@article {pmid41814325,
year = {2026},
author = {Zhang, J and Zhou, Y and Mei, X and Yan, S and Mao, J and Li, Y and Bian, Z and Li, L and Ji, D and Lu, T and Chen, J and Su, L},
title = {Molecular mechanisms and therapeutic potential of tryptophan metabolism in gut-brain signaling transduction: a narrative review.},
journal = {Journal of neuroinflammation},
volume = {23},
number = {1},
pages = {},
pmid = {41814325},
issn = {1742-2094},
support = {2023YFC3504200//National Key Research and Development Program of China/ ; ZYXYL2024-006//The "leading plan" project of the first-class discipline of Nanjing University of Chinese Medicine/ ; 82304723//National Natural Science Foundation of China/ ; },
abstract = {As an essential amino acid, tryptophan (Trp) serves as a pivotal mediator in gut-brain axis (GBA) communication through three primary metabolic pathways: kynurenine (Kyn), indole, and serotonin (5-HT), which together regulate neuroimmune and neuroendocrine homeostasis via the vagus and spinal afferent nerves, circulatory system, and hypothalamic-pituitary-adrenal (HPA) axis. This review systematically examines Trp metabolism’s critical roles in GBA, emphasizing molecular pathways, rate-limiting enzymes, and receptor-mediated signaling. We discuss the bidirectional interplay between gut microbiota and host Trp metabolism, encompassing microbial modulation of host enzyme activities such as indoleamine 2,3-dioxygenase and direct production of bioactive indole derivatives like indole-3-propionic acid. Characteristic disruptions in Trp metabolism patterns are identified across GBA-associated disorders including irritable bowel syndrome, inflammatory bowel disease, depression, Alzheimer’s disease, schizophrenia and Parkinson’s disease, marked by aberrant neurotoxic to neuroprotective metabolite ratios and enzymatic dysregulation. The aryl hydrocarbon receptor (AhR) emerges as a molecular hub connecting Trp metabolites to GBA functions, with distinct metabolites eliciting opposing effects through AhR activation. Therapeutic strategies targeting Trp metabolism are critically evaluated, including fecal microbiota transplantation, probiotic supplementation, metabolite administration, and enzyme inhibitors. Future research directions address mechanistic gaps and translational challenges in restoring GBA homeostasis via Trp pathway modulation.},
}

@article {pmid42007101,
year = {2026},
author = {Tang, H and Wu, M and Tan, S and Liu, C and Cui, Y},
title = {Uterine microbiota dynamics and new therapeutic opportunities in gynecological diseases.},
journal = {American journal of translational research},
volume = {18},
number = {3},
pages = {1768-1791},
pmid = {42007101},
issn = {1943-8141},
abstract = {Traditional view holds that the uterus is a sterile environment. However, with the increased development of molecular biology technologies, this classical theory has been re-examined. Increasing evidence shows that a low-biomass, uniquely structured microecosystem exists in the healthy uterus. Its composition and dynamic changes are crucial in maintaining endometrial homeostasis, regulating immune responses, and influencing embryo implantation. Uterine microecological imbalance is associated with different gynecological diseases, such as chronic endometritis, endometriosis, and uterine-related tumors. This paper systematically reviews the compositional features of the uterine microecology and the dynamic changes in bacterial communities, as well as summarizes the evidence linking these changes to major gynecological diseases. This work examines current treatment and intervention strategies including antibiotics, probiotics, uterine cavity colonization, and fecal microbiota transplantation, and discusses their potential clinical value and methodological challenges. A deeper investigation of the relationship between uterine microecology and gynecological diseases is expected to provide new biomarkers and therapeutic targets for the precise diagnosis and treatment of gynecological disorders.},
}

@article {pmid42007373,
year = {2026},
author = {Poznyak, AV and Vatlin, AA and Pavshintsev, VV and Mitkin, NA and Maltseva, ON and Utkina, AS and Orekhov, AN},
title = {An overview of the role of the gut microbiota in rheumatoid arthritis.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {3},
pmid = {42007373},
issn = {2771-5965},
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disease preceded by a prolonged preclinical phase marked by the emergence of autoantibodies and mucosal immune dysregulation. Evidence from human studies and animal models consistently demonstrates that gut microbiota dysbiosis contributes to this transition, particularly through impaired intestinal barrier function, activation of pro-inflammatory pathways, and molecular mimicry. Specific taxa - including Prevotella copri, Collinsella aerofaciens, and reductions in butyrate-producing bacteria - have been linked to heightened systemic inflammation, increased T helper 17 responses, and the generation of RA-associated autoantibodies. Current research also indicates that anti-rheumatic medications such as methotrexate, sulfasalazine, and minocycline produce measurable shifts in gut microbial composition, suggesting that microbiota-drug interactions may influence treatment response. Therapeutic approaches aimed at modifying gut ecology - including dietary interventions, prebiotics, probiotics, and fecal microbiota transplantation - show early potential in restoring microbial balance, improving intestinal barrier integrity, and reducing inflammatory markers, although evidence in the preclinical RA stage remains limited. Additionally, emerging data highlight the importance of intestinal autophagy and microRNA networks in regulating epithelial integrity and systemic immune activation. Taken together, the literature supports a mechanistic link between gut dysbiosis and the onset of RA. It points to microbiota-targeted strategies as promising avenues for delaying or preventing disease progression. Future studies should prioritize longitudinal analyses and interventional trials focusing specifically on individuals at risk for RA.},
}

@article {pmid42008253,
year = {2026},
author = {Narang, H and Talukdar, D and Kumar, B and Mathur, P and Ningombam, A and Singh, M and Bajaj, A and Markandey, M and Kalaivani, M and Verma, M and Kaur, M and Bakshi, S and Jana, P and Jamdhade, M and Bhardwaj, N and Puraswani, M and Ashita, and Ahmed, N and Goyal, MK and Mubbunu, M and Thomas, DM and Mundhra, S and Prasad, S and Garg, R and Gupta, A and Shalimar, and Gunjan, D and Mahapatra, SJ and Agarwal, S and Saraya, A and Garg, P and Makharia, G and Kedia, S and Das, B and Ahuja, V},
title = {Fecal Microbiota Transplant and Multidrug-Resistant Organism Decolonization in Gastrointestinal Disease: A Randomized Clinical Trial.},
journal = {JAMA internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1001/jamainternmed.2026.0655},
pmid = {42008253},
issn = {2168-6114},
abstract = {IMPORTANCE: Gut colonization by multidrug-resistant organisms (MDROs) is a risk factor for infection with these pathogens. There are no approved therapeutic interventions to combat it.

OBJECTIVE: To assess the efficacy of fecal microbiota transplant (FMT) in causing MDRO decolonization and decreasing antimicrobial resistance (AMR) genes and its impact on gut microbiome, virome, and mycobiome composition in patients with gastrointestinal (GI) diseases.

