, metabolites, and AD-related indicators. Antibiotic treatment inhibited the neuroprotective benefits of CMD, whereas FMT from CMD-treated donors successfully replicated its therapeutic benefits. Network pharmacology analysis indicated that the active components of CMD might target inflammatory pathways. Additionally, CMD exhibited a significant restorative impact on markers associated with the AKT/NF-κB signaling pathway.

CONCLUSION: CMD exerts anti-AD effects by modulating the microbiota-gut-brain axis through remodeling gut microbiota, regulating metabolic homeostasis, and reducing brain inflammation. Notably, CMD demonstrated superior efficacy compared to single herbs or herb pairs.},
}

Animals
*Alzheimer Disease/drug therapy/chemically induced/metabolism
*Drugs, Chinese Herbal/pharmacology
Male
Rats
Amyloid beta-Peptides
*Gastrointestinal Microbiome/drug effects
Rats, Sprague-Dawley
Peptide Fragments
Inflammation/drug therapy/metabolism
Feces/chemistry
Brain/drug effects/metabolism/pathology
Disease Models, Animal
Chromatography, High Pressure Liquid

@article {pmid41947174,
year = {2026},
author = {Wu, L and Zhang, Y and Zhang, G and Feng, X and Zhu, W and Yang, H and Ji, X and Yin, M and Li, S and Li, Y and Shi, W and Cong, B},
title = {Microbiota-associated metabolite pantothenic acid enhances skeletal muscle contusion repair via epigenetic regulation of macrophage M2 polarization.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {41947174},
issn = {1479-5876},
support = {82293651//Major Projects of the National Natural Science Foundation of China/ ; 82130055//Key Projects of the National Natural Science Foundation of China/ ; 253A5601D//Hebei Province Innovation Capability Improvement Project/ ; },
mesh = {Animals ; *Macrophages/metabolism/drug effects ; *Muscle, Skeletal/pathology/injuries/drug effects ; *Epigenesis, Genetic/drug effects ; *Pantothenic Acid/pharmacology/metabolism ; *Cell Polarity/drug effects ; Mice, Inbred C57BL ; *Wound Healing/drug effects ; Cell Line ; Mice ; Male ; Cell Differentiation/drug effects ; *Gastrointestinal Microbiome ; Myoblasts/drug effects ; Macrophage Activation/drug effects ; Fecal Microbiota Transplantation ; },
abstract = {BACKGROUND: The quality of skeletal muscle contusion repair hinges on the timely resolution of inflammation and the initiation of regeneration, processes in which M2 macrophage polarization plays a critical role. Nevertheless, the upstream signals that regulate this polarization—particularly specific instructions mediated via the “gut-muscle axis”—remain poorly defined. METHODS: The study was conducted as follows. First, intestinal barrier integrity following skeletal muscle contusion was assessed using histochemical staining and molecular assays. To elucidate the role of the gut microbiota in skeletal muscle repair, dysbiosis models and fecal microbiota transplantation (FMT) were established. Key gut microbiota and metabolites were subsequently identified through 16S rDNA sequencing and untargeted metabolomics analysis of fecal and serum samples. Based on these findings, targeted metabolite intervention experiments were conducted to evaluate their effects on the repair process of skeletal muscle contusion. To delineate the role of macrophages in this context, macrophage depletion was achieved via administration of clodronate liposomes. The impact of the key metabolites on macrophage polarization was then tested both in vivo and in vitro and the subsequent effect of polarized macrophages on C2C12 myoblast differentiation was examined in co-culture system. Finally, we explored the underlying epigenetic mechanisms through which the important metabolites regulates macrophage polarization. RESULTS: Here, we identify a gut microbiota-dependent pathway that facilitates skeletal muscle injury repair. We observed that gut microbiota dysbiosis following skeletal muscle contusion was accompanied by a marked enrichment of the microbial metabolite pantothenic acid (vitamin B5). Functional assays demonstrated that depletion of the gut microbiota severely compromised muscle repair, whereas exogenous supplementation with pantothenic acid significantly enhanced regeneration and attenuated fibrosis. Mechanistically, pantothenic acid exerted its beneficial effects not by acting directly on myocytes, but through remodeling the immune microenvironment. In cultured macrophages, pantothenic acid elevated intracellular acetyl-CoA levels, promoted histone H3 lysine 27 acetylation (H3K27ac) at the promoter of the M2-associated gene Arg1, and acted synergistically with IL-4 to drive macrophage polarization toward the M2 phenotype. This epigenetic regulation was validated in vivo by ChIP-qPCR on macrophages sorted from contused muscles of pantothenic acid-treated mice, confirming that the modification occurs within the muscle microenvironment. This shift in macrophage polarization subsequently promoted myoblast differentiation and maturation. CONCLUSION: Collectively, our findings delineate a comprehensive mechanism whereby a gut microbiota-associated metabolite, pantothenic acid, epigenetically programs macrophage M2 polarization via a “metabolism-epigenetics” axis to accelerate skeletal muscle repair. This work provides a novel conceptual framework for therapeutic interventions targeting the gut-muscle axis.},
}

Animals
*Macrophages/metabolism/drug effects
*Muscle, Skeletal/pathology/injuries/drug effects
*Epigenesis, Genetic/drug effects
*Pantothenic Acid/pharmacology/metabolism
*Cell Polarity/drug effects
Mice, Inbred C57BL
*Wound Healing/drug effects
Cell Line
Mice
Male
Cell Differentiation/drug effects
*Gastrointestinal Microbiome
Myoblasts/drug effects
Macrophage Activation/drug effects
Fecal Microbiota Transplantation

@article {pmid41947394,
year = {2026},
author = {Li, H and Zhao, Y and Luo, Y and Bao, B and Hao, J and Duan, S and Liu, Z},
title = {Goat Milk Fat Globule Membrane Supplementation Ameliorates Alzheimer Disease Cognitive Impairment by Modulating the Gut Microbiota.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {15},
pages = {12054-12068},
doi = {10.1021/acs.jafc.5c11966},
pmid = {41947394},
issn = {1520-5118},
mesh = {Animals ; *Glycolipids/administration & dosage ; *Alzheimer Disease/microbiology/drug therapy/psychology/metabolism ; *Glycoproteins/administration & dosage/metabolism ; *Gastrointestinal Microbiome/drug effects ; Humans ; Lipid Droplets ; Mice ; Male ; Goats ; Dietary Supplements/analysis ; Amyloid beta-Peptides/metabolism ; Bacteria/isolation & purification/classification/genetics ; *Cognitive Dysfunction/drug therapy/microbiology/psychology/metabolism ; Milk/chemistry ; Brain/metabolism/drug effects ; Female ; },
abstract = {Research has found Alzheimer disease (AD) is accompanied by cognitive dysfunction and gut microbiota imbalance. Goat milk fat globule membrane (GMFGM) derived from goat milk, is a membrane primarily composed of proteins and polar lipids that regulates the gut microbiota. However, its role in AD remains unclear. Therefore, we examined the neuroprotective effects of GMFGM in 5xFAD mice. Supplementation with GMFGM (400 mg/kg bw, 8 weeks) improved cognitive performance, reduced brain Aβ deposition, alleviated neuroinflammation, and upregulated neurotrophic factors. Moreover, GMFGM preserved gut barrier integrity, lowered serum LPS levels, and reshaped gut microbiota composition, decreasing Alistipes, Dorea formicigenerans, and Duncaniella dubosii while increasing Stenotrophomonas. Further fecal microbiota transplantation validated the mechanism by which GMFGM ameliorates AD cognitive impairment by modulating the gut microbiota. These results indicate that GMFGM may rescue cognition by modulating the gut microbiota, alleviating gut damage, reducing LPS levels, and consequently inhibiting neuroinflammatory.},
}

Animals
*Glycolipids/administration & dosage
*Alzheimer Disease/microbiology/drug therapy/psychology/metabolism
*Glycoproteins/administration & dosage/metabolism
*Gastrointestinal Microbiome/drug effects
Humans
Lipid Droplets
Mice
Male
Goats
Dietary Supplements/analysis
Amyloid beta-Peptides/metabolism
Bacteria/isolation & purification/classification/genetics
*Cognitive Dysfunction/drug therapy/microbiology/psychology/metabolism
Milk/chemistry
Brain/metabolism/drug effects
Female

@article {pmid41948377,
year = {2026},
author = {Wang, L and Sha, YY and Hu, GY and Qian, YM and Guo, J},
title = {Da Yuan Yin Regulates Gut Microbiota and Improves Intestinal Injury in Sepsis.},
journal = {Food science & nutrition},
volume = {14},
number = {4},
pages = {e71456},
pmid = {41948377},
issn = {2048-7177},
abstract = {Sepsis is a common disease, which is a life-threatening organ dysfunction caused by the host's dysfunctional response to infection. Da Yuan Yin (DYY) is a traditional Chinese medicine that has anti-inflammatory and purgative effects. Sepsis mouse model was conducted by lipopolysaccharide induction to explore the effects of DYY in vivo. Hematoxylin-eosin staining was performed to observe mouse ileum tissue. ELISA and western blot were carried out to measure the levels of inflammatory factors and tight junction proteins. Moreover, proliferation and apoptosis were measured by immunohistochemistry (Ki67) and TUNEL staining. 16S rRNA sequencing was implemented to predict the effects of DYY on gut microbiota in sepsis. Metabolic function was predicted by PICRUSt2 and experimentally validated by measuring short-chain fatty acids (SCFAs) and β-glucuronidase activity. A fecal microbiota transplantation (FMT) experiment was performed to establish causality. In this study, DYY alleviated sepsis-induced intestinal injury. Additionally, DYY inhibited inflammation (TNF-α, IL-1β, and IL-6), cell apoptosis, and promoted proliferation in sepsis, as well as the promotion of tight junction proteins (claudin-1, occludin, and ZO-1). 16S rRNA sequencing revealed that DYY could regulate the alteration in the abundance of gut microbiota in sepsis and promote the growth of bacilli, such as Lactobacillales and Enterobacteriaceae. Functionally, DYY increased protective SCFA levels and suppressed β-glucuronidase activity. Crucially, FMT from DYY-treated donors replicated these protective effects in septic recipients, directly demonstrating the mediatory role of gut microbiota. Collectively, DYY can mitigate intestinal injury and modulates gut microbiota in sepsis; the protective role of DYY on sepsis was mediated through the regulation of gut microbiota, which may be a promising therapeutic strategy for sepsis.},
}

@article {pmid41948520,
year = {2026},
author = {Rynikova, M and Bojcukova, V and Demeckova, V},
title = {One therapy, many targets: redefining ulcerative colitis treatment through fecal microbiota transplantation.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261437918},
pmid = {41948520},
issn = {1756-283X},
abstract = {Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease driven by a multifactorial interplay between gut microbiota dysbiosis, immune dysregulation, and epithelial barrier dysfunction. Accurate diagnosis and a deeper understanding of UC pathogenesis are essential for developing durable and mechanism-based therapies. Despite major advances, conventional treatments such as immunosuppressants and biologics often fail to achieve sustained remission and carry significant adverse effects, underscoring the need for novel, multi-target interventions. This review synthesizes current insights into UC pathogenesis, diagnostic approaches, and therapeutic strategies, with a particular focus on fecal microbiota transplantation (FMT) as a single therapy acting on multiple disease axes. By restoring microbial equilibrium, FMT can modulate host immunity and reinforce epithelial integrity, collectively promoting mucosal healing. We summarize mechanistic evidence, findings from preclinical and clinical studies, and key variables influencing FMT efficacy, including donor selection, preparation, and delivery routes. While evidence supports the therapeutic promise of FMT, challenges remain regarding standardization, long-term engraftment, and sustained safety. Nonetheless, FMT represents a transformative therapeutic platform that redefines UC treatment by bridging microbial restoration, immune modulation, and barrier repair. Future research should aim to refine FMT protocols and develop next-generation microbiota-based therapeutics, such as defined microbial consortia and live biotherapeutic products, to enable safer, more consistent, and personalized modulation of the gut ecosystem in UC.},
}

@article {pmid41948584,
year = {2026},
author = {Yu, J and Liu, X},
title = {Gut microbiota and sepsis: mechanisms, clinical correlations, and therapeutic prospects.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1793041},
pmid = {41948584},
issn = {2296-858X},
abstract = {Sepsis is a life-threatening organ dysfunction triggered by a dysregulated host response to infection. According to the Global Burden of Disease Study, this condition affects over 50 million people annually and causes approximately 5.3 million deaths, with fatality rates varying significantly across populations and healthcare settings, ranging from about 20% to 50%, representing a major challenge in critical care medicine. In recent years, the gut microbiota, as the largest microbial ecosystem in the human body, has increasingly demonstrated a central role. It is not only essential for maintaining intestinal barrier integrity, immune homeostasis, and metabolic balance but also actively participates in the pathogenesis, progression, and outcomes of sepsis through modulating immune responses, influencing the production of key metabolites, and mediating gut-organ axes. This article systematically reviews the characteristics of sepsis-induced gut microbiota dysbiosis, delves into the molecular mechanisms by which dysbiosis drives immune disorders, metabolic disturbances, and multi-organ injury, evaluates the clinical potential and current limitations of microbiome-associated biomarkers, and summarizes recent advances and controversies in microbiota-targeted therapeutic strategies, including probiotics, fecal microbiota transplantation, precision nutrition, and antibiotic stewardship. This review aims to analyze the shortcomings and translational challenges in current research, providing a theoretical basis and forward-looking perspective for developing precise microbiome-based individualized management strategies for sepsis.},
}

@article {pmid41950979,
year = {2026},
author = {Khoruts, A and Kuchma, N and Vaughn, BP},
title = {Fecal Microbiota Transplantation Rapidly Reduces Systemic Inflammation and Resolves Clostridioides difficile Pseudomembranous Colitis.},
journal = {Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cgh.2026.03.023},
pmid = {41950979},
issn = {1542-7714},
}

@article {pmid41951277,
year = {2026},
author = {Bajer, L and Polakovicova, P and Heczkova, M and Holm, K and Hole, MJ and Hlavaty, M and Bohdanecka, A and Drastich, P and Tichanek, F and Meyer-Myklestad, MH and Medhus, AW and Reikvam, DH and Jørgensen, KK and Brezina, J and Macinga, P and Wohl, P and Fabian, O and Hov, JR and Cahova, M},
title = {Geography-independent mucosal microbiota alterations in primary sclerosing cholangitis persist after liver transplantation.},
journal = {JHEP reports : innovation in hepatology},
volume = {8},
number = {4},
pages = {101716},
pmid = {41951277},
issn = {2589-5559},
abstract = {BACKGROUND & AIMS: Primary sclerosing cholangitis (PSC)-associated alterations of fecal gut microbiota have already been described, but data on the mucosal microbiota are still limited. We aimed to further define disease-specific mucosal microbial patterns independent of geography and assess the relationship to liver transplantation (LTx), gut inflammation (inflammatory bowel disease), and PSC recurrence (rPSC).

METHODS: We performed 16S ribosomal RNA gene (V3-V4) sequencing of ileocolonic biopsies from 115 patients with PSC (pre-LTx), 159 liver-transplanted patients (post_LTx, recurrence occurred in 38), and 96 healthy controls (HC) from Norway and the Czech Republic.

RESULTS: Alpha diversity was lower in all PSC groups compared with HC. Elastic net models discriminated pre_LTx (AUC ileum 0.97; colon 0.93; p <0.001) and post_LTx PSC patients (AUC ileum 0.97; colon 0.97; p <0.001) from HC, and distinguished pre_LTx from post_LTx (AUC ileum 0.83; colon 0.83; p <0.001). The shared, cohort-independent PSC microbiota was dominated by Enterococcus, Pseudomonas, Veillonella, Klebsiella, and Streptococcus, while several common commensals were underrepresented. A microbial dysbiosis index calculated from PSC-associated genera correlated negatively with alpha diversity and serum albumin, while a positive correlation was observed with markers of cholestatic disease (ALP, GGT) and liver fibrosis (APRI). There were no associations with the presence of inflammatory bowel disease or fecal calprotectin. Differences between post-LTx patients with and without recurrence were limited, but several genera deregulated in pre-LTx PSC (Klebsiella, Bilophila, Coprococcus, Odoribacter) showed similar trends in rPSC.

CONCLUSIONS: Our findings in two European countries revealed a distinct mucosal microbiota composition associated with PSC that persists after LTx. These microbial patterns correlate with the severity of liver injury in PSC but not with markers of intestinal inflammation.

IMPACT AND IMPLICATIONS: This study provides an extensive evaluation of mucosa-associated microbiota in primary sclerosing cholangitis (PSC) before and after liver transplantation across two European cohorts. The persistence of PSC-related dysbiosis after transplantation highlights the importance of the gut-liver axis in PSC and supports further investigation into microbiota-driven mechanisms. Together with the strong association between microbiota composition and markers of cholestasis and fibrosis, this suggests potential clinical utility as an indicator of disease activity or even as a target for prevention or therapy.},
}

@article {pmid41951653,
year = {2026},
author = {He, L and Yuan, D and Li, Q and Zhang, X and Niu, K and Li, X and Ou, Y and Du, H and Yuan, J and Duan, Y and Niu, H},
title = {Fecal virome transplantation attenuates arthritis in mice by remodeling gut ecology, systemic tryptophan metabolism, and innate immune responses.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {41951653},
issn = {2055-5008},
support = {2024VPPC-S02//the Open Project of the Key Laboratory of Viral Pathogenesis and Infection Prevention and Control (Jinan University), Ministry of Education/ ; 2025A1515012786//the Natural Science Foundation of Guangdong Province/ ; 2022YFF0710702 and 2022YFF0710701//the National Key &D Programs of China/ ; 202201020381//the Guangzhou Joint Fund for Key Laboratory/ ; YXJC2022004//the Medical Joint Fund of Jinan University/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; *Tryptophan/metabolism ; Mice ; *Immunity, Innate ; RNA, Ribosomal, 16S/genetics ; *Arthritis, Rheumatoid/therapy/immunology ; *Virome ; Disease Models, Animal ; Feces/microbiology/virology ; Cytokines/blood ; Metabolomics ; Bacteria/classification/genetics ; Male ; },
abstract = {Rheumatoid arthritis (RA) is an autoimmune disorder characterized by chronic joint inflammation and systemic immune dysregulation. Emerging evidence suggests that the gut microbiome plays an important role in immune modulation in RA, yet the role of the gut virome remains poorly understood. Here, using the K/BxN serum-transfer arthritis model, we systematically evaluated the potential role of fecal virome transplantation (FVT) in modulating gut ecology and innate inflammatory responses. Arthritic mice exhibited marked alterations in gut virome composition compared with healthy controls. Administration of purified virus-like particles (VLPs) from healthy donors correlated with reductions in paw swelling, histopathological inflammation, bone erosion, circulating proinflammatory cytokines, and myeloid cell infiltration in inflamed tissues. In parallel, 16S rRNA sequencing showed that FVT remodeled the gut bacterial community toward a composition more similar to that of healthy controls. Targeted serum metabolomics revealed increased levels of microbiota-derived tryptophan metabolites, including indole-3-lactic acid and related indole derivatives, suggesting a link between gut microbial remodeling and systemic immunometabolic regulation. Collectively, these findings indicate that FVT may attenuate inflammatory arthritis by remodeling gut microbial ecology, potentially involving virome-bacteriome interactions and immunometabolic pathways.},
}

Animals
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
*Tryptophan/metabolism
Mice
*Immunity, Innate
RNA, Ribosomal, 16S/genetics
*Arthritis, Rheumatoid/therapy/immunology
*Virome
Disease Models, Animal
Feces/microbiology/virology
Cytokines/blood
Metabolomics
Bacteria/classification/genetics
Male

@article {pmid41951771,
year = {2026},
author = {Liu, LM and He, XF and Zhang, YL and Zhou, JT and Miao, H and Zhao, YY},
title = {Gut microbiota and renal fibrosis: novel mechanistic insights and therapeutic potential.},
journal = {Acta pharmacologica Sinica},
volume = {47},
number = {8},
pages = {2023-2034},
pmid = {41951771},
issn = {1745-7254},
mesh = {Humans ; Animals ; *Gastrointestinal Microbiome/drug effects/physiology ; Probiotics/therapeutic use ; Fibrosis ; Dysbiosis ; *Acute Kidney Injury/microbiology/pathology/therapy ; *Renal Insufficiency, Chronic/microbiology/pathology/therapy ; *Kidney/pathology ; },
abstract = {Kidney diseases, including acute kidney injury (AKI) and chronic kidney disease (CKD), are associated with changes in the composition and function of gut microbiota. Available evidence has delineated that both AKI and CKD were associated with microbial dysbiosis that led to impairment of the intestinal epithelial cell barrier, decreasing the abundance of beneficial bacteria (Lactobacillus reuteri and Bifidobacterium animalis), and increasing the abundance of pathogenic bacteria (Eggerthella lenta and Fusobacterium nucleatum). This was accompanied by the alteration in microbial-derived metabolites, including reducing short-chain fatty acid production and accumulating uremic toxins, such as indoxyl sulphate, indole-3-acetic acid (IAA), and trimethylamine-N-oxide (TMAO), thereby exacerbating renal inflammation and fibrosis. However, supplementation with probiotics, such as Parabacteroides goldsteinii, Lactobacillus johnsonii, Bacteroides ovatus and Bacteroides fragilis, attenuated renal fibrosis by the regulation of nuclear factor κB, NLR family pyrin domain containing 3 inflammasome, aryl hydrocarbon receptor, sodium-glucose transport 2, farnesoid X receptor, glucagon-like peptide-1 receptor, and nuclear factor erythroid 2-related factor 2 signalling pathways via microbial-derived metabolites, such as IAA, TMAO, indole-3-aldehyde, hyodeoxycholic acid and 1,5-anhydroglucitol. This review elaborates on the microbial dysbiosis-related renal pathogenesis and discusses therapeutic potential and targets of renal fibrosis. Further, targeting modulation of gut microbiota by several cardinal approaches, such as probiotics, natural products (neohesperidin, madecassoside, and polysaccharides), and fecal microbiota transplant, are also highlighted. However, these therapeutic approaches need to be further evaluated by large controlled trials. These findings expand the understanding of microbial dysbiosis-associated underlying molecular mechanisms of renal fibrosis in the host and elucidate a clear pathophysiological rationale for the intervention of renal fibrosis.},
}

Humans
Animals
*Gastrointestinal Microbiome/drug effects/physiology
Probiotics/therapeutic use
Fibrosis
Dysbiosis
*Acute Kidney Injury/microbiology/pathology/therapy
*Renal Insufficiency, Chronic/microbiology/pathology/therapy
*Kidney/pathology

@article {pmid41952403,
year = {2026},
author = {El-Salhy, M and Corsetti, M and Gilja, OH and Gonlachanvit, S and Hatlebakk, JG and Hoff, DAL and Lahtinen, P and Lunding, JA and Mazzawi, T and Monaghan, TM and Ohlsson, B and Patcharatrakul, T and Kim, YS and Shin, CM},
title = {Towards a Standard Protocol for Fecal Microbiota Transplantation in Irritable Bowel Syndrome.},
journal = {Journal of neurogastroenterology and motility},
volume = {32},
number = {2},
pages = {185-197},
pmid = {41952403},
issn = {2093-0879},
abstract = {Randomized controlled trials (RCTs) of fecal microbiota transplantation (FMT) in patients with irritable bowel syndrome (IBS) have produced outcomes varying from no effect at all to high efficacy and durable effects over time. This review analyzed differences in the protocols used in FMT RCTs for IBS in the recently published literature with the aim of identifying the factors responsible for the success or failure of these RCTs. The results of this analysis might be useful in formulating an effective standard protocol for FMT in IBS. A systematic search was conducted in the PubMed database of the literature published in English from January 2015 to December 2023 using several search phrases comprising MeSH expressions. Those RCTs that carefully selected donors based on environmental factors that are known to affect the gut microbiota positively and ensured bacterial diversity before and during FMT produced successful outcomes. Furthermore, direct freezing of the donor's fecal transplant, storing it at -80°C until the FMT is performed, and then thawing it at 4°C and mixing it manually appear to be factors associated with the success of FMT in IBS. Administering the donor's fecal transplant into the small intestine results in durable effects of FMT and long-term colonization of beneficial bacteria. A standard protocol for FMT with large and durable effects should include (1) careful donor selection, (2) handling the donor's fecal transplant in a way that preserves its microbiota contents, and (3) administering the transplant into the small intestine.},
}

@article {pmid41953022,
year = {2026},
author = {Han, W and Li, Q and Yuan, G},
title = {The gut microbiome as an actionable drug-sensitivity modulator for immune checkpoint blockade: clinical evidence for FMT, live biotherapeutics, and defined consortia.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1802676},
pmid = {41953022},
issn = {1664-3224},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/adverse effects ; Animals ; },
abstract = {Immune checkpoint inhibitors (ICIs) deliver durable benefit to only a subset of patients and can be limited by immune-related adverse events (irAEs). The gut microbiome has emerged as an actionable, host-level modulator of ICI drug sensitivity and toxicity. This mini-review links microbial ecology to antigen presentation, T-cell priming and fitness, metabolite signaling, and barrier inflammation, and summarizes interventional evidence across three modalities. Responder-derived fecal microbiota transplantation (FMT) provides the strongest proof-of-concept for re-sensitization in anti-PD-1-refractory melanoma. Microbiome repair can also improve refractory ICI-associated colitis. Early trials of live biotherapeutics and defined consortia support scalability but highlight context dependence and design pitfalls, including antibiotic preconditioning. We discuss practical determinants of reproducibility, including co-medications, diet, engraftment and functional readouts, and conclude with safety, regulatory, and reporting priorities for clinically deployable microbiome engineering.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/adverse effects
Animals

@article {pmid41953448,
year = {2026},
author = {Bautista, J and López-Cortés, A},
title = {Biohacking the human gut microbiome for precision health and therapeutic innovation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1776983},
pmid = {41953448},
issn = {1664-302X},
abstract = {Biohacking, the self-directed application of biotechnology, digital tools, and lifestyle interventions, has rapidly converged with gut microbiome science to create adaptive, individualized, and minimally invasive precision-health paradigms. This narrative review integrates current evidence on diet-based modulation, microbial therapeutics (probiotics, prebiotics, postbiotics, and fecal microbiota transplantation), and synthetic-biology approaches (engineered strains and phage or synthetic consortia) within a multi-omics and continuous-phenotyping framework. Mechanistically, short-chain fatty acids (SCFAs), bile-acid derivatives, and tryptophan catabolites operate as endocrine-like mediators linking gut microbial ecology with host immunity, metabolism, and neuroendocrine signaling. Pathways mediated by microbial metabolites underpin translational applications that span metabolic optimization, through improved insulin sensitivity, reduced adiposity, and attenuation of inflammation, and neurocognitive enhancement via the microbiome-gut-brain axis. Evidence from oncology further indicates that microbial metabolites and engineered taxa remodel stromal and immune niches, shaping therapeutic response and disease progression. Concurrently, emerging digital infrastructures, wearables, biosensors, metabolic avatars, and AI-driven "health twins," enable real-time, closed-loop modulation of host-microbe dynamics. Persistent challenges include methodological heterogeneity, safety concerns regarding live biotherapeutics and unsupervised fecal microbiota transplantation (FMT), fragmented regulation, and vulnerabilities in cyberbiosecurity and data equity. We propose a translational roadmap emphasizing standardized metadata (STORMS), validated reference frameworks, longitudinal multi-omics for causal inference, strain-level safety genomics, and governance integrating ethical and cybersecurity oversight. Under these conditions, microbiome-focused biohacking may evolve from anecdotal experimentation into a more reproducible and scientifically grounded component of preventive and personalized medicine. This manuscript is presented as a narrative and conceptual review, integrating validated microbiome research with emerging biohacking frameworks while explicitly distinguishing evidence-based findings from exploratory or speculative concepts.},
}

@article {pmid41955275,
year = {2026},
author = {Santens, P and Bruggeman, A and Laukens, D and Vandenbroucke, RE},
title = {Faecal microbiota transplant for Parkinson's disease.},
journal = {Brain : a journal of neurology},
volume = {149},
number = {8},
pages = {e65},
doi = {10.1093/brain/awag123},
pmid = {41955275},
issn = {1460-2156},
}

@article {pmid41956787,
year = {2026},
author = {Ye, JJ and Pan, YL and Wang, J and Lyu, Y},
title = {[Research advances on hepatic encephalopathy following transjugular intrahepatic portosystemic shunt].},
journal = {Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology},
volume = {34},
number = {3},
pages = {249-255},
pmid = {41956787},
issn = {1007-3418},
support = {82370619//National Natural Science Foundation of China/ ; XJZT24LY33//Medical Staff Training Promotion Project of Xijing Hospital, Air Force Medical University/ ; },
mesh = {*Hepatic Encephalopathy/etiology/prevention & control ; Humans ; *Portasystemic Shunt, Transjugular Intrahepatic/adverse effects ; Hypertension, Portal/surgery ; *Postoperative Complications/prevention & control/etiology ; Risk Factors ; },
abstract = {Transjugular intrahepatic portosystemic shunt (TIPS) is an important therapeutic method for complications of portal hypertension in cirrhosis, but the high incidence rate of postoperative hepatic encephalopathy seriously affects patient prognosis. Current research focuses on the core mechanisms and intervention methods specific to or related to TIPS, clarifying that the risk factors for hepatic encephalopathy are centered on perioperative TIPS parameters (stent diameter, portosystemic venous pressure gradient, spontaneous portosystemic shunt). The pathogenesis is key to shunt-related ammonia metabolism imbalance, hemodynamic abnormalities, and gut-hepatic-brain axis abnormalities. Prevention and treatment strategies revolve around a comprehensive management system of "preoperative risk stratification-intraoperative precise shunt-postoperative targeted intervention," emphasizing TIPS-specific procedures such as stent optimization, spontaneous portosystemic shunt closure, and flow-limiting stents, as well as targeted technologies like fecal microbiota transplantation and artificial intelligence risk prediction, ultimately providing practical evidence for the precise prevention and treatment of hepatic encephalopathy following TIPS.},
}

*Hepatic Encephalopathy/etiology/prevention & control
Humans
*Portasystemic Shunt, Transjugular Intrahepatic/adverse effects
Hypertension, Portal/surgery
*Postoperative Complications/prevention & control/etiology
Risk Factors

@article {pmid41957048,
year = {2026},
author = {Wang, X and Song, Y and Zhao, W and Liu, Y and Fu, Y and Zhang, Y and Zhao, Q and Miao, M and Zhao, W and Wang, X and Li, Z},
title = {Cinnamaldehyde mitigates MASLD through SIRT1/FOXO1-induced autophagy and synergistic gut microbiota modulation.},
journal = {NPJ science of food},
volume = {10},
number = {1},
pages = {},
pmid = {41957048},
issn = {2396-8370},
support = {ZYYZDXK-2023005//National Administration of Traditional Chinese Medicine Key Discipline Construction Project of High-Level TCM/ ; 82304831//National Natural Science Foundation of China/ ; 242300421090//Henan Science Fund for Excellent Young Scholars/ ; 2023TQ0109, GZB20230196//China Postdoctoral Science Foundation/ ; 232301420077//Associates Fund of Henan Province science and technology research and development program/ ; 2025HYTP092//Young Talent Support Program of Henan Association for Science and Technology/ ; NA (2024)//Central Plains Science and Technology Innovation Young Top Talent Project/ ; },
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is a global health burden with limited therapeutic options. Cinnamomum cassia, a medicinal-food homologous plant, contains principal bioactive cinnamaldehyde (CA), whose anti-MASLD mechanisms require clarification. ‌This study employed both a high-fat diet (HFD)-induced MASLD model and a free fatty acid (FFA)-stimulated cell model. CA administration attenuated intracellular lipid accumulation in vitro and ameliorated both hepatic steatosis and systemic hyperlipidemia in vivo, while inhibiting hepatic lipid peroxidation. Mechanistically, integrated RNA-seq, network pharmacology, siRNA, immunofluorescence, and transmission electron microscopy analyses identified the SIRT1/FOXO1-autophagy axis as CA's key regulatory pathway. Gut microbiome profiling revealed CA's capacity to ameliorate HFD-induced dysbiosis, particularly enriching Lachnospiraceae_NK4A136. Fecal microbiota transplantation (FMT) and Spearman correlations link serum lipids and hepatic injury factors to gut microbiota, indicating partially microbiota-mediated metabolic modulation by CA. Collectively, CA ameliorates MASLD through coordinated autophagy enhancement and microbial homeostasis restoration, holding promise as a functional food ingredient for ‌metabolic liver disease prevention.},
}

@article {pmid41957631,
year = {2026},
author = {Cheng, J and Le, S and Wang, D and Liu, P and Liu, C and Shen, D and Wang, D},
title = {Gut microbiota dysfunction mediates stress-exacerbated aortic dissection via the bacteroides vulgatus-outer membrane vesicles-stearic acid-JNK/MAPK axis.},
journal = {Journal of nanobiotechnology},
volume = {24},
number = {1},
pages = {},
pmid = {41957631},
issn = {1477-3155},
support = {LHGJ20230213//Joint Construction project of Henan Medical Science and Technology/ ; },
mesh = {Animals ; Mice ; *Gastrointestinal Microbiome/physiology ; Male ; *Aortic Dissection/metabolism/microbiology ; Mice, Inbred C57BL ; *Bacteroides/metabolism ; Disease Models, Animal ; MAP Kinase Signaling System ; Bacterial Outer Membrane/metabolism ; Fecal Microbiota Transplantation ; Myocytes, Smooth Muscle/metabolism ; Dissection, Thoracic Aorta ; Stearic Acids ; },
abstract = {BACKGROUND: Aortic dissection (AD) is a lethal condition involving vascular smooth muscle cell (VSMC) transformation and extracellular matrix degradation. While gut microbiota dysbiosis is implicated in cardiovascular diseases, its role in stress-exacerbated AD pathogenesis is unknown. This study investigates the mechanism linking chronic restraint stress (CRS) to AD progression via gut microbiota modulation.

METHODS: A β-aminopropionitrile (BAPN)-induced AD mouse model combined with CRS was utilized. Aortic dilation, mortality, and VSMC phenotype shift (assessed via α-SMA/SM22α and OPN/MMP2 expression) were evaluated. Gut microbiota composition was analyzed using 16 S rRNA sequencing. Microbiota depletion was achieved via antibiotics, and fecal microbiota transplantation (FMT) from CRS-exposed mice was performed. Serum metabolomics analysis, incorporating liquid chromatography-mass spectrometry (LC-MS), has demonstrated that outer membrane vesicles (OMVs) derived from Bacteroides vulgatus (B. vulgatus) contain high levels of the key metabolite stearic acid (SA). In vitro effects of stearic acid (SA) on AngII-induced JNK phosphorylation in VSMCs were tested, with validation using the JNK agonist anisomycin. Statistical analyses included correlation tests and appropriate comparisons (e.g., t-tests, ANOVA).

RESULTS: CRS significantly accelerated aortic dilation, increased mortality, and promoted a synthetic VSMC phenotype (decreased α-SMA/SM22α, increased OPN/MMP2) in BAPN-treated mice. 16 S sequencing revealed CRS reduced gut microbiota diversity, particularly depleting B. vulgatus, which correlated negatively with AD severity. Antibiotic-mediated microbiota ablation mitigated CRS-aggravated AD, while FMT from CRS mice exacerbated it. Metabolomics identified stearic acid (SA), a metabolite derived from OMVs of B. vulgatus, as negatively correlated with aortic diameter. SA supplementation inhibited VSMC synthetic transformation, reduced AD incidence, and suppressed JNK/MAPK pathway activation in vivo. Mechanistically, SA attenuated AngII-induced JNK phosphorylation in VSMCs in vitro, an effect reversed by the JNK agonist anisomycin.

CONCLUSIONS: CRS exacerbates the pathogenesis of AD by disrupting the gut microbiota, particularly by reducing the abundance of B. vulgatus and the levels of SA, which is a metabolite encapsulated in the OMVs of B. vulgatus. This leads to unchecked JNK/MAPK signaling, driving detrimental VSMC transformation. Restoration of SA inhibits this pathway and mitigates AD progression. Targeting the gut microbiota-B. vulgatus-SA axis presents a novel therapeutic strategy for stress-aggravated AD.},
}

Animals
Mice
*Gastrointestinal Microbiome/physiology
Male
*Aortic Dissection/metabolism/microbiology
Mice, Inbred C57BL
*Bacteroides/metabolism
Disease Models, Animal
MAP Kinase Signaling System
Bacterial Outer Membrane/metabolism
Fecal Microbiota Transplantation
Myocytes, Smooth Muscle/metabolism
Dissection, Thoracic Aorta
Stearic Acids

@article {pmid41959053,
year = {2026},
author = {Midani, FS and Lee, DH and Moon, Y and Seale, M and Horvath, TD and Ardis, AK and Cantú, J and Coles, E and Pizzini, JD and Zhu, D and Dooling, SW and Ahern, GJ and Ardis, CK and Beckford, A and Ruggiero, NM and Shin, J and Joos, R and Stanton, C and Ross, RP and Dai, DLY and Mandhane, PJ and Petersen, C and Turvey, SE and Kiely, ME and Murray, DM and Costa-Mattioli, M and Tolias, KF and Britton, RA and Danhof, HA},
title = {Infant gut microbiomes contribute to metabolic states that impact brain function.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
pmid = {41959053},
issn = {2692-8205},
abstract = {Alterations in the gut microbiome are associated with neurodevelopmental disorders, but causal mechanisms and therapeutic strategies remain undefined. Here, we demonstrate that human infant microbiomes isolated during the first six months of life drive behavioral impairments in mice and that microbiota-based interventions restore mice to normal behavior. Early-life microbiomes from twelve infants who later exhibited cognitive deficits at 2 years old (low-scoring) transferred adverse metabolic, brain, and behavioral phenotypes to mice, in contrast to microbiomes from twenty-three cognitively typical or high-scoring infants. Deficits in mice were rescued by fecal microbiota transplant from high-scoring infants or a rationally designed consortium that promoted amino acid levels. We confirmed lower fecal amino acid concentrations in low-scoring infants and replicated the association between early-life microbiome composition and cognitive outcomes in a second geographically independent infant cohort. Altogether, we discovered an early-life microbiome-mediated metabolic state causally linked to cognitive deficits and amenable to microbial intervention.},
}

@article {pmid41959551,
year = {2026},
author = {Lv, W and Hu, H and Huang, Y and Yang, J and Li, Y and He, J and Wang, K and Liu, Y and Wang, Q},
title = {Microbial mechanisms and therapeutic interventions in the periodontitis-inflammatory bowel disease axis: a comprehensive review.},
journal = {Journal of oral microbiology},
volume = {18},
number = {1},
pages = {2656084},
pmid = {41959551},
issn = {2000-2297},
abstract = {BACKGROUND: Periodontitis and inflammatory bowel disease (IBD) are chronic inflammatory conditions of the oral and gastrointestinal tracts that exhibit bidirectional microbial and immunological crosstalk.

OBJECTIVE: Aimed at elucidating the bidirectional crosstalk between periodontitis and IBD at both microbiological and immunological levels and evaluate related therapeutic interventions, this review comprehensively summarizes recent evidence on their interaction via the oral-gut-bone axis, focusing on microbial ecology, host responses, and innovative therapies.

DESIGN: Distinct yet overlapping dysbiotic signatures are observed in both diseases, with periodontal pathogens such as Porphyromonas gingivalis and Fusobacterium nucleatum capable of translocating to the gut and perturbing intestinal homeostasis, while gut inflammation reciprocally reshapes the oral microbiome. Mechanistic links include a spectrum of convergent pathways: (i) microbial metabolites-short-chain fatty acids, choline metabolites, indole derivatives, polyamines, and bile acids-that modulate barrier integrity and immune responses; (ii) shared immune cells and inflammatory mediators driving mucosal damage at both sites; (iii) bacterial extracellular vesicles (BEVs) and lysine lactylation (Kla)-mediated signaling; and (iv) oxidative stress, iron metabolism dysregulation, and ferroptosis contributing to tissue destruction.

RESULTS: Therapeutic strategies targeting this axis encompass bidirectional interventions: periodontal and IBD treatments that mutually influence oral and gut health, natural anti-inflammatory and antimicrobial compounds, probiotics and prebiotics, oral and fecal microbiota transplantation, and emerging bacteriophage therapy. Critically, the clinical translation of collaborative dentistry-gastroenterology management is highlighted as a promising avenue for integrated care.

CONCLUSIONS: By integrating findings across microbial ecology, host response, and therapeutic innovation, this review provides a comprehensive framework for understanding and targeting the periodontitis-IBD axis.},
}

@article {pmid41960434,
year = {2026},
author = {Yao, W and Yan, S and Du, R and Zhao, Y and Zhang, H and Wang, B and Cheng, X and Ma, Z and Bao, S and Li, X and Song, Y},
title = {Eucommia polysaccharides alleviate experimental colitis by reshaping colonic microbiota composition, metabolites, and modulating the IL-17 signaling pathway.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1769429},
pmid = {41960434},
issn = {1664-302X},
abstract = {Intake of plant polysaccharides are associated with a reduced risk of ulcerative colitis (UC). Eucommia polysaccharides (EUPs) are promising nutritional supplements with notable antibacterial, anticancer, and anti-inflammatory properties. They exhibit a moderate molecular weight and are resistant to gastric acid degradation. Yet, the action mechanisms of microorganisms and metabolites in EUPs for UC treatment remain incompletely elucidated. The current study was formulated to assess the therapeutic efficacy of EUPs against fecal microbiota transplantation (FMT)-induced colitis, focusing on comparing the effects of low-dose and high-dose EUPs. After East Frisian sheep received dextran sulfate sodium (DSS) intervention, their fecal microbiota was used to prepare fecal bacterial suspensions for mouse FMT. Administration of high-dose EUPs alleviated key colitis symptoms, improved colonic epithelial barrier, preserved microbial diversity, and significantly reduced harmful bacterial (e.g., g_Klebsiella and g_unidentified_Enterobacteriaceae). Furthermore, this treatment significantly enriched the bile secretion pathways, particularly those involving deoxycholic acid (DCA) and hyodeoxycholic acid (HDCA). Additionally, DCA and HDCA were significantly negatively correlated with g_unidentified_Enterobacteriaceae and g_Klebsiella, and these two bile acids were also negatively correlated with key genes associated with the IL-17 signaling pathway. Overall, this study elucidates that EUPs ameliorate FMT-induced colitis in a mouse model via restoring gut microbes and metabolites and modulating the IL-17 pathway, thereby providing novel insights into therapeutic strategies for UC.},
}

@article {pmid41960919,
year = {2026},
author = {van Leeuwen, PT and Gadaleta, P and Brul, S and Seppen, J and Wortel, MT},
title = {Environmentally mediated interactions predict community assembly and invasion success in a gut microbiota synthetic community.},
journal = {mSystems},
volume = {11},
number = {5},
pages = {e0011326},
pmid = {41960919},
issn = {2379-5077},
mesh = {*Gastrointestinal Microbiome/physiology ; Coculture Techniques ; Bacteroides/growth & development ; Escherichia coli/growth & development ; Humans ; *Microbial Interactions ; Models, Biological ; },
abstract = {The gut microbiome plays a crucial role in host homeostasis, with implications for nutrition, immune development, metabolism, and protection against pathogens. Disturbance of the microbiome by microbial invasion can be negative or positive: invasions of opportunistic pathogens can cause disease while dysbiotic states need invasions to recover. However, the complexity of the microbiome challenges our understanding of what factors determine the ability of microbes to invade. In this study, we measure interactions between members of a synthetic community of prominent gut bacteria using supernatant assays, which quantify the growth of one species in the cell-free culture medium of another. We measure relative abundances of co-cultures of up to four species to validate a generalized Lotka-Volterra model parameterized with these supernatant assays. We predict differential invasion outcomes of the opportunistic pathogens Escherichia coli and Bacteroides ovatus based on their monoculture growth profiles and interactions with other species, and we experimentally confirm model predictions of invasion success. The predictive value of our model indicates that environmentally mediated interactions, e.g., through soluble chemicals, primarily determine co-culture abundances and invasion success. Furthermore, model analyses show that negative interactions within the resident community and neutral to positive interactions with the invading species promote invasion success, but the interactions toward the invading species dominate. Our validated approach opens the way for testing of interactions of human gut microbiome species, thereby developing interventions to avoid pathogenic overgrowth and therapies to enhance health-benefitting invasions.IMPORTANCEThe stability of the human gut microbiome is crucial for host health, with opportunistic pathogen invasions causing diseases and healthy strain replacements needed for recovery. The microbiota's complexity complicates the understanding of invasion outcomes. This study uses a 10-species synthetic community of common gut microbiota to predict stable communities and invasion success. We grow cells in the growth medium of other species with the cells removed to parameterize a computational model, accurately predicting community composition up to four species and invasion success of Escherichia coli and Bacteroides ovatus. Our findings show that interactions through soluble compounds in the environment dictate co-culture growth and invasions. Furthermore, model analysis shows that interactions within the resident community and toward the invader are both important, but the latter dominate. These results pave the way for larger-scale studies to characterize gut microbiome interactions and properties that resist invasions, potentially benefiting health through improved probiotics and fecal microbiota transplants.},
}