This randomized, double-blind, sham-controlled clinical trial was conducted in a gastroenterology ward and intensive care unit at a tertiary care center in India. Participants were patients with GI diseases with persistent MDRO colonization. Patient recruitment occurred from July 2022 to June 2024, with follow-up completed in July 2024. Data were analyzed from October 1, 2024, to April 25, 2025.

INTERVENTION: FMT via colonoscopy or sham intervention (sigmoidoscopy with saline injection).

MAIN OUTCOMES AND MEASURES: Co-primary outcomes were MDRO decolonization rate and decrease in antimicrobial resistance genes (AMR) at 4 weeks after the intervention. Secondary outcomes included changes in stool microbiome (16S ribosomal RNA amplicon sequencing), virome (viruslike particles shotgun sequencing), and mycobiome (ITS2 sequencing); incidence of MDRO infections; and adverse events within 4 weeks.

RESULTS: Of 114 randomized patients (mean [SD] age, 40.6 [12.5] years; 80 [70.2%] male; 52 patients [45.6%] with pancreatitis; 43 patients [37.7%] with cirrhosis; 19 patients [16.7%] with other GI disorders), 58 received FMT and 56 received the sham intervention. Most patients were colonized with carbapenem-resistant Enterobacteriaceae or extended-spectrum β-lactamase-producing Enterobacteriaceae at baseline (55 patients [94.8%] in the FMT group and 56 patients [100%] in the sham group). Five patients (2 in the FMT group, 3 in the sham group) were lost to follow-up. Intention-to-treat analysis showed no significant differences in MDRO decolonization (18 patients [31.0%] in the FMT group vs 17 patients [30.4%] in the sham group; absolute difference, 0.6% [95% CI, -16.2% to 17.6%]; P = .94) or AMR genes (median [IQR], 2.5 [1.2 to 3.0] genes in the FMT group vs 2.0 [1.0 to 3.0] genes in the sham group; P = .68), with comparable adverse events. Among 71 patients who underwent 16S ribosomal RNA gene sequencing at 4 to 6 weeks after the intervention, enrichment of bacteria capable of producing short-chain fatty acids was observed in the FMT group. These microbial alterations were not observed in the sham group. However, viral diversity remained unchanged after FMT. Mycobiome analysis revealed that FMT induced only modest, transient alterations in the gut mycobiome.

CONCLUSIONS AND RELEVANCE: This randomized clinical trial found that while a single session of FMT did not significantly enhance MDRO decolonization or decrease AMR genes in patients with GI diseases, it modulated gut microbiome diversity and composition.

TRIAL REGISTRATION: Clinical Trials Registry-India Registration No. 2022/07/043847.},
}

@article {pmid42008254,
year = {2026},
author = {Kelly, BJ and Woodworth, MH and Kwon, JH},
title = {Fecal Microbiota Transplant for Multidrug Resistance-No Benefit Without Disruption?.},
journal = {JAMA internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1001/jamainternmed.2026.0668},
pmid = {42008254},
issn = {2168-6114},
}

@article {pmid42009386,
year = {2026},
author = {Couturier, J and Kenner, E and Nicula, M and Chowdhury, F and Surette, M and Pai, N},
title = {Protocol for a pilot feasibility randomised controlled trial of fecal microbiota transplantation for adolescent anorexia nervosa.},
journal = {BMJ open},
volume = {16},
number = {4},
pages = {e109115},
doi = {10.1136/bmjopen-2025-109115},
pmid = {42009386},
issn = {2044-6055},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; Adolescent ; *Anorexia Nervosa/therapy/psychology ; Pilot Projects ; Feasibility Studies ; Child ; Female ; Male ; Randomized Controlled Trials as Topic ; Gastrointestinal Microbiome ; },
abstract = {INTRODUCTION: Despite its serious impact, anorexia nervosa (AN) remains one of the least understood mental illnesses, with significant gaps in effective treatment options. No medications have been deemed effective and only 50% of individuals respond to conventional psychotherapies. Gastrointestinal (GI) bacteria have been found to be altered in individuals with AN. While, Fecal microbiota transplantation (FMT) has shown potential for alleviating anxiety and depression, its effects remain understudied for individuals with AN. This study aims to determine whether oral capsular FMT is acceptable to adolescents with AN and results in clinical improvement in weight and/or psychological symptoms.

METHODS: This study will randomise 20 adolescents with AN, ages 12-17 years, to receive either FMT or placebo capsules. These 20 youth, as well as an additional 10 youth who decline trial enrolment, will participate in qualitative interviews. We will track recruitment rates and collect psychological and biological measures (blood, stool, urine and saliva) at multiple timepoints to assess how gut microbiota and their metabolites may influence the symptoms of AN. Interviews with participants and caregivers will explore their experiences and views on FMT as a treatment approach.

ETHICS AND DISSEMINATION: This study has received ethics approval by the Hamilton Integrated Research Ethics Board (#17493) and investigational drug approval by Health Canada (Dossier ID: c292423). Informed consent will be obtained by research staff from all participants. Findings will be disseminated through academic conferences, clinical forums and partnerships with advocacy organisations to reach clinicians, researchers and individuals with lived experience.

TRIAL REGISTRATION NUMBER: NCT06593366.},
}

Humans
*Fecal Microbiota Transplantation/methods
Adolescent
*Anorexia Nervosa/therapy/psychology
Pilot Projects
Feasibility Studies
Child
Female
Male
Randomized Controlled Trials as Topic
Gastrointestinal Microbiome

@article {pmid42009997,
year = {2026},
author = {Swain, MP and Mehta, CH and Padya, BS and Sharma, S and Velagacherla, V and Mitra, A and Mohanty, S and Mukherjee, T},
title = {Microbiome modulating remedies for chronic diseases: a review of current interventions and future directions.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {42009997},
issn = {1568-5608},
}

@article {pmid42010713,
year = {2026},
author = {Tang, J and Wang, L and Yang, Z and Song, Y and Wu, S and Liang, Q and Li, Z and Zhou, S and Xiong, H and Chen, D and Li, J and Li, F},
title = {Gut microbiota induces dysspermatogenesis via microbial-derived phenylacetylglycine in Ggt1-deficient mice.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02401-0},
pmid = {42010713},
issn = {2049-2618},
support = {32272874//National Natural Science Foundation of China/ ; 2021YFF1000601//National Key R&D Program of China/ ; 2662025DKPY008//Fundamental Research Funds for the Central Universities/ ; },
abstract = {BACKGROUND: Male infertility represents a global health concern, with emerging evidence linking gut microbiota dysbiosis to dysspermatogenesis and subfertility. However, the molecular mediators and regulatory mechanisms by which gut microbiota influences testicular functions remain poorly defined.

RESULTS: This study demonstrates that male gamma-glutamyl transferase 1-deletion (Ggt1[-/-]) mice exhibits infertility phenotypes, including reduced germ and testicular Leydig cell numbers, increased rates of abnormal sperm, and altered reproductive hormone levels. Metabolomic analysis reveals elevated levels of the gut microbial-derived metabolite phenylacetylglycine (PAGly) in serum and testes of Ggt1[-/-] mice, with in vivo injection experiments indicating its role in impairing spermatogenesis. Moreover, blocking PAGly effectively restores the impaired spermatogenesis in Ggt1[-/-] mice. Fecal metagenomic and metabolomic analyses show that gut microbiota in Ggt1[-/-] mice induces elevation of phenylacetic acid, a precursor metabolite of PAGly. Strikingly, fecal microbiota transplantation from Ggt1[-/-] mice (Ggt1[-/-]-FMT) recapitulates the infertility phenotypes including reduced germ cells and increased rates of abnormal sperm. Mechanistically, integrated CUT&Tag and ATAC-Seq analyses reveal that transcription factor STAT5B occupies regulatory elements near Klk1b transcription start sites (TSS), confirming that transcription factor STAT5B directly regulates Klk1b gene transcription. Concretely, PAGly activates β2-adrenergic receptor (β2AR) on Leydig cells, triggering STAT3 phosphorylation, subsequent SOCS3 upregulation, and STAT5B phosphorylation suppression; p-STAT5B with transcriptional activation function is reduced, then Klk1b gene transcription is compromised, and therefore spermatogenesis is disrupted.

CONCLUSION: Ggt1 deletion-induced gut microbiota dysbiosis disrupts spermatogenesis via β2AR-STAT3-SOCS3-STAT5B-Klk1bs signaling pathway. Specifically, PAGly-induced β2AR activation promotes STAT3 phosphorylation, which induces SOCS3 to suppress p-STAT5B dependent Klk1bs transcription. This mechanism underscores the critical role of gut-derived metabolites in regulating testicular function and identifies potential targets for microbiota-modulated male infertility. Video Abstract.},
}

@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},
doi = {10.1080/19490976.2026.2658915},
pmid = {41997890},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Bile Acids and Salts/metabolism/analysis/chemistry ; *Vancomycin/administration & dosage/therapeutic use ; *Clostridium Infections/therapy/microbiology ; Feces/chemistry/microbiology ; Male ; *Clostridioides difficile/physiology ; Middle Aged ; Female ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; Aged ; Bacteria/classification/genetics/isolation & purification/metabolism ; Gastrointestinal Microbiome ; Adult ; Recurrence ; Administration, Oral ; },
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.},
}

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

@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 = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.04.016},
pmid = {42002228},
issn = {2666-6367},
abstract = {BACKGROUND: 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.

OBJECTIVES: 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.

STUDY DESIGN: 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.

RESULTS: 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 50-55% 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.

CONCLUSIONS: Current evidence indicates that FMT has been explored as a context-dependent therapy for selected gastrointestinal complications following allo-HSCT, particularly in patients with aGVHD. 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.},
}

@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 ; *Liver Cirrhosis/drug therapy/metabolism/pathology/chemically induced ; *Gastrointestinal Microbiome/drug effects ; *Lycium/chemistry ; *Ferroptosis/drug effects ; Mice ; Male ; *Polysaccharides/pharmacology/chemistry ; Mice, Inbred C57BL ; *Fructans/pharmacology/chemistry ; 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
*Liver Cirrhosis/drug therapy/metabolism/pathology/chemically induced
*Gastrointestinal Microbiome/drug effects
*Lycium/chemistry
*Ferroptosis/drug effects
Mice
Male
*Polysaccharides/pharmacology/chemistry
Mice, Inbred C57BL
*Fructans/pharmacology/chemistry
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 = {},
number = {},
pages = {},
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/ ; },
}

@article {pmid42002835,
year = {2026},
author = {Morineau, N and Tessoulin, B and Guimard, T and Papin, M and Roquilly, A and Le Gouill, S and Montassier, E},
title = {Longitudinal gut microbiome dynamics are associated with clinical outcome and toxicity during ibrutinib therapy.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2659397},
doi = {10.1080/19490976.2026.2659397},
pmid = {42002835},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Piperidines/adverse effects/therapeutic use ; *Adenine/analogs & derivatives/adverse effects/therapeutic use ; Male ; Female ; Middle Aged ; Aged ; Longitudinal Studies ; *Bacteria/classification/genetics/isolation & purification/metabolism/drug effects ; Feces/microbiology ; Treatment Outcome ; *Antineoplastic Agents/adverse effects/therapeutic use ; Adult ; },
abstract = {Accumulating evidence indicates that the gut microbiome influences therapeutic efficacy and toxicity across cancer treatments; however, its longitudinal dynamics during targeted therapies remain poorly characterized. Here, we performed whole-genome shotgun metagenomic sequencing of 291 longitudinal stool samples collected over one year from 30 patients with hematologic malignancies treated with ibrutinib. Overall gut microbial diversity remained stable at the population level but exhibited markedly divergent temporal trajectories according to clinical outcome, with progressive recovery in responders and blunted or delayed restoration in non-responders. Longitudinal modeling revealed distinct species- and pathway-level microbial dynamics between patients with treatment response or nonresponse, including enrichment of saccharolytic, short-chain fatty acid-associated taxa and metabolic pathways in responders, and expansion of bile acid-modifying, proteolytic, and inflammation-associated microbial features in non-responders. Functional profiling further demonstrated opposing temporal trends in pathways related to carbohydrate fermentation, amino-acid metabolism, and secondary bile acid synthesis. In addition, both baseline microbiome composition and longitudinal remodeling were associated with the development of ibrutinib-associated diarrhea. Together, these findings reveal coordinated, outcome-specific remodeling of the gut microbiome during ibrutinib therapy and highlight longitudinal microbiome trajectories, rather than static baseline features, as potential biomarkers of treatment response and toxicity, as well as targets for microbiome-directed interventions. In conclusion, our findings highlight a potential role of gut microbiome dynamics in modulating response to BTK inhibition and support the need for larger, prospective studies to validate these observations.},
}

Humans
*Gastrointestinal Microbiome/drug effects
*Piperidines/adverse effects/therapeutic use
*Adenine/analogs & derivatives/adverse effects/therapeutic use
Male
Female
Middle Aged
Aged
Longitudinal Studies
*Bacteria/classification/genetics/isolation & purification/metabolism/drug effects
Feces/microbiology
Treatment Outcome
*Antineoplastic Agents/adverse effects/therapeutic use
Adult

@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},
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.},
}