*Gastrointestinal Microbiome/physiology
Coculture Techniques
Bacteroides/growth & development
Escherichia coli/growth & development
Humans
*Microbial Interactions
Models, Biological

@article {pmid41963684,
year = {2026},
author = {Mc Closkey, C and El-Hakeem, AA and Gafar, ME and Slattery, E},
title = {Trends in Clostridioides Difficile Hospitalisations in Ireland (2009-2022).},
journal = {Irish journal of medical science},
volume = {},
number = {},
pages = {},
pmid = {41963684},
issn = {1863-4362},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired infection associated with significant morbidity, mortality and healthcare costs. Comparisons of disease burden between countries are complicated by heterogeneity in diagnostic testing and surveillance practices. AIMS: To quantify CDI-related hospitalisations in Ireland between 2009 and 2022 and to examine temporal trends in patient demographics, length of stay (LOS), admission type, and in-hospital mortality. METHODS: We conducted a retrospective analysis of the national Hospital Inpatient Enquiry (HIPE) database, including all discharges from Irish public hospitals coded with CDI (ICD-10-AM A04.7) between 2009 and 2022. Temporal trends were examined, and multivariable logistic regression was conducted using SPSS (v30) to identify factors independently associated with in-hospital mortality. RESULTS: Between 2009 and 2022, 20,956 CDI-related hospitalisations were recorded, accounting for approximately 0.2% of all hospitalisations in Ireland. Annual CDI-related hospitalisations increased by 66%, from 1,301 in 2009 to 1,962 in 2022. Over the same period, in-hospital mortality declined from 21.0% to 11.8%, and mean LOS decreased from 44.0 to 31.5 days. Logistic regression adjusting for age, sex, LOS, admission type, and year of hospitalisation, found the odds of in-hospital mortality were approximately 45% lower in 2022 versus 2009. Increasing age was the strongest independent predictor of mortality; patients aged ≥ 85 years had 72-fold higher odds of mortality compared with the youngest age group. CDI was recorded as the primary diagnosis in 28% of hospitalisations and was associated with lower mortality (adjusted OR 0.36, p < 0.001). Male sex (adjusted OR 1.26, p < 0.001) and elective admission (adjusted OR 1.31, p < 0.001) were independently associated with higher mortality. CONCLUSIONS: CDI-related hospitalisations in Ireland increased substantially between 2009 and 2022, while in-hospital mortality rates and LOS declined. Despite these improvements, CDI is still associated with significant mortality among the elderly. Further research should examine the impact of acute hospital bed availability, faecal microbial transplant (FMT) access, and recurrent infections on CDI case rates.},
}

@article {pmid41963962,
year = {2026},
author = {Li, Y and Wu, H and Yang, J and Weedor, JG and Ding, H and Cui, W and Cui, B and He, Z and Zhang, W and Xing, Y and Zeng, F and Huang, X and Zheng, K and Shen, Y and Yu, Y and Pan, W and Yang, X},
title = {Clostridium butyricum ameliorates Toxoplasma gondii-induced neuropsychiatric disorders by attenuating glial-mediated synaptic pruning via the gut-brain axis.},
journal = {Journal of neuroinflammation},
volume = {23},
number = {1},
pages = {},
pmid = {41963962},
issn = {1742-2094},
support = {Nos. 202310313083Y//the Training Programs of innovation and Entrepreneurship for College Students in Jiangsu Province/ ; Nos. X202510313020//the Training Programs of innovation and Entrepreneurship for College Students in Jiangsu Province/ ; Nos. X202510313017//the Training Programs of innovation and Entrepreneurship for College Students in Jiangsu Province/ ; No. JC20250007//the Faculty Development Grant of Basic Medical Sciences in Xuzhou Medical University/ ; Nos. 82372283//the National Natural Science Foundation of China/ ; No. QL-YB022//the XZHMU-QL Joint Research Fund/ ; No. 2022M710120//China Postdoctoral Science Foundation/ ; },
mesh = {Animals ; *Clostridium butyricum ; Mice ; *Neuroglia/metabolism ; *Neuronal Plasticity/physiology ; Toxoplasma ; *Brain-Gut Axis/physiology ; *Gastrointestinal Microbiome/physiology ; *Toxoplasmosis/psychology ; Mice, Inbred C57BL ; Male ; *Mental Disorders/microbiology ; Humans ; Fecal Microbiota Transplantation/methods ; *Brain ; Dysbiosis/microbiology ; },
abstract = {Gut microbiota dysbiosis contributes to Toxoplasma gondii (T. gondii)-induced neuropsychiatric disorders (TNDs); however, the underlying mechanisms remain largely elusive. Here, we identified the critical role of butyrate-producing bacteria in TNDs in mice. Decreased abundance of butyrate-producing bacteria was consistently observed in patients with Alzheimer’s disease and T. gondii-infected mice. Dietary supplementation with Clostridium butyricum (C. butyricum), a gut commensal butyrate-producing bacterium, reversed gut microbiota dysbiosis, ameliorated intestinal barrier disruption and inflammation, and reduced endotoxemia. Coincidentally, C. butyricum administration suppressed microglial and astrocytic activation, rescued synaptic ultrastructure damage and synaptic loss, thus alleviating cognitive impairment and anxiety/depression-like behaviors. Mechanistically, C. butyricum treatment mitigated the abnormal synaptic pruning mediated by glial cells and C1q to prevent the neuropathology induced by T. gondii infection. Importantly, fecal microbiota transplantation from C. butyricum-supplemented mice into antibiotic-treated recipients recapitulated the therapeutic effects on gut and brain pathology observed in infected mice. Together, our findings suggest that C. butyricum ameliorates TNDs by modulating glial cell-mediated abnormal synaptic pruning via the gut-brain axis, highlighting the therapeutic potential efficacy of butyrate-producing bacteria against TNDs.},
}

Animals
*Clostridium butyricum
Mice
*Neuroglia/metabolism
*Neuronal Plasticity/physiology
Toxoplasma
*Brain-Gut Axis/physiology
*Gastrointestinal Microbiome/physiology
*Toxoplasmosis/psychology
Mice, Inbred C57BL
Male
*Mental Disorders/microbiology
Humans
Fecal Microbiota Transplantation/methods
*Brain
Dysbiosis/microbiology

@article {pmid41964110,
year = {2026},
author = {Deng, L and Wang, X and Mebratie, DY and Tang, Y and Hu, J and Qi, J and Tian, M and Bao, Y and Zhu, L and Wang, S},
title = {Dietary conjugated linoleic acid enhances resistance to Salmonella infection by promoting PPARγ-mediated metabolic reprogramming and effector function in CD8[+] T cells.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2657625},
pmid = {41964110},
issn = {1949-0984},
mesh = {Animals ; *Linoleic Acids, Conjugated/administration & dosage ; *PPAR gamma/metabolism/genetics/immunology ; *CD8-Positive T-Lymphocytes/immunology/metabolism/drug effects ; Salmonella typhimurium/immunology/physiology ; Mice ; *Salmonella Infections/immunology/microbiology/prevention & control ; Mice, Inbred C57BL ; Gastrointestinal Microbiome/drug effects ; Intestinal Mucosa/immunology/microbiology ; Female ; Immunity, Mucosal ; Dietary Supplements ; },
abstract = {Conjugated linoleic acid (CLA) is a dietary lipid that modulates host-microbiota-immune interactions, yet its mechanistic impact on mucosal defense remains unclear. Here, we show that oral CLA supplementation enhances resistance to Salmonella Typhimurium infection and is associated with coordinated changes in gut microbial composition and mucosal immune responses. CLA-enriched commensals, including Dubosiella and Lactobacillus, were associated with increased production of CLA-derived oxylipins and activation of immune surveillance genes. Functionally, CLA pretreatment reduced Salmonella colonization, preserved epithelial integrity, and decreased neutrophilic inflammation without direct antibacterial effects. Single-cell RNA sequencing of ileal intraepithelial lymphocytes revealed that CLA predominantly reprogrammed intestinal CD8[+] T cells toward an oxidative phenotype and enhanced effector activity. ATAC-seq revealed increased chromatin accessibility at loci associated with metabolic regulation, consistent with transcriptional reprogramming toward oxidative fitness. Mechanistically, CLA directly activated PPARγ signaling to promote mitochondrial biogenesis, oxidative phosphorylation, and the production of IFN-γ and granzyme B in CD8[+] T cells; pharmacologic inhibition of PPARγ attenuated these effects both in vitro and in vivo. Notably, depletion of CD8[+] T cells eliminated CLA-mediated protection and abolished early restriction of bacterial dissemination at Peyer's patches and mesenteric lymph nodes. Although CLA enhanced CD8[+] T-cell effector programs, antibiotic depletion and fecal microbiota transplantation experiments demonstrated that an intact gut microbiota is necessary for effective protection in vivo. Together, these findings identify CLA as a dietary modulator that strengthens mucosal resistance to Salmonella by promoting PPARγ-mediated metabolic reprogramming and enhanced effector fitness in intestinal CD8[+] T cells.},
}

Animals
*Linoleic Acids, Conjugated/administration & dosage
*PPAR gamma/metabolism/genetics/immunology
*CD8-Positive T-Lymphocytes/immunology/metabolism/drug effects
Salmonella typhimurium/immunology/physiology
Mice
*Salmonella Infections/immunology/microbiology/prevention & control
Mice, Inbred C57BL
Gastrointestinal Microbiome/drug effects
Intestinal Mucosa/immunology/microbiology
Female
Immunity, Mucosal
Dietary Supplements

@article {pmid41964572,
year = {2026},
author = {Li, K and Ran, X and Ding, H and Han, J and Zhang, L and Wang, X and Guo, W and Li, Y and Fu, S and Bi, J},
title = {Lycium Barbarum Polysaccharide Attenuates Staphylococcus aureus-Induced Mastitis via the Gut Microbiota-Derived Indole-3-Propionic Acid/AhR-IL-22-STAT3 Axis.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {15},
pages = {12038-12053},
doi = {10.1021/acs.jafc.5c06224},
pmid = {41964572},
issn = {1520-5118},
mesh = {Animals ; Female ; *Staphylococcus aureus/physiology/drug effects ; *STAT3 Transcription Factor/genetics/immunology/metabolism ; Mice ; *Indoles/metabolism/immunology ; *Mastitis/microbiology/drug therapy/metabolism/genetics/immunology ; *Staphylococcal Infections/microbiology/drug therapy/genetics/metabolism ; *Drugs, Chinese Herbal/administration & dosage ; *Gastrointestinal Microbiome/drug effects ; *Receptors, Aryl Hydrocarbon/genetics/metabolism/immunology ; Interleukin-22 ; Humans ; Signal Transduction/drug effects ; },
abstract = {Mastitis caused by Staphylococcus aureus (S. aureus) is marked by inflammation and disruption of the blood-milk barrier (BMB), posing health risks to humans and animals. We investigated the therapeutic effects of Lycium barbarum polysaccharide (LBP) in lactating mice with S. aureus-induced mastitis. Oral LBP reduced bacterial colonization, inflammatory cytokines, oxidative stress, and BMB damage. 16S rRNA sequencing and fecal microbiota transplantation (FMT) confirmed that protective effects depended on gut microbiota modulation. Metabolomic analysis revealed that LBP promoted microbial tryptophan metabolism, elevating indole-3-propionic acid (IPA). Mechanistically, IPA activated the aryl hydrocarbon receptor (AhR) and upregulated IL-22-STAT3 signaling, thereby enhancing the epithelial integrity and suppressing inflammation. Pharmacological inhibition of AhR or STAT3 abolished these benefits. Collectively, our results demonstrate that LBP mitigates S. aureus-induced mastitis through a microbiota-dependent IPA-AhR-IL-22-STAT3 axis, providing new insights into microbiota-targeted strategies for infection-associated inflammation.},
}

Animals
Female
*Staphylococcus aureus/physiology/drug effects
*STAT3 Transcription Factor/genetics/immunology/metabolism
Mice
*Indoles/metabolism/immunology
*Mastitis/microbiology/drug therapy/metabolism/genetics/immunology
*Staphylococcal Infections/microbiology/drug therapy/genetics/metabolism
*Drugs, Chinese Herbal/administration & dosage
*Gastrointestinal Microbiome/drug effects
*Receptors, Aryl Hydrocarbon/genetics/metabolism/immunology
Interleukin-22
Humans
Signal Transduction/drug effects

@article {pmid41964647,
year = {2026},
author = {Khanna, S and Bloom, PP},
title = {Difficile to treat: advanced management strategies in difficult to treat Clostridioides difficile infections.},
journal = {Expert review of anti-infective therapy},
volume = {24},
number = {4},
pages = {413-424},
doi = {10.1080/14787210.2026.2659725},
pmid = {41964647},
issn = {1744-8336},
mesh = {Humans ; *Anti-Bacterial Agents/administration & dosage ; *Clostridium Infections/therapy/microbiology ; Fecal Microbiota Transplantation/methods ; Clostridioides difficile/isolation & purification ; Fidaxomicin/administration & dosage ; Recurrence ; Cross Infection/microbiology/therapy ; Animals ; Diarrhea/microbiology ; Practice Guidelines as Topic ; Broadly Neutralizing Antibodies ; Antibodies, Monoclonal ; },
abstract = {INTRODUCTION: Clostridioides difficile infection (CDI) remains a leading cause of healthcare-associated infectious diarrhea, with a major burden driven by recurrences and severe or even fulminant disease in vulnerable hosts. The therapeutic landscape has shifted toward fidaxomicin-based antibiotic regimens and microbiota restoration strategies, including standardized microbiota-based products.

AREAS COVERED: Recent international guidelines, outcome studies, and pivotal trials focused on difficult-to-treat phenotypes such as refractory or fulminant CDI, multiply recurrent CDI, and CDI in high-risk populations (immunocompromised, inflammatory bowel disease, critical illness) were reviewed. A PubMed search was supplemented by hand-searching additional references, guidelines and regulatory documents. Evidence is summarized for optimized antibiotic regimens, bezlotoxumab, conventional fecal microbiota transplantation (FMT), FDA-approved microbiota-based products, and salvage strategies including intracolonic therapy and surgery.

EXPERT OPINION: Advanced CDI management is moving from repeated antibiotic cycling toward individualized recurrence prevention and microbiota restoration strategies. Implementation requires diagnostic stewardship, early recognition of recurrences, clear pathways for microbiota-based therapy access, and multidisciplinary care for fulminant infection. Over the next five years, standardized microbiota therapeutics and better risk tools should shift care toward earlier, more durable recurrence prevention.},
}

Humans
*Anti-Bacterial Agents/administration & dosage
*Clostridium Infections/therapy/microbiology
Fecal Microbiota Transplantation/methods
Clostridioides difficile/isolation & purification
Fidaxomicin/administration & dosage
Recurrence
Cross Infection/microbiology/therapy
Animals
Diarrhea/microbiology
Practice Guidelines as Topic
Broadly Neutralizing Antibodies
Antibodies, Monoclonal

@article {pmid41965671,
year = {2026},
author = {Li, Z and Yang, M and Zhang, Y and He, J and Li, J},
title = {Cross-species fecal microbiota transplantation alters the carbohydrate metabolic phenotype: insights from Gansu zokor (Eospalax cansus).},
journal = {BMC veterinary research},
volume = {22},
number = {1},
pages = {},
pmid = {41965671},
issn = {1746-6148},
support = {No. 2024JC-ZDXM-14//Natural Science Basic Research Program of Shaanxi Province/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/veterinary ; *Carbohydrate Metabolism ; Male ; *Gastrointestinal Microbiome/physiology ; Hypoxia/metabolism ; Liver/metabolism ; Rats, Sprague-Dawley ; Brain/metabolism ; Rats ; RNA, Ribosomal, 16S/genetics ; },
abstract = {The Gansu zokor (Eospalax cansus), a subterranean rodent endemic to China, exhibits remarkable adaptability to hypoxic conditions. Although it is known that the gut microbiota of Gansu zokor undergoes changes under hypoxia, thereby influencing carbohydrate metabolism, it remains unclear whether such a hypoxia adaptation mechanism can be simulated in surface-dwelling animals. In this study, we established a cross-species fecal microbiota transplantation model from Gansu zokor to SD rats to investigate carbohydrate metabolic adaptations under hypoxia. Using 16 S rRNA sequencing, we characterized the features of gut microbiota. Furthermore, we examined molecular markers associated with glycolysis and the tricarboxylic acid cycle in the liver and brain of SD rats exposed to prolonged hypoxia. The results demonstrated that fecal microbiota transplantation altered the composition of gut microbiota in SD rats, leading to modifications in carbohydrate metabolic networks in the liver and brain under prolonged hypoxia. This shift rendered their carbohydrate metabolic patterns more similar to those observed in Gansu zokor. In conclusion, this study provides new evidence supporting the role of gut microbiota in hypoxia adaptation in subterranean rodent and offers a valuable animal model reference for the treatment of hypoxia-induced injuries via fecal microbiota transplantation.},
}

Animals
*Fecal Microbiota Transplantation/veterinary
*Carbohydrate Metabolism
Male
*Gastrointestinal Microbiome/physiology
Hypoxia/metabolism
Liver/metabolism
Rats, Sprague-Dawley
Brain/metabolism
Rats
RNA, Ribosomal, 16S/genetics

@article {pmid41966031,
year = {2026},
author = {Wu, J and Yang, Z and Chen, L and Xu, Q and Zhang, Y and Yang, Y and Beloved, M and Zhan, S and Cao, W and Li, Z and Wang, G and Lv, Q and Han, J},
title = {A polysaccharide from Pueraria lobata ameliorates hepatic fibrosis via gut microbiota-dependent suppression of ferroptosis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {155},
number = {},
pages = {158123},
doi = {10.1016/j.phymed.2026.158123},
pmid = {41966031},
issn = {1618-095X},
mesh = {Animals ; *Pueraria/chemistry ; *Gastrointestinal Microbiome/drug effects ; *Polysaccharides/pharmacology/chemistry ; Mice ; *Liver Cirrhosis/drug therapy/chemically induced ; Male ; *Ferroptosis/drug effects ; Carbon Tetrachloride ; Oxidative Stress/drug effects ; Liver/drug effects/pathology ; Mice, Inbred C57BL ; Drugs, Chinese Herbal/pharmacology ; },
abstract = {BACKGROUND: Hepatic fibrosis, driven by oxidative stress and subsequent hepatocellular injury, represents a major worldwide health challenge. Pueraria lobata Radix, a traditional Chinese herb, contains polysaccharides with demonstrated hepatoprotective properties, though their mechanisms remain incompletely defined.

PURPOSE: This study aims to characterize the structure of P. lobata polysaccharide (PLP2) and to decipher its protective mechanisms against hepatic fibrosis.

METHODS: PLP2, a homogeneous, water-soluble polysaccharide, was purified from P. lobata and structurally characterized. Subsequently, the hepatoprotective activity of PLP2 was investigated in a CCl₄-induced murine model of hepatic fibrosis.

RESULTS: Structural analysis indicated that PLP2 (Mw = 142.9 kDa) was mainly composed of (1→4)-α-D-Glc and (1→4)-α-D-GalA units, with a minor presence of →4,6)-α-D-Glc-(1→ residues. In a CCl₄-induced murine model of hepatic fibrosis, PLP2 treatment effectively ameliorated liver injury, histopathological damage, and inflammatory responses. Mechanistically, PLP2 treatment restored mitochondrial ultrastructure and hepatic ATP levels, thereby suppressing hepatic ferroptosis through the activation of the Nrf2/HO-1/GPX4 axis. The indispensable role of Nrf2 was further validated using the inhibitor ML385, which abolished PLP2's protection. Notably, the hepatoprotective effects of PLP2 were predominantly dependent on gut microbiota integrity, as direct PLP2 treatment failed to protect hepatocytes in vitro. This role was further confirmed by the abolition of protection with antibiotic treatment and the transfer of benefits via fecal microbiota transplantation.