@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.},
}

@article {pmid42006318,
year = {2026},
author = {Kang, L and Feng, C and Tang, Z and Gu, W and Wang, Y and Pei, A and Piao, M},
title = {Pueraria flavones attenuate DSS-induced colitis by regulating the microbiota-bile acid-FXR/TGR5 axis and suppressing mtDNA-cGAS-STING signaling.},
journal = {iScience},
volume = {29},
number = {4},
pages = {115275},
pmid = {42006318},
issn = {2589-0042},
abstract = {Ulcerative colitis (UC) is characterized by inflammation and impaired barrier function. Pueraria flavones (PFs) possess anti-inflammatory properties, though their underlying mechanisms remain poorly understood. This study assessed PFs in a dextran sulfate sodium (DSS)-induced colitis mouse model. PFs alleviated colitis symptoms, including weight loss and colon shortening, in a dose-dependent manner, while restoring barrier integrity and reducing pro-inflammatory cytokines. Mechanistically, PFs inhibited cGAS-STING activation by decreasing mitochondrial DNA (mtDNA) release, thereby limiting cytokine production. Furthermore, fecal microbiota transplantation (FMT) confirmed that PFs exert protective effects through the modulation of the gut microbiota. Metabolomic analysis revealed that PFs increased bile acids, such as tauroursodeoxycholic acid (TUDCA) and ursodeoxycholic acid (UDCA), which activated the farnesoid X receptor (FXR)/TGR5 signaling pathway to enhance barrier function. Collectively, these findings suggest that PFs mitigate colitis by remodeling the microbiota-bile acid-FXR axis and suppressing mtDNA-cGAS-STING signaling, presenting a promising therapeutic approach for UC.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.017},
pmid = {41990750},
issn = {1934-6069},
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.},
}

@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 = {},
number = {},
pages = {},
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},
doi = {10.1111/jog.70272},
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 ; Mice ; Mice, Inbred C57BL ; *Estrogens/deficiency ; *Sesquiterpenes/pharmacology/administration & dosage ; *Lactones/pharmacology/administration & dosage ; *Lipid Metabolism Disorders/drug therapy/etiology ; *Inflammation/drug therapy ; Gastrointestinal Microbiome/drug effects ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Intestines/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
Mice
Mice, Inbred C57BL
*Estrogens/deficiency
*Sesquiterpenes/pharmacology/administration & dosage
*Lactones/pharmacology/administration & dosage
*Lipid Metabolism Disorders/drug therapy/etiology
*Inflammation/drug therapy
Gastrointestinal Microbiome/drug effects
Disease Models, Animal
Fecal Microbiota Transplantation
Intestines/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 ; *Gastrointestinal Microbiome/drug effects ; *Berberine/pharmacology ; Mice ; *Hypoxia/complications/metabolism ; *Bile Acids and Salts/metabolism ; Intestinal Mucosa/metabolism/drug effects/pathology ; Male ; Disease Models, Animal ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; *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
*Gastrointestinal Microbiome/drug effects
*Berberine/pharmacology
Mice
*Hypoxia/complications/metabolism
*Bile Acids and Salts/metabolism
Intestinal Mucosa/metabolism/drug effects/pathology
Male
Disease Models, Animal
Mice, Inbred C57BL
Fecal Microbiota Transplantation
*Intestinal Diseases/etiology/metabolism/prevention & control

@article {pmid41993317,
year = {2026},
author = {Chaki, T and Maruyama, D and Doan, TN and Xiaoli, T and Prakash, A},
title = {Dietary tryptophan mitigates lung ischemia-reperfusion injury via microbiota-derived indole-3-propionate and aryl hydrocarbon receptor signaling.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.04.02.714281},
pmid = {41993317},
issn = {2692-8205},
abstract = {BACKGROUND: Lung ischemia-reperfusion (IR) injury drives early morbidity after lung transplantation and cardiothoracic surgery, yet targeted preventive therapies are lacking. The gut-lung axis and microbiota-derived tryptophan metabolites, including indole-3-propionate (IPA), may regulate pulmonary immunity and inflammation. We investigated whether a tryptophan-rich (Trp-Rich) diet attenuates sterile lung IR injury by increasing microbiota-derived indole metabolites and reprogramming alveolar macrophage (AM) inflammatory responses.

METHODS: C57BL/6 mice received isocaloric tryptophan-standard (Trp-Std; 0.18%) or Trp-Rich (0.60%) diets for 14 days, then underwent unilateral left lung IR (60 min ischemia followed by 60 min reperfusion). Oxygen saturation, lung cytokines, and aryl hydrocarbon receptor (AhR) signaling readouts (Cyp1a1 / Cyp1b1) were evaluated. Gut microbiota was profiled by 16S rRNA sequencing, and targeted metabolomics quantified tryptophan metabolites in feces, portal vein (PV) plasma, and lung tissue. To further assess inflammatory priming in vivo , mice were additionally challenged with intratracheal lipopolysaccharide (LPS). Mechanistic studies compared IPA with related indole metabolites in MH-S cells and primary human AMs, including ex vivo nutritional IR, LPS stimulation, and AhR stimulation and blockade using synthetic agonists and antagonists.

RESULTS: Trp-Rich feeding improved post-IR oxygenation, reduced lung IL-1β, and increased pulmonary Cyp1a1 / Cyp1b1 gene expression. Trp-Rich diet remodeled the gut microbiota, including enrichment of Bifidobacterium and Lactobacillus , and increased IPA levels across feces, PV plasma, and lung tissue, with lower kynurenine/IPA ratios across matrices. In the LPS intratracheal challenge, Trp-Rich feeding reduced IL-6 levels in lung tissue and systemic plasma. Primary murine AMs isolated from Trp-Rich mice also showed reduced IL-1β and IL-6 release in an ex vivo nutritional IR model. Among tested indole metabolites, IPA showed the strongest dose-dependent suppression of LPS-induced cytokines and chemokines in MH-S cells and primary human AMs, remained active in the ex vivo nutritional IR model, and its anti-inflammatory effect was abrogated by AhR blockade and enhanced by co-treatment with other indole metabolites.