CONCLUSION: These findings provide evidence that PLP2 exerts its anti-fibrotic effects through the gut microbiota-dependent suppression of ferroptosis via the Nrf2/HO-1/GPX4 axis, providing a solid scientific foundation for the clinical application of P. lobata.},
}

Animals
*Pueraria/chemistry
*Gastrointestinal Microbiome/drug effects
*Polysaccharides/pharmacology/chemistry
Mice
*Liver Cirrhosis/drug therapy/chemically induced
Male
*Ferroptosis/drug effects
Carbon Tetrachloride
Oxidative Stress/drug effects
Liver/drug effects/pathology
Mice, Inbred C57BL
Drugs, Chinese Herbal/pharmacology

@article {pmid41966334,
year = {2026},
author = {Premikha, M and Rajendiran, U and Wahab, MT and Venkatachalam, I},
title = {Interventions targeting gut colonization by multi-drug-resistant organisms in healthcare settings: a systematic review and meta-analysis of randomized controlled trials.},
journal = {The Journal of hospital infection},
volume = {172},
number = {},
pages = {228-241},
doi = {10.1016/j.jhin.2026.03.035},
pmid = {41966334},
issn = {1532-2939},
mesh = {Humans ; Randomized Controlled Trials as Topic ; *Drug Resistance, Multiple, Bacterial ; Probiotics/therapeutic use ; *Anti-Bacterial Agents/therapeutic use ; Fecal Microbiota Transplantation ; *Cross Infection/prevention & control/microbiology ; *Gastrointestinal Microbiome/drug effects ; *Bacterial Infections/prevention & control ; },
abstract = {Gut colonization with multi-drug-resistant organisms (MDROs) increases risks of infection, transmission and mortality in healthcare settings. Although decolonization strategies have been attempted to reduce the impact of gut MDROs, no consensus exists on their effectiveness. Our study evaluates the effectiveness of these strategies. We searched PubMed, Embase, CENTRAL, CINAHL and Web of Science for randomized controlled trials (RCTs) published from January 2005 to December 2024. Eligible studies included patients in healthcare settings with baseline MDRO colonization confirmed by rectal swab or stool sample. The primary outcome was reduction in colonization rates in the short term (<28 days) and long term (≥28 days). Two reviewers independently screened studies, extracted data and assessed bias using the Cochrane RoB 2 tool. A random-effects model was used for meta-analysis. This study was registered on PROSPERO (CRD42025625291). Of 900 studies screened, 14 RCTs were included. Interventions included probiotics (N = 7), oral non-absorbable antibiotics (N = 6) and fecal microbiota transplantation (FMT) with antibiotics (N = 1). No significant effect was observed for short-term (risk ratio [RR] = 1.18; 95% confidence interval [CI]: 0.81-1.71; P = 0.39) and long-term decolonization (RR = 1.12; 95% CI: 0.95-1.32; P = 0.16). Post-hoc subgroup analyses showed no significant differences across immune status, target organisms, intervention types and timing of outcome assessment. Risk of bias was low in four studies, with seven having some concerns and three at high risk. Certainty of evidence was low. Current evidence does not support routine use of interventions for gut MDRO decolonization. Well-powered RCTs focused on pathogen-specific interventions and clinically meaningful endpoints are needed to evaluate promising strategies for sustained decolonization (e.g. FMT) and emerging strategies (e.g. bacteriophages).},
}

Humans
Randomized Controlled Trials as Topic
*Drug Resistance, Multiple, Bacterial
Probiotics/therapeutic use
*Anti-Bacterial Agents/therapeutic use
Fecal Microbiota Transplantation
*Cross Infection/prevention & control/microbiology
*Gastrointestinal Microbiome/drug effects
*Bacterial Infections/prevention & control

@article {pmid41966656,
year = {2026},
author = {Gavi, F and Bracco, M and Testori, N and Rossi, F and Fettucciari, D and Panio, E and Assumma, S and Russo, P and Gandi, C and Foschi, N and Ragonese, M and Turri, F and Bientinesi, R and Palermo, G and Ciccarese, C and Iacovelli, R and Kröner, PT and Gasbarrini, A and Sighinolfi, MC and Rocco, B},
title = {Gut microbiome impact on systemic therapy outcomes in metastatic renal cell carcinoma: a systematic review.},
journal = {World journal of urology},
volume = {44},
number = {1},
pages = {},
pmid = {41966656},
issn = {1433-8726},
mesh = {Humans ; *Carcinoma, Renal Cell/therapy/secondary/drug therapy ; *Kidney Neoplasms/pathology/therapy/drug therapy ; *Gastrointestinal Microbiome ; Probiotics/therapeutic use ; Treatment Outcome ; *Immune Checkpoint Inhibitors/therapeutic use ; Fecal Microbiota Transplantation ; Anti-Bacterial Agents/therapeutic use ; *Protein Kinase Inhibitors/therapeutic use ; },
abstract = {BACKGROUND AND OBJECTIVE: Metastatic renal cell carcinoma (mRCC) treatment with immune checkpoint inhibitors (ICIs) and vascular endothelial growth factor–tyrosine kinase inhibitors (VEGF-TKIs) yields durable benefit in a subset of patients, yet primary resistance remains frequent. Emerging data implicate the gut microbiome as a determining factor of systemic therapy efficacy. This review systematically evaluates clinical evidence on antibiotics (ATBs), probiotics, dietary interventions, and fecal microbiota transplantation (FMT) in modulating the gut microbiome to influence outcomes in adult patients with mRCC. METHODS: Eligible studies included adult (≥ 18 year) RCC cohorts receiving microbiome interventions versus standard care, reporting objective response rate (ORR), progression-free survival (PFS), overall survival (OS), or immune-related adverse events (irAEs). KEY FINDINGS AND LIMITATIONS: Six studies (N = 4738) met criteria: three retrospective cohorts linking peri-ICI ATB exposure to inferior ORR (12.9–34.8%), shorter PFS (hazard ratios [HR] 1.96–3.10), and OS (HR 3.5); one prospective RCT (n = 20) demonstrating engraftment of Bifidobacterium animalis yogurt during VEGF-TKI therapy with enrichment of Akkermansia muciniphila and trends to longer PFS; and one phase II RCT abstract (n = 50) showing FMT from an ICI responder improved 1-year PFS (66.7% vs. 35.0%, p = 0.036) and ORR (54% vs. 28%) in pembrolizumab + axitinib recipients. CONCLUSIONS AND CLINICAL IMPLICATIONS: ATB-induced dysbiosis compromises ICI efficacy in mRCC; probiotics and FMT exhibit promise to augment immunotherapy and targeted therapy. Prospective, biomarker-driven RCTs with standardized microbiome assays are needed before routine clinical implementation.},
}

Humans
*Carcinoma, Renal Cell/therapy/secondary/drug therapy
*Kidney Neoplasms/pathology/therapy/drug therapy
*Gastrointestinal Microbiome
Probiotics/therapeutic use
Treatment Outcome
*Immune Checkpoint Inhibitors/therapeutic use
Fecal Microbiota Transplantation
Anti-Bacterial Agents/therapeutic use
*Protein Kinase Inhibitors/therapeutic use

@article {pmid41966990,
year = {2026},
author = {Maseng, MG and Hansen, SH and Grännö, O and Bang, C and Lund, C and Huppertz-Hauss, G and Perminow, G and Valeur, J and Bengtson, MB and Opheim, R and Boyar, R and Frigstad, SO and Aabrekk, TB and Detlie, TE and Kristensen, VA and Strande, V and Hovde, Ø and Asak, Ø and Franke, A and Halfvarsson, J and Høivik, ML and Hov, JR},
title = {Disentangling the gut microbiome and inflammation in inflammatory bowel diseases: longitudinal observations from the IBSEN III study.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag051},
pmid = {41966990},
issn = {1536-4844},
support = {//Takeda Pharmaceuticals, Pfizer, Ferring Pharmaceuticals, Tillotts Pharma, Foundation Dam, and the Norwegian South-Eastern Health Authorities/ ; 90569 to J.H.//NordForsk/ ; 2019-01185 to JH//Vinnova/ ; 2988039 to MLH//Research Council of Norway/ ; No: 2020066//Regional Health Authorities South-Eastern Norway/ ; //DFG Excellence Cluster 2167 "Precision Medicine in Chronic Inflammation" (PMI) and the DFG Research Unit 5042 "miTarget"/ ; no: 327634//Research Council of Norway/ ; },
abstract = {BACKGROUND AND AIM: Despite the well-established involvement of the gut microbiome in inflammatory bowel disease (IBD), less is known about how the gut microbiome changes over time and how it varies with clinical disease activity and fecal calprotectin (f-calprotectin). To address this gap, we utilized samples from the population-based inception cohort of the Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) study.

METHODS: Data and stool samples from study participants with IBD and symptomatic controls were collected at diagnosis and after 3, 6, and 12 months. Microbiome profiling of stool samples was performed targeting the V3-V4 region of the 16S rRNA gene, and a consensus-based approach of mixed models was employed for the longitudinal microbiome analysis.

RESULTS: We included 1251 samples from 744 patients with ulcerative colitis, 618 samples from 356 patients with Crohn' s disease and 266 samples from 164 symptomatic non-IBD controls. In the IBD population, we observed that levels of f-calprotectin decreased over time, as did the patient-reported disease activity (P < .001). Distinct changes in the gut microbiome of IBD patients were observed throughout the first year, such as increased alpha diversity (P < .001) and significant taxonomic changes.Notably, there was no covariation between the changes in alpha diversity and f-calprotectin or symptom score.

CONCLUSION: The gut microbiome during the first year after IBD diagnosis showed changes that paralleled inflammation and clinical disease activity, albeit without covariation, suggesting that there may be a disease-driving impact of gut microbiome independent of inflammation and inflammation-driven symptoms.},
}

@article {pmid41967083,
year = {2026},
author = {Pum, K and Lou, E and Goffredo, P and Jahansouz, C and Subramanian, S and Prakash, A},
title = {Immunotherapy with guts: a review of microbial therapeutic adjuncts for immunotherapy in solid tumors.},
journal = {The oncologist},
volume = {31},
number = {6},
pages = {},
pmid = {41967083},
issn = {1549-490X},
support = {R21 CA267707/CA/NCI NIH HHS/United States ; //Minnesota Colorectal Cancer Foundation and The Mezin-Koats Foundation/ ; },
mesh = {Humans ; *Neoplasms/therapy/immunology/microbiology ; *Immunotherapy/methods ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/immunology ; *Probiotics/therapeutic use ; *Immune Checkpoint Inhibitors/therapeutic use ; },
abstract = {BACKGROUND: Immunotherapy has transformed the management of some solid tumor types, but its impact has been limited to the subset of cancer patients who have "hot" or immunogenic tumors. Num2erous studies are based on strategies for turning "cold," or immune-unresponsive, tumors into a "hot" state. The gut microbiome has emerged as a potential co-therapy for standard immune checkpoint inhibitors (ICIs) to achieve this goal. Recent approaches have primarily focused on the use of probiotics, microbial consortia, or fecal microbiota transplantations in combination with anti-PD-1 and anti-CTLA-4 antibodies.

METHODS: This review highlights the current status of microbiome modulation and its potential impact on clinical practice. Probiotics, such as CMB588, and microbial consortia have been selected following successful preclinical studies. These taxa may initiate T cell infiltration and are commonly found in the microbial profiles of individuals who have previously responded to immunotherapy.

RESULTS: Several trials with these therapies have had success and noted minimal safety concerns compared to monotherapy treatments. Fecal microbiota transplantation (FMT), originally used to treat Clostridium difficile infections, has also demonstrated promising results in increasing immune checkpoint inhibitor (ICI) efficacy across various cancer types and is being utilized in multiple ongoing trials.

CONCLUSION: These therapeutics form the foundation for exciting possibilities in immunotherapy and improving patient outcomes.},
}

Humans
*Neoplasms/therapy/immunology/microbiology
*Immunotherapy/methods
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/immunology
*Probiotics/therapeutic use
*Immune Checkpoint Inhibitors/therapeutic use

@article {pmid41967501,
year = {2026},
author = {Deschamps, C and Tronel, A and Bailly, E and Sohnagou Tanfede, MR and Gilibert, S and Denis, S and Soranzo, T and Van De Wiele, T and Marinelli, L and Blanquet-Diot, S},
title = {Small intestinal microbiome, the underrated maestro of SIMO disease.},
journal = {FEMS microbiology reviews},
volume = {50},
number = {},
pages = {},
pmid = {41967501},
issn = {1574-6976},
support = {BOFGOA2022000803//Ghent University/ ; //FWO/ ; FWOEOS202200603//FNRS/ ; },
mesh = {Humans ; *Intestine, Small/microbiology ; *Gastrointestinal Microbiome/physiology ; Animals ; *Blind Loop Syndrome/microbiology ; },
abstract = {Small intestinal microbial overgrowth (SIMO) results from a breakdown in the delicate equilibrium between luminal environment, gut motility, and microbial ecology. Despite extensive research, these factors have largely been investigated as separate entities, with limited integrative insights into their interplay. This review is the first comprehensive synthesis of physicochemical, mechanical, and microbial parameters shaping SIMO pathogenesis. By reviewing both clinical and experimental data, we reveal how alterations in pH, transit time, digestive secretion dynamics, bile acid composition and impaired intestinal absorption collectively reshape microbial load, diversity, and metabolic output, establishing a self-perpetuating loop of dysfunction. We further discuss the limitations of current diagnostic tools and the transformative potential of emerging approaches, from sampling capsules enabling molecular analyses, to in vitro models simulating human small intestinal ecosystem. This integrative perspective shifts the paradigm from a microbe-centered to an ecosystem-based understanding of SIMO, outlining key challenges and opportunities for personalized diagnostics, mechanistic research, and microbiota-targeted next-generation therapeutics including pre-, pro-, postbiotics and faecal transplantation.},
}

Humans
*Intestine, Small/microbiology
*Gastrointestinal Microbiome/physiology
Animals
*Blind Loop Syndrome/microbiology

@article {pmid41968703,
year = {2026},
author = {Si, Y and Hu, Y and Zhou, Y and Ju, H and Shi, Y and Fang, H},
title = {The Key Genus of Gut Microbiota in Cognition Improvement Following Metformin Treatment in T2DM: A Two-sample Mendelian Randomization Study Combined 16s Rrna Sequencing.},
journal = {Endocrine, metabolic & immune disorders drug targets},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715303475583260405213850},
pmid = {41968703},
issn = {2212-3873},
abstract = {INTRODUCTION: Diabetes increases the risk of cognitive impairment. Metformin, a standard treatment for type 2 diabetes mellitus (T2DM), may potentially improve cognitive dysfunction. This study aims to explore the role of metformin in the cognitive performance of diabetic mice.

METHODS: We divided experimental animals into five groups, including a control group, a diabetes group, a Metformin + Diabetes group, a Control + Fecal Microbiota Transplantation (FMT) group, and a Diabetes + FMT group. These groups assessed cognitive function and plasma longchain fatty acid levels. Gut microbiota composition and the relationship between diabetes and gut microbiota were analyzed using 16S rRNA sequencing of stool samples and Mendelian randomization analysis.

RESULTS: Compared to the Diabetes group and Control + FMT group, mice receiving metformin or FMT treatment showed improved long-term memory, short-term memory, and spatial cognition (P < 0.05), accompanied by increased phosphatidic acid and decreased phosphatidylcholine, phosphatidylethanolamine, and lysophosphatidylcholine (P < 0.05). Bioinformatics analysis of 16S rRNA sequencing (P < 0.01) and Mendelian Randomization analysis (OR: 1.071, 95% CI: 1.003-1.144, P = 0.040) showed changed gut microbial composition, and Lachnospiraceae_ NK4A136 was the common significantly differential genus.

DISCUSSION: Metformin appears to enhance cognitive function in diabetic mice through mechanisms independent of blood sugar control, likely involving the brain-gut axis. Metformin increased the abundance of Lachnospiraceae_NK4A136, a genus found at lower levels in T2DM patients compared to healthy individuals. Thus, supplementing Lachnospiraceae_NK4A136 might improve cognitive function in diabetics.

CONCLUSION: Metformin can improve cognitive function in diabetic mice by modulating the gutbrain axis and altering plasma long-chain fatty acids.},
}

@article {pmid41968757,
year = {2026},
author = {Wu, M and Zhang, Y and Yu, J},
title = {How the gut microbiome affects the immunotherapy response in hepatocellular carcinoma.},
journal = {Cancer biology & medicine},
volume = {23},
number = {5},
pages = {561-579},
pmid = {41968757},
issn = {2095-3941},
support = {2023ZD0500200//Non-communicable Chronic Diseases-National Science and Technology Major Project/ ; 3133344//Strategic Seed Funding Collaboration Research Scheme CUHK/ ; 3135509//Strategic Impact Enhancement Fund CUHK/ ; 3134277//Impact Case for RAE CUHK/ ; },
mesh = {Humans ; *Liver Neoplasms/immunology/therapy/microbiology ; *Carcinoma, Hepatocellular/therapy/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; *Immunotherapy/methods ; Animals ; Dysbiosis/immunology ; Tumor Microenvironment/immunology ; Fecal Microbiota Transplantation ; },
abstract = {Hepatocellular carcinoma (HCC) remains a major global health challenge with limited long-term survival despite advances in surgical, locoregional, and systemic treatments. Although immune checkpoint blockade (ICB) has reshaped HCC therapy, only a subset of patients achieves durable responses, reflecting substantial heterogeneity in tumor biology and immune microenvironments. Dysbiosis, involving the loss of beneficial bacteria, like Lactobacillus reuteri and Akkermansia muciniphila, and the expansion of pathogens, such as Klebsiella pneumoniae and Catenibacterium mitsuokai, drives HCC by promoting microbial translocation and chronic inflammation. This process is mediated by microbiota-derived metabolites. Pro-carcinogenic agents, like deoxycholic acid (DCA) and quinolinic acid, induce inflammation and activate oncogenic pathways, while protective short-chain fatty acids (SCFAs), like acetate and butyrate, modulate T-cell and ILC3 responses to influence antitumor immunity. Tryptophan catabolites, acting via the aryl hydrocarbon receptor (AhR), further fine tune immune and barrier functions. In addition, emerging data implicate intratumoral microbiota as active modulators of immune suppression and metastatic behavior. These mechanistic insights have accelerated the development of microbiome-targeted interventions, such as probiotics, prebiotics, engineered bacterial strains, and fecal microbiota transplantation, to enhance ICB responsiveness. This review synthesizes current advances linking the gut microbiome to HCC immunobiology and highlights emerging therapeutic strategies aimed at optimizing immunotherapy through precise microbial modulation.},
}

Humans
*Liver Neoplasms/immunology/therapy/microbiology
*Carcinoma, Hepatocellular/therapy/immunology/microbiology
*Gastrointestinal Microbiome/immunology
*Immunotherapy/methods
Animals
Dysbiosis/immunology
Tumor Microenvironment/immunology
Fecal Microbiota Transplantation

@article {pmid41969116,
year = {2026},
author = {Shakirov, R and Pankratova, Y and Shakurov, A and Senina, A and Boulygina, E and Grigoryeva, T and Yarullina, D and Karpukhin, O},
title = {Comparative characteristics of the microbiota of diverticula in complicated diverticulitis.},
journal = {The new microbiologica},
volume = {49},
number = {1},
pages = {65-70},
pmid = {41969116},
issn = {1121-7138},
mesh = {Humans ; *Diverticulitis/microbiology ; *Bacteria/classification/isolation & purification/genetics ; Male ; *Gastrointestinal Microbiome ; RNA, Ribosomal, 16S/genetics ; *Microbiota ; },
abstract = {We present a comparison of the mucosal microbiota within different diverticula in a patient with diverticular disease (DD) complicated by diverticulitis and pelvic abscess. The conventional culture method and the 16S rRNA-based sequencing approach were employed to characterize the microbiota of perforated diverticulum (PD) and adjacent visually intact diverticulum (ID) from the same surgically resected colonic segment. Compared to PD, the microbiota of ID demonstrated depletion in butyrate-producing genera and increased abundances of Proteobacteria, Enterobacteriaceae, and Bacteroides. The predominantly pro-inflammatory character of the microbiota in ID suggests its probable pathological role in the progression of DD towards more complicated forms, up to inflammatory destruction (perforation) of the diverticulum wall. The insights of this study pave the way for the development of forthcoming clinical trials focusing on microbiota-related therapies, including the use of antibiotics, probiotics, and fecal microbiota transplantation (FMT), to potentially treat or manage DD and its complications.},
}

Humans
*Diverticulitis/microbiology
*Bacteria/classification/isolation & purification/genetics
Male
*Gastrointestinal Microbiome
RNA, Ribosomal, 16S/genetics
*Microbiota

@article {pmid41969207,
year = {2026},
author = {Saha, P and Roy, S and More, M and Bose, D and Trivedi, A and Brooks, BW and Syn, WK and Diehl, AM and Chatterjee, S},
title = {Underlying MASLD-induced gut microbiome dysbiosis and intestinal inflammation are key to poor outcomes in vibriosis infections in a preclinical model.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2652474},
pmid = {41969207},
issn = {1949-0984},
mesh = {Animals ; *Vibrio Infections/microbiology/pathology ; *Dysbiosis/microbiology ; Mice ; *Gastrointestinal Microbiome ; Disease Models, Animal ; Mice, Inbred C57BL ; Vibrio vulnificus/physiology ; Inflammation/microbiology ; Male ; Liver/pathology ; Intestines/microbiology ; *Non-alcoholic Fatty Liver Disease/microbiology ; Intestinal Barrier Function ; Anti-Bacterial Agents ; },
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of chronic liver disease globally, especially in developed countries, including the United States. The etiology of MASLD is closely associated with several other cardiometabolic conditions and can further aggravate to more severe stages of liver disease, including steatohepatitis and cirrhosis. Moreover, patients with underlying MASLD conditions have altered gut microbiome signatures and intestinal homeostasis, leading to gut barrier dysfunction, thereby making them more vulnerable to acute gastrointestinal infections like non-cholera vibriosis. However, the exact role of the gut microbiome and intestinal pathophysiology in increasing susceptibility to infection in patients with MASLD remains poorly understood. In this study, we used oral inoculation of the bacterium Vibrio vulnificus to investigate the pathophysiological outcomes in both control and diet-induced MASLD mouse cohorts. Our results showed that non-cholera vibriosis in mice with underlying MASLD caused increased liver damage, an inflammatory surge, followed by the onset of fibrotic lesions compared to the chow-diet fed control mice, depicting a worsened outcome. Depletion of the gut bacteriome by antibiotic treatment and following fecal microbiota transplantation in these mouse cohorts showed decreased pathophysiology in the livers, indicating that an altered gut microbiome in MASLD could be a key factor in the increased likelihood of non-cholera vibriosis in patients with MASLD.},
}

Animals
*Vibrio Infections/microbiology/pathology
*Dysbiosis/microbiology
Mice
*Gastrointestinal Microbiome
Disease Models, Animal
Mice, Inbred C57BL
Vibrio vulnificus/physiology
Inflammation/microbiology
Male
Liver/pathology
Intestines/microbiology
*Non-alcoholic Fatty Liver Disease/microbiology
Intestinal Barrier Function
Anti-Bacterial Agents

@article {pmid41969481,
year = {2026},
author = {Huang, M and Chen, Y and Cui, X},
title = {Targeting the gut microbiota-metabolite-immune axis in cancer immunotherapy: mechanistic interplay, therapeutic strategies, and translational applications-a narrative review.},
journal = {Translational cancer research},
volume = {15},
number = {3},
pages = {214},
pmid = {41969481},
issn = {2219-6803},
abstract = {BACKGROUND AND OBJECTIVE: Microbiota and their metabolites form a dynamic regulatory network that modulates the tumor microenvironment (TME) and immune cell functionality, emerging as critical targets in cancer immunotherapy. Despite remarkable advances in immune checkpoint inhibitors (ICIs), clinical efficacy remains limited by primary or acquired resistance in a substantial proportion of patients. Accumulating evidence indicates that the gut microbiota-metabolite-immune axis is a critical determinant of ICI responsiveness, but the underlying molecular mechanisms and tumor-specific regulatory patterns remain incompletely elucidated. This narrative review aims to systematically dissect the mechanistic interplay of this axis across diverse cancer types and synthesize current microbiota-targeted therapeutic strategies for improved immunotherapy outcomes.

METHODS: We conducted a systematic literature search of PubMed for studies published between January 2019 and December 2025, with a particular focus on basic and translational research elucidating the roles of gut microbiota and their metabolites in cancer immunotherapy across various malignancies.

KEY CONTENT AND FINDINGS: This review elucidates the molecular mechanisms by which core metabolites regulate antitumor immunity, synthesizes characteristic microbial signatures across gastrointestinal and non-gastrointestinal cancers. Furthermore, we evaluate the translational potential of intervention strategies, including fecal microbiota transplantation, probiotic supplementation, and engineered microbes, as adjuvants to enhance ICI efficacy and overcome resistance.