CONCLUSIONS: A Trp-Rich diet attenuated sterile lung IR injury, coinciding with gut microbiota remodeling, increased systemic and pulmonary IPA, reduced inflammatory priming, and reprogrammed AM responses. These data support diet- or microbiome-directed strategies targeting IPA-AhR signaling to mitigate perioperative lung IR injury.},
}

@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},
doi = {10.1097/MD.0000000000048307},
pmid = {41995553},
issn = {1536-5964},
mesh = {Humans ; *Vancomycin/therapeutic use/administration & dosage ; *Fidaxomicin/therapeutic use/administration & dosage ; Male ; Female ; Taiwan ; Retrospective Studies ; Aged ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; *Clostridium Infections/drug therapy ; *Diarrhea/drug therapy/microbiology ; Middle Aged ; *Clostridioides difficile ; Aged, 80 and over ; Fecal Microbiota Transplantation ; Treatment Outcome ; 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
*Vancomycin/therapeutic use/administration & dosage
*Fidaxomicin/therapeutic use/administration & dosage
Male
Female
Taiwan
Retrospective Studies
Aged
*Anti-Bacterial Agents/therapeutic use/administration & dosage
*Clostridium Infections/drug therapy
*Diarrhea/drug therapy/microbiology
Middle Aged
*Clostridioides difficile
Aged, 80 and over
Fecal Microbiota Transplantation
Treatment Outcome
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/microbiology ; Immune Checkpoint Inhibitors/therapeutic use ; Melanoma/therapy ; Animals ; Carcinoma, Non-Small-Cell Lung/therapy ; Clinical Trials as Topic ; },
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/microbiology
Immune Checkpoint Inhibitors/therapeutic use
Melanoma/therapy
Animals
Carcinoma, Non-Small-Cell Lung/therapy
Clinical Trials as Topic

@article {pmid41786895,
year = {2026},
author = {Hu, S and Liu, H and Song, F and Huang, D and Wei, Q},
title = {CFD protein deficiency induce slow transit constipation is correlated with gut microbial dysbiosis.},
journal = {Scientific reports},
volume = {16},
number = {1},
pages = {},
pmid = {41786895},
issn = {2045-2322},
abstract = {UNLABELLED: Dysregulation of complement factor D (CFD) has been associated with various diseases, such as metabolic, cardiovascular, and renal disorders. However, its role in intestinal function has been less studied. Our research found that CFD-deficient (Cfd[–/–]) mice exhibited spontaneous slow transit constipation (STC) compared to wild-type (WT) mice. Moreover, the fecal weight and water content in Cfd[–/–] mice were significantly reduced, despite no specific changes in feeding behavior. Reduced C-kit protein expression, colon injury, complement dysfunction and dysbiosis of the fecal microbiota are also observed in Cfd[–/–] mice. After microbiota transplantation from WT mice into Cfd[–/–] mice, reduced stool output, water content, decreased C-kit protein expression and colon injury were significantly improved. These results indicate that CFD is critical for controlling microbial homeostasis in the colon and, in its absence, leads to colon injury and promotes slow transit constipation.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1038/s41598-026-41597-x.},
}

@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 (FMT). 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/microbiology/complications ; *Gastrointestinal Microbiome/drug effects ; *Ciprofloxacin/adverse effects ; *Seizures/etiology/microbiology/chemically induced/metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Blood-Brain Barrier/metabolism ; Fecal Microbiota Transplantation ; Disease Susceptibility ; *Brain/metabolism ; *Brain-Gut Axis ; Disease Models, Animal ; },
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/microbiology/complications
*Gastrointestinal Microbiome/drug effects
*Ciprofloxacin/adverse effects
*Seizures/etiology/microbiology/chemically induced/metabolism
Male
Rats
Rats, Sprague-Dawley
Blood-Brain Barrier/metabolism
Fecal Microbiota Transplantation
Disease Susceptibility
*Brain/metabolism
*Brain-Gut Axis
Disease Models, Animal

@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},
}

@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 = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-48522-2},
pmid = {41981196},
issn = {2045-2322},
support = {0008147//Ministry of Innovation, Science and Technology/ ; },
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.},
}

@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},
doi = {10.1080/19490976.2026.2657048},
pmid = {41983510},
issn = {1949-0984},
mesh = {*Methylamines/metabolism/blood ; Animals ; *Gastrointestinal Microbiome/physiology ; *Peritoneal Fibrosis/microbiology/metabolism/etiology/pathology ; Mice ; Fecal Microbiota Transplantation ; Peritoneal Dialysis/adverse effects ; Humans ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Peritoneum/pathology/metabolism ; Bacteria/metabolism/classification/genetics/isolation & purification ; Transforming Growth Factor beta1/metabolism ; Disease Models, Animal ; Female ; },
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.},
}

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

@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},
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.

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.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00345-026-06386-1.},
}

@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 ; Rats ; *Hepatitis E virus/drug effects/genetics ; *Cytidine/analogs & derivatives/pharmacology/therapeutic use ; Disease Models, Animal ; Ribavirin/pharmacology/therapeutic use ; *Hydroxylamines/pharmacology/therapeutic use ; Sofosbuvir/pharmacology/therapeutic use ; Hepatocytes/virology ; Male ; Humans ; RNA, Viral ; Rats, Sprague-Dawley ; },
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
Rats
*Hepatitis E virus/drug effects/genetics
*Cytidine/analogs & derivatives/pharmacology/therapeutic use
Disease Models, Animal
Ribavirin/pharmacology/therapeutic use
*Hydroxylamines/pharmacology/therapeutic use
Sofosbuvir/pharmacology/therapeutic use
Hepatocytes/virology
Male
Humans
RNA, Viral
Rats, Sprague-Dawley

@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 ; *Clostridium Infections/therapy ; *Inflammatory Bowel Diseases/therapy ; *Autism Spectrum Disorder/therapy ; Treatment Outcome ; },
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
*Clostridium Infections/therapy
*Inflammatory Bowel Diseases/therapy
*Autism Spectrum Disorder/therapy
Treatment Outcome

@article {pmid41975274,
year = {2026},
author = {Nikolaidis, M and Hu, C and Juran, BD and McCauley, BM and Schlicht, EM and Bianchi, JK and Ali, AH and Tragaki, V and Atkinson, EJ and Johnson, S and Mars, RA and Eaton, JE and Carey, EJ and Franke, A and Schramm, C and Kashyap, PC and Go, YM and Tran, V and Teeny, S and Jones, DP and Grant, CW and Athreya, AP and Miller, GW and LaRusso, NF and Gores, GJ and Karlsen, TH and Hov, JR and Amoutzias, GD and Lazaridis, KN},
title = {Compositional and functional differences of gut microbiome and metabolome inform pathogenesis of cholestatic liver disease.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2655793},
doi = {10.1080/19490976.2026.2655793},
pmid = {41975274},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Metabolome ; Female ; Male ; Middle Aged ; Feces/microbiology/chemistry ; Adult ; *Bacteria/classification/genetics/isolation & purification/metabolism ; *Liver Cirrhosis, Biliary/microbiology/metabolism/pathology ; *Cholangitis, Sclerosing/microbiology/metabolism/pathology ; Aged ; },
abstract = {Primary sclerosing cholangitis (PSC) and primary biliary cholangitis (PBC) are rare, idiopathic, chronic cholestatic liver diseases that respond differently to limited medical therapies and often lead to liver transplantation. We examined the compositional and functional differences in the gut microbiome, mycobiome, and metabolome of these diseases to better understand their impact on pathogenesis and outcomes. Stool sample metagenomes and metabolomes from patients with PSC (n = 245), PBC (n = 280) and matched controls (n = 245 and n = 278, respectively) were analyzed by shotgun sequencing and ultrahigh-resolution mass spectrometry. Comparisons were conducted with covariate-adjusted linear models. The gut microbiomes of patients with PSC and PBC were characterized by reduced diversity and increased abundance of pathobionts and virulence factors, coupled with altered microbial metabolism, including a reduction of short-chain fatty acids and B-vitamins. Untargeted stool metabolomics supported these results. Patients were stratified into groups using their microbial signatures, and each group had distinct patterns of microbiome-related changes. Cox regression analysis revealed that pathogenic microbial species were predictive of hepatic decompensation, whereas beneficial species had a protective effect. Based on previous groundwork and our new results, microbiome-based interventions such as probiotics, short-chain fatty acid supplementation, and phage therapy represent promising therapeutic options for cholestatic liver diseases.},
}