CONCLUSIONS: Microbiota-based personalized therapeutic strategies are increasingly recognized as promising tools to modulate antitumor immunity and improve immunotherapy outcomes. Systematic profiling of the gut microbiota-metabolite-immune axis across cancer types will facilitate the development of precision interventions to overcome ICI resistance. Future research integrating multi-omics approaches and large-scale clinical trials is pivotal to translate mechanistic insights into clinically viable therapies, ultimately revolutionizing the landscape of cancer immuno-oncology.},
}

@article {pmid41970392,
year = {2026},
author = {Peng, Y and Hu, Q and Gao, C},
title = {Fecal microbiota transplantation for intestinal rehabilitation after GI bleeding and perforation post-cardiac transplant: a case report.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1766362},
pmid = {41970392},
issn = {2296-858X},
abstract = {Gastrointestinal complications present a critical challenge following heart transplantation. These issues often stem from multifactorial mechanisms, including immunosuppressive therapy and physiological stress, which compromise mucosal defenses. We report a case of a 53-year-old heart transplant recipient who developed severe gastrointestinal bleeding and perforation due to stress ulcers. Following embolization therapy, the clinical course was further complicated by secondary intestinal cicatricial obstruction, necessitating effective intestinal rehabilitation. To address the resulting malabsorption and facilitate recovery while maintaining immunosuppressive stability, fecal microbiota transplantation (FMT) was employed to restore gut microbiota diversity. This intervention successfully promoted intestinal functional recovery. This case offers a practical reference for managing complex post-transplant gastrointestinal complications, highlighting the therapeutic potential of FMT.},
}

@article {pmid41971318,
year = {2026},
author = {Jin, L and Bian, X and Zhang, G and Zhu, J and Li, X and Yang, D},
title = {Combined polysaccharides from Angelica sinensis, Crataegus pinnatifida, Prunus persica, and Carthamus tinctorius attenuate cold exposure-induced bone loss by modulating the gut microbiota and fecal metabolites.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1768890},
pmid = {41971318},
issn = {1664-302X},
abstract = {BACKGROUND: Chronic cold stress is a significant risk factor for skeletal deterioration; however, effective therapeutic strategies targeting the underlying environmental-metabolic interactions remain unclear. This study investigated the osteoprotective potential of Mixed Polysaccharides (MPs) and elucidated the mediating role of the gut microbiome.

METHODS: Cold exposure-induced bone loss was established in rats. Fecal microbiota transplantation (FMT), 16S rRNA gene sequencing, and untargeted metabolomics was employed to illustrate the positive effect of MPs on the improvement of cold-exposed bone loss.

RESULTS: MPs treatment effectively reversed cold-induced trabecular microarchitecture deterioration and bone mass loss. In femoral tissue, MPs rebalanced skeletal turnover by upregulating osteogenic markers (Runx2, Osterix) and suppressing osteoclastogenic factors (TRAP, c-fos), concurrent with a marked reduction in the levels of pro-inflammatory cytokines TNF-α and IL-1β in femur. Furthermore, MPs restored intestinal barrier integrity by upregulating tight junction proteins (ZO-1, Occludin), thereby mitigating the intestinal barrier impairment driven by cold stress. FMT experiments demonstrated that the osteoprotective effects of MPs are microbiota-dependent, as the transplantation of MPs-modulated microbiota recapitulated the bone-preserving and barrier-restoring phenotypes in recipient mice. Multi-omics integration identified that MPs selectively promoted the expansion of Lactobacillus intestinalis and the accumulation of cholylhistidine. Correlation analysis further revealed a strong link between the enrichment of these microbial and metabolic signatures, reduced pro-inflammatory cytokine levels, and improved bone formation.

CONCLUSION: Our findings indicate that MPs alleviate cold-stress-induced bone loss by remodeling the gut microbiota and metabolic profile, fortifying the intestinal barrier and decreasing pro-inflammatory cytokine.},
}

@article {pmid41971324,
year = {2026},
author = {Wang, B and Deng, F and Liu, Z and Tian, J and Li, Y and Mao, Y and Song, H},
title = {Clinical application of fecal microbiota transplantation and its influencing factors.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1807071},
pmid = {41971324},
issn = {1664-302X},
abstract = {Fecal microbiota transplantation (FMT) is an emerging therapy that has received significant attention in recent years, although its origins can be traced back to 4th-century China. In modern medicine, FMT has been incorporated into clinical guidelines for the treatment of recurrent Clostridioides difficile infection. By re-establishing a healthy gut microbiota and regulating the immune system, FMT has potential therapeutic effects on various diseases, such as gastrointestinal diseases, diabetes, tumors, Alzheimer's disease, and liver disease. However, its efficacy varies based on the type of disease and individual differences. The clinical application of FMT is influenced by multiple factors, including fecal matter processing, administration route, dosage, donor screening, and recipient detection. Currently, FMT faces numerous challenges, including the need to verify the stability and durability of its efficacy, standardize donor screening criteria, and optimize fecal processing and administration. Future research is expected to reveal the mechanisms of action of FMT, optimize treatment protocols, and refine its safety, efficacy, and convenience, thereby bringing hope for patients with complex and challenging diseases.},
}

@article {pmid41974014,
year = {2026},
author = {AlAwadhi, HK and Hyesoo Chang, N and Jogendran, M and Bretthauer, M},
title = {Gastroenterology/Hepatology: What You May Have Missed in 2025.},
journal = {Annals of internal medicine},
volume = {179},
number = {5_Supplement},
pages = {e2601058},
doi = {10.7326/ANNALS-26-01058},
pmid = {41974014},
issn = {1539-3704},
mesh = {Humans ; *Gastroenterology/trends ; *Gastrointestinal Diseases/therapy/diagnosis ; },
abstract = {During 2025, gastroenterology and hepatology experienced advances in treatment and surveillance of common diseases. Technological innovations have been reported that may positively affect patients worldwide. New drug options for treatment of metabolic dysfunction-associated steatohepatitis are emerging, and old drugs have new indications and patterns of use for common gastroenterologic diseases. The 9 articles featured here were selected because they represent important information for clinicians who are not gastroenterologists but who often diagnose, treat, and follow patients with gastroenterologic conditions. Two randomized trials address potential overtreatment of patients with Barrett esophagus without high-grade dysplasia and patients with severe alcohol-associated hepatitis. For clinicians who care for patients with malignant gastric outlet obstruction, 2 new randomized trials now provide evidence that a new endoscopic approach is a good alternative to traditional surgical gastroenterostomy or duodenal stenting. Aspirin is emerging as promising adjuvant therapy for patients with colorectal cancer that is positive for PI3K pathway alterations, and fecal microbiota transplantation has been shown to be noninferior to standard vancomycin for patients with a first episode of Clostridioides difficile infection. Finally, a randomized trial showed that structured exercise and training for patients with colon cancer after surgery and adjuvant oncologic treatment reduce recurrence and increase survival.},
}

Humans
*Gastroenterology/trends
*Gastrointestinal Diseases/therapy/diagnosis

@article {pmid41974041,
year = {2026},
author = {Wu, S and Chew, NF and Ma, X and Situ, J and Shun, EH and Li, C and Ip, JD and Ho, SS and Zhang, AJ and Tsoi, JY and Chan, WM and Ma, W and Liang, Y and Mao, W and Chen, KWY and Yin, F and To, KK and Yuan, S and Chan, JF and Zhu, L and Huang, Y and Sridhar, S},
title = {Molnupiravir is effective against hepatitis E virus infection in an animal model.},
journal = {Hepatology communications},
volume = {10},
number = {5},
pages = {},
pmid = {41974041},
issn = {2471-254X},
mesh = {Animals ; *Hepatitis E/drug therapy/virology ; *Antiviral Agents/pharmacology/therapeutic use ; *Hepatitis E virus/drug effects/genetics ; Disease Models, Animal ; Rats ; Ribavirin/pharmacology/therapeutic use ; *Hydroxylamines/pharmacology/therapeutic use ; Male ; Sofosbuvir/pharmacology ; RNA, Viral ; Hepatocytes/virology ; Humans ; Cytidine/analogs & derivatives ; },
abstract = {BACKGROUND: There are few treatment options for patients with chronic hepatitis E unresponsive to ribavirin. Drug repurposing is required to identify new treatments. Molnupiravir, a nucleoside analogue, is approved for the treatment of coronavirus disease 2019 (COVID-19). This study evaluated the activity of molnupiravir against hepatitis E virus (HEV) in cell culture and animal models.

METHODS: Cytotoxicity and antiviral efficacy of molnupiravir, ribavirin, and sofosbuvir were investigated using infectious cDNA clones and wild-type HEV isolates in PLC/PRF/5 cells and primary rat hepatocytes. Immunosuppressed rats were infected with HEV and treated with molnupiravir and ribavirin. The effectiveness of molnupiravir in clearing HEV in serum, feces, and liver tissue was compared with that of untreated and ribavirin-treated animals. Mutations arising in virus populations during treatment were assessed using next-generation sequencing.

RESULTS: The antiviral effect of molnupiravir was comparable to that of ribavirin and superior to that of sofosbuvir against HEV strains in vitro, with decreased HEV RNA in supernatant (p<0.05) and cytoplasmic viral protein expression. No additive effect with sofosbuvir was observed. Rats (n=14 per group) treated with 400 mg/kg/d molnupiravir cleared viremia within 4 weeks of treatment, and 9/14 of these animals also cleared viral shedding in stool. Mean viremia and fecal viral loads were reduced compared with untreated and ribavirin-treated animals (p≤0.005). Partial effectiveness was apparent at the lower 250 mg/kg/d molnupiravir dose. Molnupiravir-treated rats had improved liver histology compared with control animals. Frequent transition mutations were observed in HEV from molnupiravir-treated animals.

CONCLUSIONS: Molnupiravir limits HEV infection in cell culture and animal models. Molnupiravir could be an alternative for ribavirin-refractory chronic hepatitis E.},
}

Animals
*Hepatitis E/drug therapy/virology
*Antiviral Agents/pharmacology/therapeutic use
*Hepatitis E virus/drug effects/genetics
Disease Models, Animal
Rats
Ribavirin/pharmacology/therapeutic use
*Hydroxylamines/pharmacology/therapeutic use
Male
Sofosbuvir/pharmacology
RNA, Viral
Hepatocytes/virology
Humans
Cytidine/analogs & derivatives

@article {pmid41975112,
year = {2026},
author = {Liu, J and Sun, X and Yuan, P and Qin, Y and Wu, W and Fan, Y and Zhang, Y and Zou, L and Ren, C and Li, S},
title = {Clinical response and risk factors of fecal microbiota transplantation in children: a systematic review and meta-analysis.},
journal = {European journal of pediatrics},
volume = {185},
number = {5},
pages = {},
pmid = {41975112},
issn = {1432-1076},
support = {No.ZF2025046//the Hebei Provincial Department of Finance/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/adverse effects/methods ; Child ; Risk Factors ; *Inflammatory Bowel Diseases/therapy ; Treatment Outcome ; *Clostridium Infections/therapy ; },
abstract = {UNLABELLED: The objective of this study is to investigate the clinical response and incidence of adverse events (AEs) following fecal microbiota transplantation (FMT) in children, across various diseases, populations, and treatment protocols. A systematic search was conducted across eight major Chinese and English databases, identifying 47 studies up to August 28, 2025, for inclusion. Study quality was assessed using the Quality Assessment with Diverse Studies (QuADS) tool. Single-arm rates were pooled via meta-analysis employing the Freeman-Tukey double arcsine transformation, followed by extensive subgroup comparisons to identify influencing factors. FMT demonstrated efficacy in pediatric recurrent Clostridium difficile infection (rCDI), inflammatory bowel disease (IBD), and autism spectrum disorder (ASD), although a higher incidence of AEs was observed in children with IBD. Subgroup analyses revealed that the use of donor feces from relatives or friends was associated with a higher clinical response rate in rCDI. The presence of comorbidities such as IBD diminished the response rate in rCDI patients. Younger age in rCDI and IBD patients showed a trend towards higher clinical response rates, though this did not reach statistical significance. No statistically or clinically significant differences were found in other subgroup comparisons. Meta-regression suggested IBD to be a risk factor for FMT-related AEs.

CONCLUSION: This study innovatively delineates the efficacy-safety profile of pediatric FMT and outlines a pathway for optimizing individualized treatment regimens, providing crucial evidence-based guidance for clinical practice.

TRIAL REGISTRATION: This study has been registered on the PROSPERO database (CRD42024614196).

WHAT IS KNOWN: • Fecal Microbiota Transplantation (FMT) demonstrates preliminary therapeutic potential in several pediatric diseases. • Existing evidence remains fragmented, with limited systematic data on factors modifying efficacy and safety in children.

WHAT IS NEW: • The study revealed FMT's high efficacy across rCDI, IBD, and ASD, and identified IBD as a risk factor for elevated FMT-related adverse events in pediatric patients. • Notably, related/friend donors improved rCDI response rates, while comorbidities like IBD reduced rCDI treatment efficacy.},
}

Humans
*Fecal Microbiota Transplantation/adverse effects/methods
Child
Risk Factors
*Inflammatory Bowel Diseases/therapy
Treatment Outcome
*Clostridium Infections/therapy

@article {pmid41976908,
year = {2026},
author = {Oommen, TT and Philips, CA and Ahamed, R and Theruvath, AH and Tharakan, A and Rajesh, S and Augustine, P},
title = {Palliative Healthy Donor Stool Transplantation (pFMT) in Patients with End-Stage Alcohol-Related Cirrhosis and Severe Unstable Decompensations-A Cohort Study.},
journal = {Journal of clinical medicine},
volume = {15},
number = {7},
pages = {},
pmid = {41976908},
issn = {2077-0383},
abstract = {Background and Aims: Severe alcohol-associated hepatitis (SAH) can trigger unstable decompensations in cirrhosis patients. They experience high rates of emergency department visits and hospitalization. We evaluated real-world clinical outcomes following palliative-faecal microbiota transplantation (pFMT) compared to best supportive care (BSC) in this critically ill population. Patients and Methods: From July 2021 to April 2024, 28 patients on pFMT were compared with 37 on BSC. Patients on pFMT received nasoduodenal healthy donor stool infusion daily for 5-days. Patients were followed up for portal hypertension-related events, infections, hospitalizations, extrahepatic organ failure and 6- and 12-months survival. 16S rRNA sequencing on stool samples collected at baseline and on follow up were analysed for changes in relative abundance (RA) of bacterial communities. Results: Patients were matched for age, type of decompensation and liver disease severity at enrolment. Twelve-month survival was 64.3% in pFMT versus 51.4% in BSC groups. pFMT dramatically reduced hospital readmissions (mean 0.76 ± 0.76 vs. 2.29 ± 1.27, p < 0.001). Unstable decompensations beyond 3 months occurred in 14.3% of pFMT versus 64.9% of BSC (p < 0.001). Organ failures were lesser with pFMT: acute kidney injury 7.7% versus 93.8% (p < 0.001), hepatic encephalopathy 7.1% versus 68.2% (p < 0.001). Infection burden was significantly lower (53.6% vs. 83.8%, p = 0.008), particularly infections requiring admission (17.4% vs. 66.7%, p < 0.001) with pFMT. Microbiome analysis revealed progressive expansion of Gram-negative genera in BSC, and beneficial Actinobacteria in pFMT-treated patients at 3, 6, and 12 months. Conclusions: Palliative FMT represents a unique disease-modifying intervention in end-stage alcohol-related cirrhosis, preventing organ failure progression, reducing healthcare utilization, and improving survival trajectories.},
}

@article {pmid41979342,
year = {2026},
author = {Cai, K and Chen, Z and Deng, S and Chen, J and Yu, J and Zhang, X and Jia, W and Huang, A and Chen, Y and Xie, Z and Li, P and Liao, Q},
title = {UPLC-Q-TOF/MS-Based Metabolomics and 16S rRNA Profiling Reveal that Corosolic Acid Ameliorates High-Fat Diet-Induced MASLD by Modulating the Gut-Liver Axis to Inhibit the cGAS-STING Pathway.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {16},
pages = {13282-13301},
doi = {10.1021/acs.jafc.5c13513},
pmid = {41979342},
issn = {1520-5118},
mesh = {Animals ; Mice ; Male ; Gastrointestinal Microbiome/drug effects ; *Membrane Proteins/metabolism/genetics ; RNA, Ribosomal, 16S/genetics ; *Liver/metabolism/drug effects ; Diet, High-Fat/adverse effects ; cGAS-STING Signaling Pathway ; *Triterpenes/administration & dosage ; Metabolomics ; Humans ; Mice, Inbred C57BL ; *Nucleotidyltransferases/metabolism/genetics ; STING Protein ; Bacteria/isolation & purification/genetics/classification/metabolism ; Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase ; *Non-alcoholic Fatty Liver Disease/metabolism/drug therapy/microbiology/genetics ; Chromatography, High Pressure Liquid ; Mass Spectrometry ; },
abstract = {Metabolic-associated steatohepatitis liver disease (MASLD) is characterized by abnormal hepatic fat accumulation and liver injury. Corosolic acid (CA) has proven lipid-lowering and hepatoprotective effects, yet the underlying mechanism by which CA mitigates MASLD remains unclear. In this study, mice were fed a high-fat diet for 8 weeks to induce MASLD, followed by 8 weeks of CA intervention. We found that CA significantly suppressed weight gain, reduced serum lipid levels, and improved liver function in the HFD-fed mice. Fecal metabolomic analysis showed that CA regulated multiple metabolic pathways including histidine metabolism and altered 10 shared metabolites between feces and serum, such as HAD-Car. 16S rRNA sequencing and fecal microbiota transplantation confirmed that CA reshaped gut microbiota, upregulating beneficial bacteria (e.g., Lachnospiraceae_NK4A136_group) and downregulating harmful strains (e.g., Blautia). Mechanistically, HAD-Car alleviated MASLD by inhibiting the cGAS-STING pathway. Collectively, CA exerts anti-MASLD effects via regulating gut microbiota and metabolites, offering new insights into MASLD treatment.},
}

Animals
Mice
Male
Gastrointestinal Microbiome/drug effects
*Membrane Proteins/metabolism/genetics
RNA, Ribosomal, 16S/genetics
*Liver/metabolism/drug effects
Diet, High-Fat/adverse effects
cGAS-STING Signaling Pathway
*Triterpenes/administration & dosage
Metabolomics
Humans
Mice, Inbred C57BL
*Nucleotidyltransferases/metabolism/genetics
STING Protein
Bacteria/isolation & purification/genetics/classification/metabolism
Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase
*Non-alcoholic Fatty Liver Disease/metabolism/drug therapy/microbiology/genetics
Chromatography, High Pressure Liquid
Mass Spectrometry

@article {pmid41979409,
year = {2026},
author = {Paaske, SE and Baunwall, SMD and Dahlerup, JF and Hvas, CL},
title = {Letter: Dose and Donor Matter-Determining the Optimal Strategy for Faecal Microbiota Transplantation in Clostridioides difficile Infection. Authors' Reply.},
journal = {Alimentary pharmacology & therapeutics},
volume = {64},
number = {3},
pages = {414-415},
pmid = {41979409},
issn = {1365-2036},
}

@article {pmid41979582,
year = {2026},
author = {Smółka, L and Strugała, M and Kursa, K and Pomianowski, B and Blady, K and Bratek, K},
title = {The impact of the gut microbiome on the development of atherosclerosis and peripheral arterial disease: A narrative review.},
journal = {Przeglad epidemiologiczny},
volume = {79},
number = {4},
pages = {580-594},
doi = {10.32394/pe/214773},
pmid = {41979582},
issn = {0033-2100},
mesh = {Humans ; *Atherosclerosis/microbiology/physiopathology ; *Peripheral Arterial Disease/microbiology/physiopathology ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis ; },
abstract = {Atherosclerosis is a chronic, progressive process affecting medium and large arteries, while peripheral artery disease (PAD) represents one of its clinical manifestations in the limb arteries. Although classical risk factors such as poor diet, hypertension, diabetes, and smoking are well established, increasing evidence indicates that the gut microbiome is an important and modifiable contributor to vascular pathophysiology. This paper reviews current knowledge on the role of the gut microbiome in the initiation and progression of atherosclerosis and PAD, with emphasis on bacterial metabolites, proinflammatory mechanisms, and potential therapeutic interventions. Gut dysbiosis-an imbalance in the intestinal microbial community-has been associated with increased cardiovascular risk. Patients with vascular diseases show higher levels of pro-atherogenic taxa, including Enterobacteriaceae, Streptococcus spp., Lachnoclostridium, and Family XI, alongside a reduction of beneficial short-chain fatty acid (SCFA)-producing bacteria such as Roseburia, Faecalibacterium, Coprococcus2, and Ruminococcaceae. Two key microbial metabolites influence vascular health. Trimethylamine N-oxide (TMAO), formed from choline and L-carnitine via microbial and hepatic metabolism, promotes endothelial dysfunction, inflammation, and platelet reactivity, thereby accelerating atherosclerosis. Conversely, SCFAs-acetate, propionate, and butyrate-exert anti-inflammatory effects, improve insulin sensitivity, and enhance nitric oxide synthesis, resulting in vascular protection. Therapeutic strategies targeting the gut microbiota show promising potential. These include the use of probiotics and prebiotics (notably Lactobacillus rhamnosus GG), adherence to a Mediterranean diet, and fecal microbiota transplantation (FMT), all aimed at restoring eubiosis and a favorable intestinal metabolic profile. In summary, the gut microbiome appears to be a key modulator of the pathogenesis of atherosclerosis and PAD. Targeted modulation of gut microbial composition and activity may emerge as an innovative and effective strategy for the prevention and treatment of cardiovascular diseases.},
}

Humans
*Atherosclerosis/microbiology/physiopathology
*Peripheral Arterial Disease/microbiology/physiopathology
*Gastrointestinal Microbiome/physiology
*Dysbiosis

@article {pmid41980626,
year = {2026},
author = {Li, K and Zhu, R and Chen, Y and Wang, X and Jiang, Y and Han, T and Yue, X and Xia, T and Xin, H},
title = {Portulaca oleracea L. polysaccharide alleviates colitis-associated bone loss through Muribaculaceae-enriched gut microbiota and elevated colonic melatonin.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.04.033},
pmid = {41980626},
issn = {2090-1224},
abstract = {AIMS: Colitis and its associated bone loss are major global health concerns with limited therapeutic options. Portulaca oleracea L. polysaccharide (POP) has been suggested to ameliorate both conditions via microbiota modulation. The study aimed to explore whether POP can alleviate colitis-associated bone loss and its underling mechanism.

METHODS: A murine model of dextran sodium sulfate (DSS)-induced colitis with bone loss was used to assess the effects of POP. The 16S rRNA sequencing and ex vivo fecal microbiota transplantation (ex-FMT) were employed to identify bacterial taxa potentially associated with POP's protective effects. The functional impact of microbial metabolites was evaluated by treating cells with fecal supernatants (FS), and their compositional profiles were analyzed using fecal metabolomics.

RESULTS: POP mitigated DSS-induced colitis and bone loss and reshaped gut microbial composition, featuring enrichment of Muribaculaceae. Transplantation of POP-modulated microbiota (POPFMT) replicated the therapeutic benefits, which were maintained following gentamicin treatment (GENFMT) but abolished by vancomycin (VANFMT). Compared with the DSSFMT group, Muribaculaceae abundance was significantly higher in the POPFMT group. This increase was maintained in the GENFMT group but markedly reduced in the VANFMT group. FS from POP group maintained gut barrier function by increasing ZO-1 and Occludin expression, while suppressing apoptosis in HT-29 cells. FS from POPFMT group suppressed inflammatory osteoclastogenesis of RAW 264.7 cells via the TRAF6/p65-NFATc1 signaling axis. Metabolomics revealed distinct tryptophan-related profiles, with POPFMT and GENFMT were characterized by elevated melatonin abundance, DSSFMT by increased indole, and VANFMT by increased indole derivatives. Colonic melatonin levels were consistently higher in the POP-treated, POPFMT, and GENFMT groups. Exogenous melatonin ameliorated DSS-induced colitis and bone loss, whereas the 4P-PDOT attenuated its protective effects.

CONCLUSION: POP ameliorates DSS-induced colitis and bone loss by modulating the gut microbiota. The POP-modulated gut microbiota is characterized by enrichment of Muribaculaceae and is associated with increased colonic melatonin levels, which contributes to the observed attenuation of colitis and bone loss.},
}

@article {pmid41981196,
year = {2026},
author = {Hamdi, L and Agranyoni, O and Goldberg, Y and Zarka, N and Fainstein, N and Theotokis, P and Salamotas, I and Grigoriadis, N and Katz, A and Ben-Hur, T and Navon-Venezia, S and Einstein, O},
title = {High-intensity exercise training alters gut microbiota to mitigate the development of experimental autoimmune encephalomyelitis.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41981196},
issn = {2045-2322},
support = {0008147//Ministry of Innovation, Science and Technology/ ; },
mesh = {Animals ; *Encephalomyelitis, Autoimmune, Experimental/microbiology/therapy/pathology/immunology ; Mice ; *Gastrointestinal Microbiome ; *Physical Conditioning, Animal ; Fecal Microbiota Transplantation ; Female ; Mice, Inbred C57BL ; T-Lymphocytes/immunology ; Fatty Acids, Volatile/blood ; Disease Models, Animal ; },
abstract = {Exercise training (ET) has demonstrated beneficial effects in autoimmune and neurological disorders, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). ET modulates the gut microbiota, which influences neuroimmune interactions via the microbiota-gut-brain and microbiota-gut-immune system axes. However, the role of gut microbiota in mediating ET's protective effects in autoimmune neuroinflammation remains unclear. We investigated whether gut microbiota mediates the beneficial effects of ET on EAE development. Healthy mice underwent high-intensity continuous training (HICT). Fecal microbiota from HICT and sedentary mice were transplanted into naïve recipients, followed by proteolipid protein (PLP) immunization to induce EAE. Disease severity, gut microbial composition (16S rDNA sequencing), short-chain fatty acid (SCFA) levels (LC-MS), and autoreactive T-cell proliferation (flow cytometry) were assessed. Faecal microbiota transplantation (FMT) from HICT donors significantly reduced EAE severity, delaying onset and decreasing CNS inflammation, demyelination, and axonal damage. These effects correlated with distinct microbial signatures, including increased Faecalimonas and Escherichia genera, and decreased Mucispirillum genus. HICT-FMT mice exhibited higher Faecalimonas abundance and reduced serum SCFA levels. PLP-reactive T-cell proliferation was suppressed in HICT-FMT recipients. Gut microbiota from HICT mice confers protection against EAE development, associated with microbial-metabolic shifts and modulation of autoreactive T-cell responses.},
}

Animals
*Encephalomyelitis, Autoimmune, Experimental/microbiology/therapy/pathology/immunology
Mice
*Gastrointestinal Microbiome
*Physical Conditioning, Animal
Fecal Microbiota Transplantation
Female
Mice, Inbred C57BL
T-Lymphocytes/immunology
Fatty Acids, Volatile/blood
Disease Models, Animal

@article {pmid41981603,
year = {2026},
author = {Liu, Y and Chen, C and Liu, H and Wang, W and Zhou, X and Guo, M and Zhao, J and Zeng, Z and Xu, L},
title = {Decoding the gut microbiota-immune dialogue: from bidirectional axis to therapeutic applications.},
journal = {Journal of nanobiotechnology},
volume = {24},
number = {1},
pages = {},
pmid = {41981603},
issn = {1477-3155},
support = {82160503, 82272812//National Natural Science Foundation of China/ ; QKHZC-2020-4Y156, QKH-JC-2018-1428, QKHJC-ZK-2022-624//Project of the Guizhou Provincial Department of Science and Technology/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; Fecal Microbiota Transplantation ; Inflammatory Bowel Diseases/immunology/microbiology/therapy ; Autoimmune Diseases/immunology/microbiology/therapy ; *Immune System ; },
abstract = {The gut microbiota (GM), a highly complex micro-ecosystem residing within the host’s gastrointestinal tract, works in conjunction with the gut immune system to form a precise bidirectional regulatory network, that maintains symbiotic homeostasis and overall host health. Cumulative evidence has demonstrated that the critical impact of the bidirectional causal relationship between the GM and the gut immune system on host development and the dynamic progression of disease. However, many challenges remain in this research field, including the mechanism complexity, therapeutic effect differences due to individual heterogeneity, long-term safety, and clinical transformation bottlenecks) that need to be urgently broken through. Therefore, the in-depth analysis of these issues is of great theoretical and practical significance for clarifying the intrinsic connection between the GM and gut immunity, particularly in elucidating the pathogenesis of related clinical diseases such as inflammatory bowel disease (IBD), tumors, and autoimmune diseases (AD). We systematically outline the interaction mechanisms between the microbiota and the immune system, including compositional structure (microbiota diversity and immune system composition), development and maturation processes (early microbiota colonization and immune system establishment), and functional regulation (immune cell differentiation and maintenance of mucosal barrier integrity), as well as their associations with clinical diseases. Finally, we discuss some key considerations for the developing of innovative treatment strategies, such as microbial-targeted interventions, fecal microbiota transplantation (FMT), and synergistic use of immunomodulatory drugs, with the aim of providing a new paradigm for the precise intervention of related diseases.},
}

Humans
*Gastrointestinal Microbiome/immunology
Animals
Fecal Microbiota Transplantation
Inflammatory Bowel Diseases/immunology/microbiology/therapy
Autoimmune Diseases/immunology/microbiology/therapy
*Immune System

@article {pmid41982910,
year = {2025},
author = {Santos, S and Salinas, I and Almeida, N and Caicedo, A},
title = {The role of microbiota dysbiosis in Parkinson's disease: Pathophysiology and therapeutic opportunities.},
journal = {Engineering microbiology},
volume = {5},
number = {3},
pages = {100222},
pmid = {41982910},
issn = {2667-3703},
abstract = {Parkinson's disease (PD) is a chronic, progressive neurodegenerative disorder characterized by debilitating motor and non-motor symptoms. Its etiology is multifactorial, with no single definitive cause identified, although aging is a significant risk factor. Additional risks include genetic predisposition, family history, and environmental factors such as pesticide exposure and Helicobacter pylori infection. Dysbiosis of the gut microbiota, and in particular bacterial imbalances, has been implicated in the disruption of the gut-brain axis, contributing to both systemic and neuroinflammation. Environmental factors such as antibiotic exposure and toxins can precipitate microbial dysregulation, potentially accelerating PD progression. Understanding the mechanisms of the gut-brain axis and identifying strategies to preserve a healthy microbiome are essential for developing novel therapeutic approaches. This review synthesizes current therapeutic strategies and ongoing research focused on restoring gut-brain balance to combat PD. These approaches include fecal microbiota transplantation, dietary interventions, and probiotic therapies, all of which show promise in mitigating both motor and non-motor symptoms. Furthermore, we emphasize the urgent need for continued research into probiotics and innovative therapeutic approaches for gut-brain axis modulation, presenting novel opportunities for effective PD management.},
}

@article {pmid41983065,
year = {2026},
author = {Zhao, X and Lv, Z and Liu, H and Zhang, J},
title = {Fecal microbiota transplantation for intractable diarrhea due to severe dysbiosis and cytomegalovirus enteritis: a case report.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1728176},
pmid = {41983065},
issn = {2296-861X},
abstract = {BACKGROUND: Cytomegalovirus (CMV) enteritis can lead to intractable diarrhea, especially when complicated by severe gut dysbiosis, posing a significant therapeutic challenge.

METHODS: We present a case of a 40-year-old woman with a history of traumatic brain injury and prolonged broad-spectrum antibiotic use, who developed persistent bloody, mucus-containing diarrhea (up to 40 episodes daily). Colonoscopy with biopsy confirmed CMV enteritis, and 16S rRNA sequencing revealed severe intestinal dysbiosis. Treatment consisted of intravenous ganciclovir combined with multiple sessions of fecal microbiota transplantation (FMT) delivered via jejunal tube, alongside tailored nutritional support.

RESULTS: Despite initial persistence of symptoms, the combined antiviral and FMT regimen led to resolution of diarrhea, normalization of inflammatory markers, and restoration of enteral tolerance. Follow-up colonoscopy showed mucosal healing and negative CMV staining. Microbiota analysis demonstrated restoration of diversity and a shift toward donor-like taxonomic profiles.

CONCLUSION: This case highlights CMV as an emerging cause of severe enteritis in non-immunosuppressed surgical patients and supports the efficacy of combined antiviral therapy and FMT for refractory diarrhea associated with dysbiosis and CMV infection.},
}

@article {pmid41983510,
year = {2026},
author = {Xie, W and Yuan, J and Feng, C and Shi, H and Zhang, C and Xi, T and Huang, J and Fang, W and Ni, Z and Gu, L and Jiang, N},
title = {Alteration of gut microbiota contributes to peritoneal fibrosis through increased production of trimethylamine N-oxide.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2657048},
pmid = {41983510},
issn = {1949-0984},
mesh = {Animals ; *Methylamines/metabolism ; *Peritoneal Fibrosis/microbiology/metabolism/pathology/etiology ; Humans ; *Gastrointestinal Microbiome/physiology ; Mice ; Peritoneal Dialysis/adverse effects ; Peritoneum/pathology/metabolism ; Fecal Microbiota Transplantation ; Mice, Inbred C57BL ; Male ; Mice, Knockout ; Transforming Growth Factor beta1/metabolism ; Disease Models, Animal ; },
abstract = {Peritoneal fibrosis is a common complication in peritoneal dialysis (PD) patients, which results in ultrafiltration failure (UFF) and PD withdrawal. PD patients demonstrate altered structural and functional profiles of the gut microbiota. Herein, we investigated the role of the gut microbiota and trimethylamine N-oxide (TMAO), a bacterial metabolite, in the pathogenesis of PD-associated peritoneal fibrosis. PD mice displayed mesenchymal transition features and fibrosis in the peritoneum, which were accompanied by an altered gut microbiota profile and elevated serum TMAO levels, and these peritoneal histologic abnormalities were ameliorated by gut microbiota depletion. Fecal microbiota transplantation (FMT) from PD patients induced mesenchymal and fibrotic alterations within the peritoneum of wild-type mice, and the effect was more pronounced in mice receiving FMT from PD patients with UFF. Intraperitoneal supplementation with TMAO enhanced PD-induced peritoneal fibrosis in wild-type mice. On the contrary, PD- or FMT-induced mesenchymal features and fibrosis within the peritoneal membrane were lessened in flavin-containing monooxygenase 3 gene knockout mice, which were incapable of synthesizing TMAO. TMAO treatment enhanced high glucose-mediated phenotypic transition and fibrogenesis in cultured peritoneal mesothelial cells and fibroblasts, partly by increasing TGF-β1 synthesis and secretion and subsequent phosphorylation of Smad2/3 and activation of the Wnt/β-catenin pathway. Collectively, we found that altered gut microbiota plays an important role in the development of PD-associated peritoneal fibrosis through dysregulated production of the bacterial metabolite TMAO.},
}

Animals
*Methylamines/metabolism
*Peritoneal Fibrosis/microbiology/metabolism/pathology/etiology
Humans
*Gastrointestinal Microbiome/physiology
Mice
Peritoneal Dialysis/adverse effects
Peritoneum/pathology/metabolism
Fecal Microbiota Transplantation
Mice, Inbred C57BL
Male
Mice, Knockout
Transforming Growth Factor beta1/metabolism
Disease Models, Animal

@article {pmid41983911,
year = {2026},
author = {Schindler, V and Zeitz, J and Bianca, A and Murray, F and Schuler, J and Pohl, D},
title = {Patients' view on fecal microbiota transplantation in disorders of gut-brain interaction: a survey-based study.},
journal = {Minerva gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.23736/S2724-5985.26.03999-9},
pmid = {41983911},
issn = {2724-5365},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) has gained popularity over the last years. So far, conflicting data regarding the effect on disorders of gut-brain interaction (DGBI) exist. In this study we aimed to access current knowledge and attitude towards potential FMT of DGBI patients.

METHODS: A survey on attitudes toward FMT was conducted in DGBI patients. Patients answered questions anonymously before and after having read a brief information sheet on FMT. Data were collected prospectively in 2017-2018 and in 2022-2023.

RESULTS: In total, 387 patients completed the survey. Forty percent of patients had heard about FMT prior to underlying survey. Prior to a brief information regarding FMT, 38% of patients would have agreed to FMT, while 50% were undecided and 12% would have declined. After a brief information sheet on FMT, decisions significantly changed to 63%, 26% and 11% respectively (P<0.001). The decision of patients to undergo FMT remained unchanged between 2017 and 2022. Type of DGBI and disease severity are significantly associated with treatment decisions (P=0.005).

CONCLUSIONS: This survey demonstrates great interest of DGBI patients in potential FMT, especially after being informed on details of the procedure. Bearing in mind that in the future FMT may be a clearer option in the treatment of certain DGBIs, patient education will be an important factor.},
}

@article {pmid41985671,
year = {2026},
author = {Wang, Y and Liu, X and Li, Z and Kang, A and Bai, Y and Wang, Y and Liu, Y and Zhang, C and Yang, J and Cai, Q and Feng, Y and Yi, H and Zhang, M and Zhang, F and Liu, H and Xu, C},
title = {Oligofructose alleviates hyperandrogenism in polycystic ovary syndrome through gut microbiota-derived bile acids.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.04.036},
pmid = {41985671},
issn = {2090-1224},
abstract = {INTRODUCTION: Polycystic ovary syndrome (PCOS) is a common endocrine disorder in reproductive-age women, characterized by hyperandrogenism and metabolic dysfunction. Dietary interventions are recommended as one of the first-line therapies. Oligofructose (OFS), a prebiotic fiber, has demonstrated clinical benefits in PCOS; however, its underlying mechanism remains unclear.

OBJECTIVES: To determine whether OFS alleviates PCOS-like phenotypes through bile acid-dependent mechanisms and to identify downstream ovarian steroidogenic responses.

METHODS: Letrozole-induced PCOS-like mice received OFS supplementation. Microbiota dependence was assessed using antibiotic depletion and fecal microbiota transplantation. Bile acid involvement was evaluated using cholestyramine. Gut microbial composition and function were profiled by 16S rRNA and metagenomic sequencing, and bile acids were quantified by UHPLC-MS/MS. Ovarian transcriptomics, ex vivo ovarian explants, and primary granulosa cells were used to examine steroidogenic changes, with pharmacological inhibition applied to assess TGR5-related signaling.

RESULTS: OFS improved reproductive and metabolic abnormalities in PCOS-like mice. These benefits were abolished by microbiota depletion and bile acid sequestration, indicating microbiota- and bile acid-dependent effects. OFS was associated with increased circulating hyodeoxycholic acid (HDCA), which negatively correlated with serum testosterone. HDCA supplementation partially reproduced endocrine improvements under microbiota-depleted conditions. Ovarian transcriptomic and functional analyses demonstrated enhanced aromatization following OFS treatment. In ex vivo ovarian explants and primary granulosa cells, HDCA increased estradiol production, reduced testosterone, and upregulated CYP19A1 (encoding aromatase). Under androgen stimulation, pharmacological inhibition of TGR5 attenuated HDCA-associated increases in estradiol and aromatase activity, supporting involvement of TGR5-related signaling.

CONCLUSION: OFS alleviates PCOS-like phenotypes in a microbiota- and bile acid-dependent manner and enhances ovarian aromatization. These findings move beyond descriptive bile acid alterations in PCOS by providing functional evidence that dietary fiber-induced bile acid remodeling is associated with modulation of ovarian steroidogenic regulation.},
}

@article {pmid41988171,
year = {2026},
author = {Zou, Q and Zhang, Y and Zou, S and Li, Y and Li, H and Yang, M and Lai, H and Niu, R and Yang, X and Zhou, L},
title = {Ciprofloxacin-induced microbiota dysbiosis triggers seizure susceptibility through the microbiota-gut-brain axis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1670694},
pmid = {41988171},
issn = {1664-3224},
mesh = {Animals ; *Dysbiosis/chemically induced ; Male ; *Seizures/chemically induced/etiology/microbiology/metabolism ; Rats ; *Gastrointestinal Microbiome/drug effects ; *Ciprofloxacin/adverse effects ; Blood-Brain Barrier/metabolism ; Rats, Sprague-Dawley ; *Brain-Gut Axis/drug effects ; Disease Susceptibility ; Fecal Microbiota Transplantation ; Disease Models, Animal ; Intestinal Barrier Function ; },
abstract = {BACKGROUND: Epilepsy is linked to inflammation and gut microbiota dysbiosis. Ciprofloxacin-induced microbiota disruption may increase seizure susceptibility. This study investigates underlying mechanisms and the therapeutic potential of fecal microbiota transplantation (FMT).

METHODS: A total of 64 male Sprague-Dawley rats were categorized into four experimental groups: Control (CTRL), Ciprofloxacin-treated (CPF), CPF with fecal microbiota transplantation (CPF-FMT), and CPF with phosphate-buffered saline (CPF-PBS). Gut microbiota dysbiosis was induced with ciprofloxacin for 14 days, followed by either FMT or PBS for 14 days. Seizure susceptibility was assessed using pentylenetetrazole (PTZ), alongside molecular analyses of gut and blood-brain barrier integrity, neuroinflammatory markers, and cortical transcriptomics.

RESULTS: Microbiota dysbiosis was associated with increased seizure susceptibility, accompanied by disruption of intestinal and blood-brain barrier (BBB) integrity, thereby exacerbating systemic and neuroinflammation. Dysbiotic rats exhibited significant reductions in microbial diversity and depletion of protective taxa, including f_Muribaculaceae, f_Prevotellaceae, and Lachnospiraceae_NK4A136_group, which correlated with intestinal barrier dysfunction. This dysfunction was associated with reduced tight junction proteins (ZO-1, Occludin, Claudin-5) and inflammatory cell infiltration. Systemic inflammation and disrupted blood-brain barrier integrity resulted in microglial activation and astrocytic proliferation in the brain. Notably, FMT was related to restoration of microbial diversity, improvement of barrier-related markers, attenuation of neuroinflammatory responses, and a reduction in seizure susceptibility.