Humans
*Gastrointestinal Microbiome
*Metabolome
Female
Male
Middle Aged
Feces/microbiology/chemistry
Adult
*Bacteria/classification/genetics/isolation & purification/metabolism
*Liver Cirrhosis, Biliary/microbiology/metabolism/pathology
*Cholangitis, Sclerosing/microbiology/metabolism/pathology
Aged

@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 = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c13513},
pmid = {41979342},
issn = {1520-5118},
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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1111/apt.70671},
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 ; *Gastrointestinal Microbiome/physiology ; *Atherosclerosis/microbiology ; *Peripheral Arterial Disease/microbiology ; *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
*Gastrointestinal Microbiome/physiology
*Atherosclerosis/microbiology
*Peripheral Arterial Disease/microbiology
*Dysbiosis

@article {pmid41785880,
year = {2026},
author = {Petersen, AØ and Damholt, B and Grove, M and Hink, J and Marotte-Hurbon, T and Söderqvist, J and Troy, A and Zdravkovic, M and Bayer, L and Brunner, K and Bryde, T and Clube, J and Gencay, YE and Gram, A and Haaber, JK and Hallström, B and Jasinskytė, D and Pascal, R and Petersen, M and Semsey, S and Torio, AS and Turcu, IC and Smrekar, F and Taur, Y and Satlin, MJ and Sommer, MOA and van der Helm, E and Grøndahl, C},
title = {Safety, recovery, and pharmacodynamics of CRISPR-Cas therapeutic SNIPR001: a phase 1, randomised, double-blind, first-in-human, dose-escalation study.},
journal = {The Lancet. Microbe},
volume = {7},
number = {4},
pages = {101257},
doi = {10.1016/j.lanmic.2025.101257},
pmid = {41785880},
issn = {2666-5247},
mesh = {Humans ; Double-Blind Method ; Adult ; Middle Aged ; Male ; Female ; Young Adult ; Aged ; Escherichia coli/virology ; Adolescent ; *CRISPR-Cas Systems ; Feces/microbiology ; Gastrointestinal Microbiome ; Healthy Volunteers ; *Bacteriophages/genetics ; *Escherichia coli Infections/therapy ; },
abstract = {BACKGROUND: Patients with haematological cancer who receive stem-cell transplantation are at risk of bloodstream infections, often caused by multidrug resistant gut pathogens such as Escherichia coli. SNIPR001 is a cocktail of four CRISPR-Cas-armed bacteriophages that reduce colonisation of E coli in the gastrointestinal tract in animal models and is designed to not affect other members of the commensal microbiota. We aimed to investigate the safety and tolerability of SNIPR001 in healthy participants.

METHODS: In this randomised, placebo-controlled, double-blind, first-in-human, dose-escalation trial conducted at a single centre (Medpace Clinical Pharmacology Unit; Cincinnati, OH, USA), we sequentially enrolled healthy participants (aged 18-65 years) with more than 10[7]E coli colony-forming units per gram of stool into cohorts 1, 2, and 3, pending a safety review of the previous enrolment group where applicable. Participants in each cohort were randomly assigned to treatment or placebo using a unique three-digit participant identification number. Participants were orally administered 10[8] plaque-forming units (PFU) per dose (cohort 1), 10[10] PFU per dose (cohort 2), and 10[12] PFU per dose (cohort 3) of SNIPR001 or placebo (phosphate-buffered saline buffer), twice daily for 7 days. All personnel, except for a pharmacy staff member who prepared both SNIPR001 and placebo vials, were masked to the administered dose and assignment; masking was ensured by fully covering the surface of each vial. Participants were followed up to day 187. The primary outcome was the incidence and severity of adverse events and medically attended adverse events from the first administration of the study drug until 4 weeks after the last dose administration on day 35 of the study. Recovery and biodistribution of SNIPR001 in faeces, blood, and urine; pharmacodynamics, including the ability of SNIPR001 to reduce E coli levels in stool (assessed using a linear mixed-effects model); and microbiome composition (using Bray-Curtis dissimilarity) were secondary outcomes. Primary safety analyses were assessed per-protocol (ie, all enrolled participants who received at least one administration of the study drug). This trial was conducted under an Investigational New Drug application from the US Food and Drug Administration, is registered with ClinicalTrials.gov (NCT05277350), and is closed to new participants.

FINDINGS: The trial was carried out between March 24, 2022, and Nov 30, 2022. 36 eligible participants were randomly assigned to receive SNIPR001 or placebo in cohorts 1 (six assigned to 10[8] PFU per dose and two assigned to placebo), 2 (six to 10[10] PFU per dose and two to placebo), and 3 (12 to 10[12] PFU per dose and eight to placebo). The mean age of participants was 42·1 years (SD 13·8), with 14 (39%) female participants and 22 (61%) male participants. During the trial and 4-week follow-up period, only mild and moderate adverse events were observed, with most adverse events occurring in the placebo group (13, six, one, and nine for participants receiving either placebo or SNIPR001 at 10[8], 10[10], and 10[12] PFU twice a day, respectively). The number of participants who had adverse events was not significantly higher in treatment groups than in the placebo group (p=0·94, one-sided Fisher's exact test). The most frequently reported adverse events were headaches and diarrhoea. No grade 3-4 adverse events were reported and no serious adverse events were reported in the SNIPR001 dose groups. During and after the dosing period, the gut microbiota composition did not significantly differ between the treatment and placebo groups (p>0·05, two-sided Mann-Whitney U test of Bray-Curtis distances, false discovery rate [FDR]-corrected). Functional SNIPR001 was recovered from stool samples in concentrations proportional to the administered dose but was not meaningfully detected in plasma (only one sample) or urine (only one sample). SNIPR001 was undetected in all samples 6 months after the last dosing, which is a favourable pharmacokinetic property and meets regulatory expectations. We observed the largest reduction in E coli levels compared with placebo 2 weeks after treatment initiation at day 14 (78%; -0·65 log10 [SE 0·64] for 10[12] PFU SNIPR001 twice-daily group), according to a linear mixed-effects model for the highest dose population; however, this change was not statistically significant (p=0·811, linear mixed-effects model, FDR-corrected).