CONCLUSION: This study provides evidence linking gut microbiota dysbiosis to seizure susceptibility through neuroinflammatory processes, contributing to the understanding of gut-brain axis involvement in fluoroquinolone-induced seizures.},
}

Animals
*Dysbiosis/chemically induced
Male
*Seizures/chemically induced/etiology/microbiology/metabolism
Rats
*Gastrointestinal Microbiome/drug effects
*Ciprofloxacin/adverse effects
Blood-Brain Barrier/metabolism
Rats, Sprague-Dawley
*Brain-Gut Axis/drug effects
Disease Susceptibility
Fecal Microbiota Transplantation
Disease Models, Animal
Intestinal Barrier Function

@article {pmid41989595,
year = {2026},
author = {Walker, MR and Schwarzfischer, M and Scharl, M},
title = {The cancer-microbiome axis: Mechanisms and emerging therapeutic strategies.},
journal = {Seminars in immunopathology},
volume = {48},
number = {1},
pages = {},
pmid = {41989595},
issn = {1863-2300},
mesh = {Humans ; *Neoplasms/therapy/etiology/metabolism/microbiology/immunology ; Animals ; Tumor Microenvironment/immunology ; Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome/immunology ; *Microbiota ; Disease Susceptibility ; Host-Pathogen Interactions/immunology ; Immunomodulation ; Dysbiosis ; },
abstract = {The human microbiome has emerged as a critical modulator of cancer development, progression, and therapeutic response. Advances in sequencing and functional profiling have revealed that commensal microorganisms—particularly bacteria—interact closely with host immune and metabolic pathways, influencing tumor immunity across multiple cancer types. Dysbiosis of the gut microbiome has been associated with tumorigenesis, immune evasion, and resistance to therapy, while specific microbial taxa and metabolites have been shown to enhance antitumor immune responses. These discoveries have catalyzed the development of microbiome-based therapeutic strategies aimed at reshaping host–tumor interactions. This review summarizes current understanding of the cancer–microbiome axis, with a particular focus on therapeutic interventions that leverage microbial modulation. We discuss fecal microbiota transplantation (FMT) as an early, proof-of-concept approach demonstrating the capacity of the microbiome to restore responsiveness to immune checkpoint inhibitors, while also highlighting its limitations related to variability, standardization, and mechanistic uncertainty. We then examine emerging reductionist strategies, including supplementation with individual bacterial strains, defined consortia, and engineered microbes designed to deliver immunomodulatory payloads directly within the tumor microenvironment. Finally, we explore how microbial modulation interfaces with conventional cancer therapies such as chemotherapy, hormonal therapy, and cellular immunotherapies. Together, these studies illustrate a rapidly evolving field transitioning from correlative observations to mechanistically informed therapeutic design. While significant technical and biological challenges remain, continued integration of microbiology, immunology, and synthetic biology holds promise for translating microbiome-based interventions into safe, precise, and effective cancer therapies.},
}

Humans
*Neoplasms/therapy/etiology/metabolism/microbiology/immunology
Animals
Tumor Microenvironment/immunology
Fecal Microbiota Transplantation
*Gastrointestinal Microbiome/immunology
*Microbiota
Disease Susceptibility
Host-Pathogen Interactions/immunology
Immunomodulation
Dysbiosis

@article {pmid41990750,
year = {2026},
author = {Gonzalez Pastor, B and Shkoporov, AN and Hill, C},
title = {Not just passengers: Phages as agents of genetic exchange in fecal microbiota transplantation.},
journal = {Cell host & microbe},
volume = {34},
number = {5},
pages = {780-789},
doi = {10.1016/j.chom.2026.03.017},
pmid = {41990750},
issn = {1934-6069},
mesh = {*Fecal Microbiota Transplantation/methods ; *Bacteriophages/genetics/physiology ; Humans ; *Gene Transfer, Horizontal ; *Gastrointestinal Microbiome/genetics ; Bacteria/genetics/virology ; Clostridium Infections/therapy ; Animals ; Clostridioides difficile ; Feces/microbiology ; Virome ; },
abstract = {Fecal microbiota transplantation (FMT) is an effective therapy for recurrent Clostridioides difficile infection and is increasingly being explored for other microbiota-associated diseases. However, general research has largely focused on bacterial engraftment, overlooking the contribution of the gut virome. In this perspective, we highlight phage-mediated horizontal gene transfer (HGT) as a potentially influential process occurring following FMT. Donor-derived phages may potentially influence community structure, engraft in resident bacteria, and modulate microbial functions or host physiology. In addition, temperate phages are well-equipped to mobilize bacterial genes, such as metabolic functions, stress-response traits, and antibiotic resistance determinants, raising the possibility that gene flow could well contribute to FMT outcomes. We propose a conceptual model in which phages act as bidirectional mediators of adaptation, not only accompanying bacterial communities but also influencing gut ecosystems in subtle, yet potentially consequential, ways.},
}

*Fecal Microbiota Transplantation/methods
*Bacteriophages/genetics/physiology
Humans
*Gene Transfer, Horizontal
*Gastrointestinal Microbiome/genetics
Bacteria/genetics/virology
Clostridium Infections/therapy
Animals
Clostridioides difficile
Feces/microbiology
Virome

@article {pmid41991237,
year = {2026},
author = {Wang, MT and Wang, D and Qi, YP and Chen, Q and Qin, XM and Wang, T and Lu, WH and Cao, YY},
title = {Fecal microbiota transplantation alleviates sepsis-induced acute lung injury by improving mitochondrial function.},
journal = {The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology},
volume = {30},
number = {5},
pages = {395-405},
doi = {10.4196/kjpp.25.304},
pmid = {41991237},
issn = {1226-4512},
abstract = {Sepsis-induced acute lung injury (ALI) remains a critical clinical challenge with limited therapeutic options. This study investigated the protective effects and underlying mechanisms of fecal microbiota transplantation (FMT) in a murine model of sepsis-induced ALI. 16S rRNA sequencing confirmed that FMT rescued sepsis-induced gut microbiota dysbiosis, restoring microbial diversity and composition. The results demonstrated that FMT significantly improved survival, attenuated pulmonary pathological damage and edema, and reduced systemic and pulmonary levels of proinflammatory cytokines (TNF-α, IL-6, and IL-1β). Furthermore, FMT preserved alveolar-capillary barrier integrity, as evidenced by reduced vascular permeability and upregulated expression levels of tight junction proteins (ZO-1 and occludin). Mechanistically, FMT ameliorated mitochondrial dysfunction in lung tissue, as evidenced by the restoration of oxidative phosphorylation capacity, increased ATP production, reduced mitochondrial reactive oxygen species accumulation, and decreased mitochondrial DNA release. These improvements were associated with a rebalancing of mitochondrial dynamics, characterized by increased expression levels of fusion proteins (OPA1, Mfn1, and Mfn2) and decreased expression of a fission protein (Drp1). Our findings highlight the gut-lung axis as a therapeutic target in sepsis and demonstrate that FMT alleviates sepsis-induced ALI by restoring gut microbiota homeostasis and subsequently preserving mitochondrial function. Further clinical studies are warranted to validate these preclinical findings and explore optimal FMT protocols for critical care applications.},
}

@article {pmid41992528,
year = {2026},
author = {Yanyan, X and Yanyu, Q and Qiao, G and Jiabo, G and Desong, K and Heiying, J},
title = {Atractylenolide III Alleviates the Lipid Metabolic Disorders in Ovariectomy-Induced Estrogen-Deficient Mice Through Repairing Intestinal Inflammation and Microenvironment.},
journal = {The journal of obstetrics and gynaecology research},
volume = {52},
number = {4},
pages = {e70272},
pmid = {41992528},
issn = {1447-0756},
support = {//National Natural Science Foundation of China/ ; SJCX23_0770//Jiangsu Provincial Department of Education/ ; SJCX23_0874//Jiangsu Provincial Department of Education/ ; MS2023047//Jiangsu Provincial Health Commission/ ; },
mesh = {Animals ; Female ; Ovariectomy/adverse effects ; *Lactones/pharmacology/administration & dosage ; Mice ; Mice, Inbred C57BL ; *Sesquiterpenes/pharmacology/administration & dosage ; *Estrogens/deficiency ; *Lipid Metabolism Disorders/drug therapy/etiology ; *Inflammation/drug therapy ; Lipid Metabolism/drug effects ; Gastrointestinal Microbiome/drug effects ; },
abstract = {OBJECTIVE: To investigate the mechanism by which Atractylenolide III (ATIII) alleviates ovariectomy-induced, estrogen-deficient lipid metabolism disorders through the repair of intestinal inflammation and the barrier microenvironment.

METHODS: Female C57BL/six mice (8 weeks old) were randomly assigned to three groups: a blank control group (Con, n = 10), a sham surgery group (Sham, n = 10), and an ovariectomized (OVX) group (n = 70). The OVX group was further subdivided into a model group (OVX + HFD), low- and high-dose ATIII groups (ATIII-L, ATIII-H), an estradiol (E2) group, and groups receiving fecal microbiota transplantation (FMT) from the blank control, model, or high-dose ATIII donors. After 60 days on a high-calorie diet, treatments were administered for 28 consecutive days. Serum, liver, and intestinal tissues, and cecal contents were collected from six randomly selected mice per group. Body weight was monitored; hepatic and colonic morphology was assessed by H&E staining; serum lipid profiles were determined using an automated biochemical analyzer; ELISA quantified estradiol and inflammatory cytokine levels; expression of colonic barrier-related proteins was evaluated by Western blot; and gut microbiota composition was analyzed via 16S rRNA sequencing.

RESULTS: Under conditions of estrogen deficiency, a high-calorie diet mimicking modern human intake predisposed mice to significant weight gain (p < 0.05) and dyslipidemia, accompanied by a spectrum of pathological alterations including intestinal barrier dysfunction (evidenced by downregulated tight junction proteins), systemic inflammation (reflected by elevated pro-inflammatory cytokines), hepatic steatosis, colonic inflammatory damage, and gut microbiota dysbiosis. ATIII intervention effectively mitigated these abnormalities, as demonstrated by reduced body weight, improved lipid profiles, repaired hepatic and colonic injuries, upregulated intestinal barrier proteins, downregulated inflammatory cytokines, a tendency toward elevated estrogen levels, and enhanced gut microbial diversity.

CONCLUSIONS: ATIII ameliorates ovariectomy-induced estrogen-deficient dyslipidemia by repairing intestinal barrier function and modulating intestinal inflammation. Concurrently, it exerts beneficial effects on estrogen levels and gut microbiota composition, in which the gut microbiota plays a mediating role. The experiment demonstrated that the active ingredients of traditional Chinese medicine hold significant value in treating lipid metabolism disorders in perimenopausal women, and there is potential for further in-depth research into the mechanism by which they enhance efficacy through modulating gut microbiota.},
}

Animals
Female
Ovariectomy/adverse effects
*Lactones/pharmacology/administration & dosage
Mice
Mice, Inbred C57BL
*Sesquiterpenes/pharmacology/administration & dosage
*Estrogens/deficiency
*Lipid Metabolism Disorders/drug therapy/etiology
*Inflammation/drug therapy
Lipid Metabolism/drug effects
Gastrointestinal Microbiome/drug effects

@article {pmid41993214,
year = {2026},
author = {Zhang, H and Ye, P and Yang, W and Dou, Y and Tian, Z and Zhang, N and Cui, N and Sun, L and Liu, Z and Chen, Y and Liu, X and Yang, H},
title = {Berberine protects against hypoxia-induced intestinal injury through modulation of gut microbiota and bile acid metabolism.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1784245},
pmid = {41993214},
issn = {1664-3224},
mesh = {Animals ; *Berberine/pharmacology ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Hypoxia/complications/metabolism ; *Bile Acids and Salts/metabolism ; Intestinal Barrier Function ; Male ; Intestinal Mucosa/metabolism/drug effects ; Disease Models, Animal ; Mice, Inbred C57BL ; *Intestines/drug effects ; *Intestinal Diseases/etiology/metabolism/prevention & control ; },
abstract = {BACKGROUND: High-altitude hypoxia disrupts intestinal homeostasis by impairing the epithelial barrier, triggering inflammation, and promoting microbial translocation. Berberine (BER), a natural isoquinoline alkaloid with antimicrobial and anti-inflammatory properties, has shown potential in protecting intestinal integrity; however, its efficacy under hypoxic conditions and its interaction with the gut microbiota remain unclear.

METHODS: A chronic hypoxia mouse model was used to investigate the protective effects of BER against intestinal injury. Microbiota dependency was assessed through antibiotic-mediated depletion and fecal microbiota transplantation (FMT), combined with 16S rRNA gene sequencing, metabolomics, and immune profiling. The functional role of a BER-responsive bacterium was validated by oral administration in antibiotic-treated mice.

RESULTS: BER supplementation restored epithelial barrier integrity, including tight junctions, antimicrobial peptide expression, and goblet cell function, while reducing inflammation and epithelial apoptosis under hypoxic conditions. BER also reshaped gut microbial composition and network structure, accompanied by coordinated alterations in cecal metabolites, particularly purine metabolites and bile acids. Microbiota depletion abolished the protective effects of BER, whereas FMT from BER-treated donors recapitulated these effects, confirming a microbiota-dependent mechanism. Among BER-responsive taxa, Bacteroides thetaiotaomicron (B. thetaiotaomicron) emerged as a key effector, correlating with metabolite profiles and barrier integrity. Oral administration of B. thetaiotaomicron alone protected against hypoxia-induced intestinal injury, restoring mucin production and antimicrobial peptide expression, and attenuating inflammation and apoptosis. Mechanistically, both BER and B. thetaiotaomicron reactivated bile acid-FXR signaling and normalized intestinal immune homeostasis, including T-cell subset distribution.

CONCLUSION: These findings demonstrate that BER protects against hypoxia-induced intestinal injury through microbiota-dependent metabolic and immune regulation. B. thetaiotaomicron acts as a central mediator of this protective effect, highlighting microbiota-targeted strategies as potential interventions for maintaining intestinal homeostasis under hypoxic stress.},
}

Animals
*Berberine/pharmacology
*Gastrointestinal Microbiome/drug effects
Mice
*Hypoxia/complications/metabolism
*Bile Acids and Salts/metabolism
Intestinal Barrier Function
Male
Intestinal Mucosa/metabolism/drug effects
Disease Models, Animal
Mice, Inbred C57BL
*Intestines/drug effects
*Intestinal Diseases/etiology/metabolism/prevention & control

@article {pmid41993582,
year = {2026},
author = {Simões, JLB and Braga, GC and Assmann, CE and Bagatini, MD},
title = {Targeting the gut-immune-brain axis: pharmacological insights from depression in inflammatory bowel disease.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1793292},
pmid = {41993582},
issn = {1663-9812},
abstract = {Inflammatory Bowel Disease (IBD), comprising Crohn's Disease and Ulcerative Colitis, is a chronic inflammatory condition of the gastrointestinal tract with a remarkably high prevalence of psychiatric comorbidities, particularly Major Depressive Disorder (MDD). The traditional monoaminergic hypothesis of depression is insufficient to explain the complex etiology of MDD, paving the way for new paradigms, such as the inflammatory hypothesis of depression. This narrative review critically explores IBD as a human clinical model to investigate the connection between chronic inflammation and depression. It is argued that gut dysbiosis, a central feature of IBD, is a fundamental trigger that, through a compromised gut barrier, drives systemic inflammation and, subsequently, neuroinflammation. We detail the molecular and cellular mechanisms that link intestinal inflammation to central nervous system (CNS) dysfunction, including microglial activation, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and kynurenine pathway activation, which diverts tryptophan metabolism from serotonin synthesis to the production of neurotoxic metabolites. Robust epidemiological evidence demonstrating a bidirectional association between IBD and depression is discussed, suggesting a shared pathophysiology rather than a simple cause-and-effect relationship. Furthermore, we review the implications and emerging therapeutics, highlighting the antidepressant effects of immunobiologicals, such as anti-TNF therapies, and the potential of emerging interventions that target the microbiome, such as probiotics, psychobiotics, fecal microbiota transplantation, and anti-inflammatory diets. Furthermore, we address the limitations of the current literature, such as the lack of a quantitative definition for dysbiosis and the scarcity of clinical trials with integrated neuropsychiatric outcomes, and propose directions for future translational research. We conclude that IBD should be considered a systemic disease with significant psychiatric repercussions, advocating for an integrated therapeutic approach that combines immunomodulatory, neuromodulatory, and microbiological interventions to treat both gut and brain pathology effectively.},
}

@article {pmid41993584,
year = {2026},
author = {Liang, X and He, J and Wu, Q and Fu, L and Liu, Y},
title = {Gut microbiome in alcohol-associated liver disease: interactions and therapeutic strategies.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1770833},
pmid = {41993584},
issn = {1663-9812},
abstract = {Alcohol-associated liver disease (ALD), a significant cause of chronic liver disease worldwide, is strongly linked to gut microbiome dysregulation. Heavy alcohol use disrupts the gut bacterial equilibrium and damages the intestinal barrier, making it more permeable to microbial toxins (e.g., endotoxins) that trigger liver inflammation. Many studies have investigated ALD, but no single microbial marker has yet been identified as diagnostic. Results from microbiome studies on this condition have been inconsistent; consequently, scientists are developing new microbiome-based indices and multi-omics approaches to improve their ability to predict diseases. The review evaluates current findings on how disturbances in the gut microbiome and deterioration of the intestinal barrier contribute to the development of ALD. The assessment includes microbiome-based treatments such as probiotics, fecal microbiota transplantation (FMT), and bacteriophage therapy. Research indicates that probiotics and FMT treatments may enhance liver function and reduce inflammation in patients with ALD. The studies present conflicting results because researchers used different methods and worked with limited numbers of participants. Bacteriophage therapy exists as an experimental treatment method. The development of personalized microbiome treatments, along with biomarker standardization and solutions to technical and ethical challenges, will enable these strategies to enter medical practice. The review integrates existing knowledge of the gut-liver axis in ALD to demonstrate the clinical potential of microbiome-based treatments while highlighting the need for additional research to enhance treatment outcomes.},
}

@article {pmid41993996,
year = {2026},
author = {Au Yong, SJ and Lestari Lee, AS and Subramaniyan, V and Long, CM and Husain, S and Reginald, K and Ser, HL},
title = {Gut microbiome modulation in allergic rhinitis: from current evidence to emerging therapies.},
journal = {Frontiers in allergy},
volume = {7},
number = {},
pages = {1761840},
pmid = {41993996},
issn = {2673-6101},
abstract = {Allergic rhinitis (AR) is a common inflammatory disorder of the upper airway that is primarily managed with pharmacotherapy, biologics and allergen immunotherapy. However, a substantial proportion of patients experience incomplete or insufficient symptom control, treatment-related adverse effects, or poor adherence. Increasing evidence has linked AR with alterations in microbial composition across multiple mucosal sites, including the gut, highlighting potential roles for host-microbiome interactions in the regulation of allergic inflammation, although causal relationships remain incompletely defined. This narrative mini-review synthesizes current evidence on gut microbiome-based interventions for allergic rhinitis (AR), including probiotics, prebiotics, synbiotics, postbiotics, and emerging approaches such as fecal microbiota transplantation, engineered microbes, and bacteriophage-based therapies. It examines proposed immunological mechanisms involving type 2 inflammation, regulatory immune pathways, and gut-airway axis signalling, while distinguishing clinically evaluated strategies from experimental or preclinical and assessing their translational readiness. Collectively, available evidence suggests that microbiome-targeted therapies represent a promising conceptual avenue for understanding and potentially modulating AR. However, their clinical application remains constrained by heterogeneous study designs, reliance on extrapolated data from preclinical studies, limited standardized outcome measures, insufficient long-term safety data, and evolving regulatory frameworks. Addressing these challenges through well-designed clinical trials and improved mechanistic characterization will be essential to clarify the role of microbiome-based interventions as adjunctive strategies in AR management.},
}

@article {pmid41994273,
year = {2026},
author = {Yu, Z and Qian, W and Chu, Y},
title = {Targeting the gut-lung axis in COPD: from microbial metabolites to fecal microbiota transplantation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1798150},
pmid = {41994273},
issn = {1664-302X},
abstract = {Chronic obstructive pulmonary disease (COPD) is a complex, multidimensional syndrome manifested by persistent airway inflammation, oxidative stress, and progressive airflow limitation, with pathology extending far beyond the lung. The gut-lung axis has emerged as a pivotal paradigm for understanding this systemic nature, underscoring the regulatory potency of gut microbiota-derived metabolites in inter-organ immune and metabolic crosstalk. Accumulating evidence suggests that COPD is intricately linked to gut microbiota dysbiosis and widespread disturbances in bioactive metabolites, particularly short-chain fatty acids (SCFAs), tryptophan-related amino acids (AAs), and bile acids (BAs). These metabolic aberrations exacerbate pulmonary inflammation by dysregulating immune homeostasis, compromising intestinal barrier integrity, and skewing redox balance. Fecal microbiota transplantation (FMT), as a strategy capable of comprehensively reconstituting gut microbial and metabolic homeostasis, has demonstrated potential in preclinical and translational settings to attenuate pulmonary injury via the gut-lung axis. This review centers on gut microbiota-associated metabolites, systematically summarizing their roles in COPD pathogenesis and critically evaluating the emerging evidence and mechanistic basis by which FMT recalibrates COPD progression through metabolic pathways, thereby providing a robust theoretical framework for developing precision gut microbiota-targeted systemic therapeutic strategies.},
}

@article {pmid41994742,
year = {2026},
author = {Vadukoot Lazar, M and C S Menon, A and Thomas, J},
title = {Type 3c Diabetes Mellitus: Epidemiology, Diagnosis, Management, and Research Imperatives With Insights From the United Arab Emirates and Global Contexts.},
journal = {Cureus},
volume = {18},
number = {3},
pages = {e105089},
pmid = {41994742},
issn = {2168-8184},
abstract = {Type 3c diabetes mellitus (T3cDM), also known as pancreatogenic diabetes, is a form of secondary diabetes resulting from pancreatic disease and is frequently misclassified as type 2 DM (type 2 DM). A narrative review of peer-reviewed literature from international databases was conducted, with emphasis on the epidemiology, clinical differences, diagnostic complexities, and management of T3cDM, with a specific focus on the United Arab Emirates (UAE) and global contexts. T3cDM accounts for a notable proportion of global diabetes cases, yet it is underreported due to a lack of dedicated registries and frequent misclassification as type 2 diabetes. The UAE has one of the highest diabetes prevalence rates worldwide, yet T3cDM remains undercaptured. Unlike type 1 DM (T1DM) and T2DM, T3cDM is characterized by both endocrine and exocrine pancreatic insufficiency (EPI). The diagnosis requires evidence of pancreatic pathology, absent autoimmunity, and exocrine dysfunction. Management includes insulin therapy, pancreatic enzyme replacement therapy (PERT), and nutritional supplementation; recent advances include the role of incretin therapies, improved enzyme preparations, and regenerative medicines. Emerging approaches also include metabolomics for prediction and fecal microbiota transplantation. Increasing awareness, dedicating regional registries, and implementing multidisciplinary management strategies are urgently needed in the UAE and globally.},
}

@article {pmid41995553,
year = {2026},
author = {Tseng, WC and Chen, KC and Chung, CS and Tseng, PC and Lin, CK and Liao, CH},
title = {Comparative effectiveness of vancomycin and fidaxomicin in the treatment of Clostridioides difficile-associated diarrhea: A single-center experience in Taiwan.},
journal = {Medicine},
volume = {105},
number = {16},
pages = {e48307},
pmid = {41995553},
issn = {1536-5964},
mesh = {Humans ; *Fidaxomicin/therapeutic use ; *Vancomycin/therapeutic use ; Female ; Aged ; Male ; Taiwan ; *Diarrhea/drug therapy/microbiology ; Retrospective Studies ; *Clostridium Infections/drug therapy/microbiology ; *Anti-Bacterial Agents/therapeutic use ; Middle Aged ; *Clostridioides difficile/drug effects ; Aged, 80 and over ; Treatment Outcome ; Fecal Microbiota Transplantation ; Adult ; },
abstract = {Clostridioides difficile-associated diarrhea (CDAD) has become an increasingly common healthcare-associated infection worldwide. Although both vancomycin and fidaxomicin are approved for treatment, real-world comparative data from Taiwan remain limited. This study aimed to evaluate the effectiveness of vancomycin and fidaxomicin in treating CDAD and to identify patients at risk of treatment failure who may benefit from fecal microbiota transplantation. This single-center retrospective observational study was conducted at Far Eastern Memorial Hospital from January 2018 to August 2020. Adult patients (≥20 years) diagnosed with CDAD and treated with oral vancomycin (125 mg 4 times daily) and/or fidaxomicin (200 mg twice daily) for 10 days were included. Treatment success and failure rates were compared between groups, and associations with age, sex, and Charlson Comorbidity Index (CCI) were analyzed using a Student t test and chi-square test, with significance defined as P ≤ .05. A total of 166 patients were analyzed (mean age = 72.36 ± 14.72 years; mean CCI = 6.80 ± 2.61). Of these, 161 received vancomycin and 48 received fidaxomicin. The treatment success rate was 53.4% for vancomycin and 79.2% for fidaxomicin. Among vancomycin-treated patients, treatment failure was significantly associated with older age (P = .009) and higher CCI (P = .004). No statistically significant associations were observed for fidaxomicin outcomes with age, sex, and CCI. Fidaxomicin demonstrated superior clinical effectiveness to vancomycin, particularly among older adults and patients with multiple comorbidities. These findings support prioritizing fidaxomicin for high-risk patients and considering fecal microbiota transplantation in refractory cases.},
}

Humans
*Fidaxomicin/therapeutic use
*Vancomycin/therapeutic use
Female
Aged
Male
Taiwan
*Diarrhea/drug therapy/microbiology
Retrospective Studies
*Clostridium Infections/drug therapy/microbiology
*Anti-Bacterial Agents/therapeutic use
Middle Aged
*Clostridioides difficile/drug effects
Aged, 80 and over
Treatment Outcome
Fecal Microbiota Transplantation
Adult

@article {pmid41997122,
year = {2026},
author = {Davar, D and Zarour, HM and Trinchieri, G},
title = {Improving immunotherapy in solid tumors using FMT.},
journal = {Cell},
volume = {189},
number = {8},
pages = {2214-2217},
doi = {10.1016/j.cell.2026.03.021},
pmid = {41997122},
issn = {1097-4172},
mesh = {Humans ; *Immunotherapy/methods ; *Fecal Microbiota Transplantation/methods ; *Neoplasms/therapy/immunology ; Animals ; Melanoma/therapy ; Immune Checkpoint Inhibitors/therapeutic use ; Carcinoma, Non-Small-Cell Lung/therapy ; },
abstract = {Recent clinical trials demonstrate that fecal microbiota transplantation (FMT) enhances first-line immune checkpoint inhibitor efficacy in renal cell carcinoma, cutaneous melanoma, and non-small cell lung cancer with acceptable safety. Benefit appears mediated by functional microbiome remodeling, depletion of deleterious taxa, and systemic immunometabolic modulation, supporting microbiome-directed therapeutic strategies for cancer immunotherapy.},
}

Humans
*Immunotherapy/methods
*Fecal Microbiota Transplantation/methods
*Neoplasms/therapy/immunology
Animals
Melanoma/therapy
Immune Checkpoint Inhibitors/therapeutic use
Carcinoma, Non-Small-Cell Lung/therapy

@article {pmid41997887,
year = {2026},
author = {Allerton, F and Whittle, MJ and Durkin, L and Prior, C and Trehy, M and Swales, H and Duplan, F and Borgonovi, S and Pinchbeck, G and Gajanayake, I and Dunning, M and Sparks, T and Watson, P and Amos, GCA and McCallum, K and Bazelle, J and Kent, A},
title = {Clinical benefit of faecal microbiota transplantation administered via a single retention enema as an adjunctive treatment in dogs with chronic enteropathy: a randomised controlled trial.},
journal = {The Journal of small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1111/jsap.70137},
pmid = {41997887},
issn = {1748-5827},
support = {//Small Animal Society/ ; //Linnaeus Veterinary Limited, which is part of Mars Veterinary Health, supported the cots of the Open Access Publication Charges/ ; },
abstract = {OBJECTIVES: To evaluate the clinical benefit of faecal microbiota transplantation administered via a single retention enema, as an adjunctive treatment in the management of dogs with chronic enteropathy.

MATERIALS AND METHODS: Blinded, randomised controlled trial. Dogs with chronic enteropathy (>3 weeks of small or mixed intestinal diarrhoea) were randomly allocated to either the faecal microbiota transplantation or standard treatment group (ratio 1:1) via blinded selection. Dogs in the standard treatment group had a diet change only, while dogs in the faecal microbiota transplantation group had a diet change and faecal microbiota transplantation. faecal microbiota transplantation was performed using fresh faecal material from donor dogs, screened for selected enteropathogens and administered via retention rectal enema. Outcomes measured included the Canine Inflammatory Bowel Disease Activity Index, faecal score and the owner's reported improvement. Group comparisons were made using Fisher's exact tests (owner-reported outcomes) and Kruskal-Wallis tests adjusted for ties (Canine Inflammatory Bowel Disease Activity Index and faecal score).

RESULTS: Forty-two dogs with chronic enteropathy (median Canine Inflammatory Bowel Disease Activity Index score 6 [range 4 to 11]) were included in the study. Twenty-five dogs were randomly assigned to receive faecal microbiota transplantation, while 17 dogs were allocated to standard treatment. A progressive improvement in stool consistency (reduced faecal score) was recorded over time for most dogs in both groups. By Day 90, the rates of owner-defined clinical improvement were 76% (CI 54% to 90%) in the faecal microbiota transplantation group and 73% (CI 40% to 92%) in the standard treatment group. No significant differences were evident between the two groups based on the proportion of owners that reported clinical improvement, Canine Inflammatory Bowel Disease Activity Index score or faecal score.

CLINICAL SIGNIFICANCE: This study did not demonstrate a clear clinical benefit for adjunctive faecal microbiota transplantation via single retention enema in dogs with chronic enteropathy compared to diet change alone, although the small sample size means that a type II error cannot be excluded. The similar outcome for both groups supports high rates of food responsiveness among this cohort of chronic enteropathy dogs.},
}

@article {pmid41997890,
year = {2026},
author = {Rode, AA and Duboc, H and Lamazière, A and Rainteau, D and Humbert, L and Gauliard, E and Chehri, M and Petersen, AM and Helms, M and Schønning, K and Nielsen, HV and Bytzer, P and Engberg, J},
title = {Re-establishing bile acid composition after treatment of recurrent Clostridioides difficile infection with fecal microbiota transplantation compared with oral vancomycin or a 12-strain bacterial mixture.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2658915},
pmid = {41997890},
issn = {1949-0984},
mesh = {Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; Administration, Oral ; *Anti-Bacterial Agents/administration & dosage ; Bacteria/classification/genetics/isolation & purification/metabolism ; *Bile Acids and Salts/metabolism/chemistry/analysis ; Clostridioides difficile/drug effects/physiology/genetics ; *Clostridium Infections/therapy/microbiology ; *Fecal Microbiota Transplantation/methods ; Feces/microbiology/chemistry ; Recurrence ; *Vancomycin/administration & dosage ; },
abstract = {Patients with Clostridioides difficile infection have high colonic levels of primary bile acids, which are potent germinators of Clostridioides difficile. Several studies have suggested that re-establishing a normal bile acid composition is a key factor in fecal microbiota transplantation (FMT) for recurrent C. difficile infection, yet former studies supporting this lacked controls. In a subgroup from a randomized controlled trial, we compared the bile acid composition in patients with recurrent C. difficile infection treated with either FMT, a bacterial mixture, or vancomycin. The fecal bile acid content was analyzed several times before and after treatments. Furthermore, we used 16S rDNA gene sequencing to analyze the presence of some bacterial species involved in bile acid metabolism. Stool donors served as healthy controls. We observed a higher proportion of primary bile acids in patients with recurrent C. difficile infection than in donors, yet a donor-like dominance of secondary bile acids was observed after successful treatment in all groups. The shift seemed to occur earliest in the FMT group, followed by the vancomycin group, and the latest in the bacterial mixture group. In approximately half of the participants, the rise in secondary bile acids was timely associated with the detection of bile acid-transforming bacteria that were absent before treatment. Our findings indicate that FMT re-establishes the bile acid composition faster than vancomycin, reducing the time of susceptibility to recurrences of C. difficile infection. Hence, bacterial mixtures developed as an alternative to donor stool for treating recurrent C. difficile infection might benefit from including bile acid-metabolizing bacteria.},
}

Adult
Aged
Female
Humans
Male
Middle Aged
Administration, Oral
*Anti-Bacterial Agents/administration & dosage
Bacteria/classification/genetics/isolation & purification/metabolism
*Bile Acids and Salts/metabolism/chemistry/analysis
Clostridioides difficile/drug effects/physiology/genetics
*Clostridium Infections/therapy/microbiology
*Fecal Microbiota Transplantation/methods
Feces/microbiology/chemistry
Recurrence
*Vancomycin/administration & dosage

@article {pmid42001079,
year = {2026},
author = {Yang, Y and Kang, C and Pang, R and Huang, S and He, X and Gou, X and Yang, Y and Yan, Y and Ma, X},
title = {Dihydromyricetin exerts neuroprotective effects in acute spinal cord injury by inhibiting NLRP3/Caspase-1 inflammasome through gut microbiome modeling.},
journal = {Journal of inflammation (London, England)},
volume = {23},
number = {1},
pages = {},
pmid = {42001079},
issn = {1476-9255},
support = {2024060//Chengdu Municipal Health Commission Medical Research Project/ ; 25MSZX488//Sichuan Provincial Administration of Traditional Chinese Medicine Research Project/ ; },
abstract = {BACKGROUND: The gut microbiota is closely associated with spinal cord injury (SCI). Dihydromyricetin (DHM), a potent anti-inflammatory compound with neuroprotective properties, has been shown to improve outcomes in various diseases. However, the role of gut microbiota mediating the mechanism neuroprotective effects of DHM in SCI is unknown. METHODS: Male Sprague-Dawley rats were randomly divided into three groups: SHAM, SCI, and DHM group. Motor function was assessed using the cylinder rearing test, and alterations in gut microbiota composition and metabolites were analyzed via 16S rRNA sequencing. Subsequently, Western blotting and immunofluorescence staining were employed to evaluate intestinal barrier integrity, as well as changes in proteins associated with the TLR4/NF-κB pathway and NLRP3/Caspase-1. Finally, fecal microbiota transplantation experiments were conducted to elucidate the necessity of gut microbiota in mediating the anti-inflammatory effects of DHM. RESULTS: DHM exhibits a therapeutic effect by attenuating the severity of pathological SCI and promoting motor function recovery. Notably, DHM restored a balanced microbiota pattern by increasing the relative abundance of Actinobacteria and Bacteroidetes, while concurrently decreasing that of Proteobacteria. Furthermore, DHM promoted intestinal barrier recovery, reduced blood lipopolysaccharide (LPS) levels, and suppressed the activation of the TLR4/NF-κB pathway and reduced the activity of the NLRP3/Caspase-1 inflammasome, thereby effectively decreasing the subsequent release of inflammatory factors in spinal cord tissue. Furthermore, the results from the two FMT groups demonstrated that the gut microbiota serves as a critical target for DHM to exert its anti-inflammatory effects. CONCLUSION: The results of this study demonstrate that restoring microbial balance, repairing intestinal barrier integrity, reducing serum LPS levels, and suppressing the TLR4/NF-κB pathway as well as NLRP3/Caspase-1 inflammasome activity constitute the key regulatory mechanisms underlying the neuroprotective effects of DHM following SCI, thereby opening up possibilities for a novel microbiome-directed therapeutic approach to SCI.},
}

@article {pmid42002228,
year = {2026},
author = {Liu, S and Huang, Z and Guo, Z},
title = {Fecal Microbiota Transplantation for Gastrointestinal Complications After Allogeneic Hematopoietic Cell Transplantation: A Systematic Review and Narrative Synthesis.},
journal = {Transplantation and cellular therapy},
volume = {32},
number = {7},
pages = {909-923},
doi = {10.1016/j.jtct.2026.04.016},
pmid = {42002228},
issn = {2666-6367},
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Diseases/therapy/etiology ; Transplantation, Homologous/adverse effects ; *Graft vs Host Disease/therapy/etiology ; Dysbiosis/therapy/etiology ; },
abstract = {Following allogeneic hematopoietic stem cell transplantation (allo-HSCT), patients frequently develop gastrointestinal complications, including microbiota dysbiosis, infectious syndromes, and graft-versus-host disease (GVHD), which remain major contributors to post-transplant morbidity and mortality. In recent years, several studies have explored microbiome-based interventions, particularly fecal microbiota transplantation (FMT), as a therapeutic strategy for these complications in this highly immunocompromised population. However, substantial variability exists across studies with respect to clinical indications, FMT protocols, and reported outcomes. To systematically evaluate the reported clinical use of FMT for gastrointestinal complications following allo-HSCT, including microbiota dysbiosis, infectious complications, and GVHD. The aim was to characterize study populations, treatment protocols, and reported clinical outcomes, and to synthesize evidence regarding efficacy and safety, with a focus on indication-specific patterns and potential translational relevance for patient management in this highly immunocompromised population. We conducted a PRISMA-compliant systematic review of studies evaluating FMT as a treatment in patients after allo-HSCT. PubMed, Embase, Web of Science, and the Cochrane Library were searched through October 2025. Eligible studies included randomized controlled trials, cohort studies, and prospective or retrospective single-arm studies reporting clinical outcomes following FMT. Given the marked heterogeneity in clinical indications, FMT administration strategies, and outcome definitions, study findings were synthesized using a structured narrative approach, with quantitative data summarized descriptively where appropriate. Twenty studies including patients after allo-HSCT were analyzed. FMT demonstrated high and consistent response rates in non-GVHD indications, whereas GVHD cohorts exhibited more variable responses, with median CR and ORR ranging 50% to 55% in steroid-refractory cases. One-year overall survival was generally favorable in dysbiosis and infection groups (>70%), but more heterogeneous in GVHD. FMT was well tolerated, with predominantly mild gastrointestinal adverse events; serious events were infrequent and mostly disease-related. Current evidence indicates that FMT has been explored as a context-dependent therapy for selected gastrointestinal complications following allo-HSCT, particularly in patients with acute GVHD. Nevertheless, substantial heterogeneity in study design, clinical indications, and outcome assessment limits definitive conclusions regarding efficacy. Well-designed prospective studies with standardized treatment indications, outcome measures, and careful consideration of concurrent immunosuppressive therapies are required to better define the optimal role, timing, and patient selection for FMT in the post-transplant treatment setting.},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Diseases/therapy/etiology
Transplantation, Homologous/adverse effects
*Graft vs Host Disease/therapy/etiology
Dysbiosis/therapy/etiology

@article {pmid42002330,
year = {2026},
author = {Zhao, Y and Qiao, M and Ma, C and Hou, Q and Hu, J and Yang, J},
title = {A fructan-type polysaccharide from Lycium ruthenicum attenuates liver fibrosis via microbiota-dependent ferroptosis inhibition.},
journal = {Carbohydrate polymers},
volume = {382},
number = {},
pages = {125243},
doi = {10.1016/j.carbpol.2026.125243},
pmid = {42002330},
issn = {1879-1344},
mesh = {Animals ; *Lycium/chemistry ; *Liver Cirrhosis/drug therapy/metabolism/chemically induced/pathology ; *Ferroptosis/drug effects ; *Gastrointestinal Microbiome/drug effects ; Male ; *Fructans/pharmacology/chemistry/therapeutic use/isolation & purification ; *Polysaccharides/pharmacology/chemistry ; Mice ; Mice, Inbred C57BL ; Liver/drug effects/metabolism/pathology ; Oxidative Stress/drug effects ; },
abstract = {Plant-derived polysaccharides represent promising candidates for hepatic fibrosis (HF) therapy through the gut-liver axis. This study investigated the structural characteristics, anti-fibrotic efficacy, and mechanisms of LRMP1, a novel polysaccharide from Lycium ruthenicum Murr. LRMP1 was identified as a homogeneous inulin-type fructan (3.055 kDa) with a → 1)-β-D-Fruf-(2 → backbone terminated by α-D-Glcp-(1 → 2)-β-D-Fruf linkages (DP 4-20). Integrated multi-omics analysis combining hepatic transcriptomics, serum metabolomics, and gut microbiome profiling revealed that LRMP1 ameliorates HF via a gut microbiota-postbiotics-ferroptosis regulatory axis. In both CCl4-induced and MCD diet-induced chronic fibrosis models, LRMP1 significantly attenuated liver injury, fibrosis, inflammation, and oxidative stress, while restoring intestinal barrier integrity. These protective effects correlated with enrichment of beneficial bacteria (Akkermansia muciniphila, Lactobacillus spp.) and pathogen depletion. Mechanistically, LRMP1 suppressed TGF-β signaling and inhibited hepatocyte ferroptosis by restoring the GPX4/SLC7A11 antioxidant system and reducing lipid peroxidation. Serum metabolomics further revealed elevated anti-ferroptotic metabolites and suppressed pro-inflammatory lipids. Crucially, antibiotic depletion abolished LRMP1's efficacy, whereas fecal microbiota transplantation and fermentation supernatant experiments confirmed that microbiota-derived postbiotics selectively protect hepatocytes from ferroptosis. These findings establish LRMP1 as a promising microbiota-targeted polysaccharide for HF intervention through the gut-liver axis.},
}

Animals
*Lycium/chemistry
*Liver Cirrhosis/drug therapy/metabolism/chemically induced/pathology
*Ferroptosis/drug effects
*Gastrointestinal Microbiome/drug effects
Male
*Fructans/pharmacology/chemistry/therapeutic use/isolation & purification
*Polysaccharides/pharmacology/chemistry
Mice
Mice, Inbred C57BL
Liver/drug effects/metabolism/pathology
Oxidative Stress/drug effects

@article {pmid42002659,
year = {2026},
author = {Pang, J and Ma, X and Hong, N and Shen, Z and Li, S and Li, X and Wang, S and Cong, H and Zhang, K and Yang, J and Wu, C},
title = {Gut microbiota mediates the antidepressant-like effects of xiaochaihutang: mechanisms involving inhibition of inflammation and enhancement of barrier function.},
journal = {Journal of natural medicines},
volume = {80},
number = {3},
pages = {881-898},
pmid = {42002659},
issn = {1861-0293},
support = {82374066//Innovative Research Group Project of the National Natural Science Foundation of China/ ; 82074041//Innovative Research Group Project of the National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Antidepressive Agents/pharmacology/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; Rats ; Male ; *Depression/drug therapy/microbiology ; Rats, Sprague-Dawley ; *Inflammation/drug therapy ; Fecal Microbiota Transplantation ; Intestinal Barrier Function/drug effects ; Disease Models, Animal ; Blood-Brain Barrier/drug effects ; },
abstract = {Depression is a common mental disorder that seriously impairs the psychological and physical health of patients. Extensive research has indicated that patients with depression exhibit disturbances in their gut microbiota. Xiaochaihutang (XCHT) is a traditional herbal recipe widely used in China, and previous studies have found it to possess antidepressant properties. However, whether XCHT can modulate depression-associated gut microbiota dysbiosis remains unclear. In this research, we investigated the impact of XCHT on the microbiota-gut-brain axis in depressed rats and elucidated the potential mechanisms. A rat model of depression was established using the chronic unpredictable mild stress (CUMS) protocol. Behavioral tests demonstrated that XCHT significantly alleviated depression-like behaviors. 16S rRNA sequencing revealed that XCHT enhanced the diversity and compositional structure of the gut microbiota and specifically increased the abundance of the beneficial bacterium Blautia. Fecal microbiota transplantation (FMT) experiments further confirmed that the antidepressant-like effects of XCHT were mediated through modulation of the gut microbiota. Furthermore, XCHT exhibited anti-inflammatory properties in both the central and peripheral systems and improved the integrity of the intestinal barrier and the blood-brain barrier. These mechanisms were also validated using the FMT approach. Collectively, these findings suggest that the antidepressant-like mechanism of XCHT may be directly linked to the regulation of the microbiota-gut-brain axis. This study demonstrates that XCHT exerts antidepressant-like effects by modulating the microbiota-gut-brain axis, providing novel insights into the potential therapeutic mechanisms and clinical applications for depression.},
}

Animals
*Antidepressive Agents/pharmacology/therapeutic use
*Gastrointestinal Microbiome/drug effects
*Drugs, Chinese Herbal/pharmacology/therapeutic use
Rats
Male
*Depression/drug therapy/microbiology
Rats, Sprague-Dawley
*Inflammation/drug therapy
Fecal Microbiota Transplantation
Intestinal Barrier Function/drug effects
Disease Models, Animal
Blood-Brain Barrier/drug effects

@article {pmid42004962,
year = {2026},
author = {Li, J and Chen, X and Xie, X},
title = {Mechanistic insights into gut microbiota-driven autoimmunity in rheumatoid arthritis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1812972},
pmid = {42004962},
issn = {1664-3224},
mesh = {Humans ; *Arthritis, Rheumatoid/immunology/microbiology/metabolism/therapy ; *Autoimmunity ; *Gastrointestinal Microbiome/immunology ; Animals ; *Dysbiosis/immunology ; },
abstract = {Rheumatoid arthritis (RA) is a systemic autoimmune disease whose pathogenic drivers and initiating immune events remain incompletely understood. Increasing evidence implicates the gut-joint axis in RA, yet the mechanisms by which intestinal microbiota contribute to disease development still require integrative clarification. This review summarizes current experimental and clinical evidence on the role of gut dysbiosis in promoting autoimmunity in RA. We discuss alterations in microbial composition and their links to barrier dysfunction, immune-cell polarization, microbial metabolites, and antigen-specific immune responses. Human cohort studies and arthritis models suggest that reduced microbial diversity, loss of short-chain fatty acid (SCFA)-producing commensals, and expansion of taxa such as Prevotella copri and Collinsella are associated with impaired epithelial integrity, enhanced Th17/Tfh differentiation, reduced regulatory T- and B-cell activity, and increased autoantibody production. Mechanistic studies further support roles for molecular mimicry, microbially derived citrullinated antigens, and metabolite-mediated signaling in the breakdown of immune tolerance and persistence of synovial inflammation. We also discuss emerging microecology-based interventions, including probiotics, prebiotics, postbiotics, and fecal microbiota transplantation, together with their translational potential and current limitations. Overall, available evidence places gut microbiota-mediated immune remodeling at the center of RA pathogenesis and supports precision microbiome modulation as a promising adjunctive strategy for disease prevention and treatment.},
}

Humans
*Arthritis, Rheumatoid/immunology/microbiology/metabolism/therapy
*Autoimmunity
*Gastrointestinal Microbiome/immunology
Animals
*Dysbiosis/immunology

@article {pmid42006120,
year = {2026},
author = {Tang, J and Liu, Y and Wu, N and Lu, J and Zhang, Y and Tong, N and Lü, Q},
title = {Gut microbiota: a potential therapeutic target for hyperuricemia and gout.},
journal = {Bioscience of microbiota, food and health},
volume = {45},
number = {2},
pages = {85-99},
pmid = {42006120},
issn = {2186-6953},
abstract = {The prevalence of hyperuricemia (HUA) and gout has increased in recent decades. Current therapeutic approaches for HUA/gout are often limited by potential risks, necessitating the exploration of safer and more effective treatment options. Emerging evidence highlights the gut microbiota as a pivotal regulator of uric acid (UA) homeostasis. This review synthesizes current advances in microbiota-targeted interventions for HUA/gout, focusing on mechanistic insights and translational potential. We aim to provide a roadmap for optimizing microbiota-based therapies in HUA/gout management by bridging mechanistic discoveries with clinical translation. Gut microbiota can mitigate HUA/gout through several mechanisms, including regulating UA and purine metabolism, alleviating inflammation and modulating immune response, and enhancing the integrity of the intestinal barrier. Therapeutic strategies targeting gut microbiota include probiotics, prebiotics, traditional Chinese medicine, and fecal microbiota transplantation, which offer multi-target and multi-pathway benefits. While these microbiota-targeted therapies offer advantages over conventional drugs, several challenges remain. Future research should prioritize mechanistic elucidation, personalized microbiota modulation, and large-scale trials to optimize therapeutic paradigms for HUA/gout.},
}