INTERPRETATION: This first-in-human study of SNIPR001 supported its safety, tolerability, and restriction to the gastrointestinal tract, while not systemically disrupting the gut microbiome. These results justify further clinical development of SNIPR001 in an ongoing phase 1b/2a trial.

FUNDING: Combating Antibiotic-Resistant Bacteria Biopharmaceutical Accelerator (CARB-X) and SNIPR Biome.},
}

Humans
Double-Blind Method
Adult
Middle Aged
Male
Female
Young Adult
Aged
Escherichia coli/virology
Adolescent
*CRISPR-Cas Systems
Feces/microbiology
Gastrointestinal Microbiome
Healthy Volunteers
*Bacteriophages/genetics
*Escherichia coli Infections/therapy

@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 = {},
number = {},
pages = {},
doi = {10.1093/oncolo/oyag131},
pmid = {41967083},
issn = {1549-490X},
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. Numerous 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.},
}

@article {pmid41967501,
year = {2026},
author = {Deschamps, C and Tronel, A and Bailly, E and Tanfede, MRS 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 = {},
number = {},
pages = {},
doi = {10.1093/femsre/fuag016},
pmid = {41967501},
issn = {1574-6976},
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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.20892/j.issn.2095-3941.2025.0761},
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/ ; },
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.},
}

@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/complications ; Male ; *Gastrointestinal Microbiome ; *Bacteria/classification/isolation & purification/genetics ; Middle Aged ; *Diverticulum/microbiology/complications ; Aged ; RNA, Ribosomal, 16S/genetics ; Female ; },
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/complications
Male
*Gastrointestinal Microbiome
*Bacteria/classification/isolation & purification/genetics
Middle Aged
*Diverticulum/microbiology/complications
Aged
RNA, Ribosomal, 16S/genetics
Female

@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},
doi = {10.1080/19490976.2026.2652474},
pmid = {41969207},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Dysbiosis/microbiology ; Mice ; Disease Models, Animal ; *Vibrio Infections/microbiology/pathology/complications ; Vibrio vulnificus/physiology ; Mice, Inbred C57BL ; Male ; Humans ; Inflammation/microbiology ; *Non-alcoholic Fatty Liver Disease/microbiology/complications ; Intestines/microbiology/pathology ; Female ; Liver/pathology ; 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
*Gastrointestinal Microbiome
*Dysbiosis/microbiology
Mice
Disease Models, Animal
*Vibrio Infections/microbiology/pathology/complications
Vibrio vulnificus/physiology
Mice, Inbred C57BL
Male
Humans
Inflammation/microbiology
*Non-alcoholic Fatty Liver Disease/microbiology/complications
Intestines/microbiology/pathology
Female
Liver/pathology
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 Chang, NH and Jogendran, M and Bretthauer, M},
title = {Gastroenterology/Hepatology: What You May Have Missed in 2025.},
journal = {Annals of internal medicine},
volume = {},
number = {},
pages = {e2601058},
doi = {10.7326/ANNALS-26-01058},
pmid = {41974014},
issn = {1539-3704},
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.},
}

@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 = {},
number = {},
pages = {e0011326},
doi = {10.1128/msystems.00113-26},
pmid = {41960919},
issn = {2379-5077},
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.},
}

@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},
doi = {10.1080/19490976.2026.2657625},
pmid = {41964110},
issn = {1949-0984},
mesh = {Animals ; *Linoleic Acids, Conjugated/administration & dosage/pharmacology/metabolism ; *CD8-Positive T-Lymphocytes/immunology/drug effects/metabolism ; *Salmonella typhimurium/immunology/physiology ; Mice ; Mice, Inbred C57BL ; *PPAR gamma/metabolism/genetics ; Gastrointestinal Microbiome/drug effects ; *Salmonella Infections/immunology/prevention & control/microbiology ; Dietary Supplements ; Intestinal Mucosa/immunology/microbiology ; Metabolic Reprogramming ; },
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/pharmacology/metabolism
*CD8-Positive T-Lymphocytes/immunology/drug effects/metabolism
*Salmonella typhimurium/immunology/physiology
Mice
Mice, Inbred C57BL
*PPAR gamma/metabolism/genetics
Gastrointestinal Microbiome/drug effects
*Salmonella Infections/immunology/prevention & control/microbiology
Dietary Supplements
Intestinal Mucosa/immunology/microbiology
Metabolic Reprogramming

@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 = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c06224},
pmid = {41964572},
issn = {1520-5118},
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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1080/14787210.2026.2659725},
pmid = {41964647},
issn = {1744-8336},
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: 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, guideline 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, earlier 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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1186/s12917-026-05469-w},
pmid = {41965671},
issn = {1746-6148},
support = {No. 2024JC-ZDXM-14//Natural Science Basic Research Program of Shaanxi Province/ ; },
}

@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},
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.},
}

@article {pmid41966334,
year = {2026},
author = {M, P and Rajendiran, U and Wahab, MT and Venkatachalam, I},
title = {Interventions Targeting Gut Colonization by Multidrug-Resistant Organisms in Healthcare Settings: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.},
journal = {The Journal of hospital infection},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jhin.2026.03.035},
pmid = {41966334},
issn = {1532-2939},
abstract = {BACKGROUND: Gut colonization with multidrug-resistant organisms (MDRO) increases risks of infection, transmission and mortality in healthcare settings. Although decolonization strategies have been attempted to reduce the impact of gut MDRO, no consensus exists on their effectiveness. Our study evaluates the effectiveness of these strategies.

METHODS: We searched PubMed, EMBASE, CENTRAL, CINAHL and Web of Science for randomized controlled trials (RCTs) published from Jan 2005 to Dec 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 RoB2 tool. A random-effects model was used for meta-analysis.

PROSPERO: CRD42025625291.

RESULTS: 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 (RR=1.18; 95% 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.

CONCLUSION: 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).},
}

@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 {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 = {},
number = {},
pages = {},
doi = {10.1038/s41538-026-00815-6},
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 = {},
number = {},
pages = {},
doi = {10.1186/s12951-026-04369-3},
pmid = {41957631},
issn = {1477-3155},
support = {LHGJ20230213//Joint Construction project of Henan Medical Science and Technology/ ; },
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.},
}

@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 = {},
doi = {10.64898/2026.03.09.710596},
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 {pmid41772613,
year = {2026},
author = {Zeng, L and Zhou, W},
title = {Deciphering the mitochondria-gut microbiota axis in irritable bowel syndrome: pathogenic insights and therapeutic frontiers.},
journal = {Journal of translational medicine},
volume = {24},
number = {1},
pages = {},
pmid = {41772613},
issn = {1479-5876},
abstract = {BACKGROUND: Irritable bowel syndrome (IBS) is a chronic gastrointestinal disorder involving multiple pathogenic mechanisms. Gut microbiota dysbiosis and mitochondrial dysfunction are key drivers of IBS, as they weaken the intestinal barrier, promote inflammation, and alter metabolism. However, the underlying mechanisms of crosstalk between these factors remain largely understudied, which hinders the clinical translation of targeted therapeutic strategies.

MAIN BODY: Drawing on recent literature, this review clarifies the intricate interplay between mitochondrial health and gut microbiota balance in IBS. We summarize the core pathophysiological mechanisms of IBS including neuroendocrine, immune-inflammatory, and gastrointestinal motility-related pathways. We further elaborate on the individual roles of mitochondrial dysfunction and gut microbiota dysbiosis in IBS pathogenesis, discussing the bidirectional crosstalk between mitochondria and the gut microbiota, and the regulatory role of diet in this axis. Current therapeutic approaches targeting IBS, such as Western medications; probiotics; fecal microbiota transplantation; low-fermentable oligosaccharide, disaccharide, monosaccharide, and polyol diet; traditional Chinese medicine; and mitochondria-targeted interventions, are also reviewed. Building on this, the review summarizes the advantages and limitations of existing research on the mechanisms and therapies for IBS and identifies the challenges and directions for future basic and clinical research.

CONCLUSIONS: The interplay between mitochondrial dysfunction and gut microbiota dysbiosis is a critical research focus for understanding IBS pathophysiology. Elucidating the underlying mechanisms of their crosstalk provides a foundation for future research and facilitates the development of innovative therapeutic strategies targeting mitochondrial health and gut microbiota balance. This multifaceted approach holds promise for improving IBS management and enhancing the quality of life of affected patients.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00980-2},
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/ ; },
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.},
}

@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 = {},
number = {},
pages = {},
pmid = {41951771},
issn = {1745-7254},
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.},
}

@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},
doi = {10.5056/jnm26011},
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 ; *Gastrointestinal Microbiome/immunology/drug effects ; *Immune Checkpoint Inhibitors/therapeutic use/adverse effects/pharmacology ; *Fecal Microbiota Transplantation/methods ; 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
*Gastrointestinal Microbiome/immunology/drug effects
*Immune Checkpoint Inhibitors/therapeutic use/adverse effects/pharmacology
*Fecal Microbiota Transplantation/methods
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 = {},
number = {},
pages = {},
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},
doi = {10.3760/cma.j.cn501113-20250527-00202},
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 = {*Portasystemic Shunt, Transjugular Intrahepatic/adverse effects ; Humans ; *Hepatic Encephalopathy/etiology/prevention & control ; *Hypertension, Portal/surgery ; *Postoperative Complications/prevention & control/etiology ; Risk Factors ; Liver Cirrhosis/surgery/complications ; Stents ; },
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.},
}

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

@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},
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.},
}

@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},
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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c11966},
pmid = {41947394},
issn = {1520-5118},
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.},
}

@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 C. 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},
doi = {10.1016/j.jhepr.2025.101716},
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 {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 = {},
number = {},
pages = {},
doi = {10.1007/s40520-026-03368-6},
pmid = {41940919},
issn = {1720-8319},
support = {G099721N//Fonds Wetenschappelijk Onderzoek/ ; },
}

@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 = {},
number = {},
pages = {1-20},
doi = {10.1080/17460913.2026.2654374},
pmid = {41942347},
issn = {1746-0921},
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.},
}

@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/microbiology ; *Polysaccharides/chemistry/pharmacology/isolation & purification/therapeutic use ; Mice ; *Allium/chemistry ; Gastrointestinal Microbiome/drug effects ; Dextran Sulfate ; Male ; Fatty Acids, Volatile/metabolism ; Mice, Inbred C57BL ; Colon/drug effects/metabolism ; Fecal Microbiota Transplantation ; 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/microbiology
*Polysaccharides/chemistry/pharmacology/isolation & purification/therapeutic use
Mice
*Allium/chemistry
Gastrointestinal Microbiome/drug effects
Dextran Sulfate
Male
Fatty Acids, Volatile/metabolism
Mice, Inbred C57BL
Colon/drug effects/metabolism
Fecal Microbiota Transplantation
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 = {*Hyaluronic Acid/pharmacology/chemistry/therapeutic use ; Animals ; Molecular Weight ; *Gastrointestinal Microbiome/drug effects ; Mice ; Dextran Sulfate ; *Colitis/chemically induced/drug therapy/microbiology ; Mice, Inbred C57BL ; Male ; *Colitis, Ulcerative/drug therapy/chemically induced ; Colon/drug effects/pathology ; Disease Models, Animal ; Intestinal Mucosa/drug effects/metabolism ; },
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.},
}

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

@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 = {},
number = {},
pages = {},
pmid = {41944837},
issn = {1437-1588},
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.},
}

@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 = {},
number = {},
pages = {},
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/ ; },
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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1039/d6fo00213g},
pmid = {41945453},
issn = {2042-650X},
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.},
}

@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 = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c15173},
pmid = {41945864},
issn = {1520-5118},
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.},
}

@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 = {},
number = {},
pages = {121524},
doi = {10.1016/j.jep.2026.121524},
pmid = {41932663},
issn = {1872-7573},
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.},
}

@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},
doi = {10.1080/19490976.2026.2652460},
pmid = {41933285},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Carcinoma, Non-Small-Cell Lung/immunology/surgery/microbiology ; Animals ; *Lung Neoplasms/immunology/surgery/microbiology ; Mice ; Prognosis ; Male ; Female ; Middle Aged ; Bacteria/classification/genetics/isolation & purification/metabolism ; Fecal Microbiota Transplantation ; Aged ; *Nutritional Status ; Retrospective Studies ; Fatty Acids, Volatile/metabolism ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; },
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.},
}

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

@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 ; *Gastrointestinal Microbiome/drug effects ; Rats ; *Osteoarthritis, Knee/therapy/pathology/microbiology/chemically induced ; Male ; Rats, Sprague-Dawley ; Disease Models, Animal ; Injections, Intra-Articular ; Fecal Microbiota Transplantation ; },
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
*Gastrointestinal Microbiome/drug effects
Rats
*Osteoarthritis, Knee/therapy/pathology/microbiology/chemically induced
Male
Rats, Sprague-Dawley
Disease Models, Animal
Injections, Intra-Articular
Fecal Microbiota Transplantation