@article {pmid41601518,
year = {2025},
author = {Sgarbossa, C and Chinna Meyyappan, A and Forth, E and Bromley, H and Milev, R},
title = {Assessing the long-term effects of microbial therapeutics as treatment within psychiatry: a systematic review.},
journal = {Frontiers in psychiatry},
volume = {16},
number = {},
pages = {1663719},
pmid = {41601518},
issn = {1664-0640},
abstract = {BACKGROUND: The management and treatment of psychiatric disorders by manipulating the gut microbiome and utilizing microbial therapeutics, via modulation of the gut-brain-axis, has been a rapidly growing field of research. Given the novelty of using microbial therapeutics within psychiatry, a growing number of studies have investigated their use as treatment for various psychiatric disorders and symptoms. However, few studies have explored the longitudinal efficacy of these treatments. This review aims to summarize the findings of any studies assessing the long-term effects of gut-related interventions on mood and psychiatric symptoms.

METHODS: A systematic search of 4 databases (Embase, PsycINFO, Medline, Web of Science) from inception to May 28, 2025, informed by Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, and using key words relating to microbial therapeutics, psychiatric disorders, and long-term effects was conducted. Findings were included or excluded using pre-determined eligibility criteria such as being been written in English and published by a peer-reviewed journal, assessed for quality using the Cochrane Handbook for Systematic Reviews of Interventions Risk of Bias tool, and qualitatively evaluated.

RESULTS: The search yielded 4175 studies, of which 1274 duplicates were removed. All remaining studies underwent abstract screening, from which 70 records were full-text screened and a total of ten clinical studies (n = 10) met eligibility criteria and were included in the review. The majority of studies explored the effects of microbial therapeutics such as fecal microbiota transplant and probiotics, as treatment for disorders of the gastrointestinal tract as the primary scope, with additional outcome measures assessing psychiatric well-being. The review presented with mixed findings: many studies reported a sustained improvement in symptoms of depression and anxiety ranging from 3- to 18-months post-treatment, while others reported the opposite with no sustained long-term improvement in mood-related symptoms. There was also a lack of consistency across follow-up duration between studies, making it difficult to compare findings.

CONCLUSIONS: Overall, this review highlighted the need for more placebo-controlled studies with larger sample sizes to effectively evaluate the longitudinal potential of microbial therapeutics as treatment for mood-disturbances and psychiatric symptoms. With consideration for the limitations of this field, these results provide evidence that there may be long-term benefits of targeting the gut microbiome as treatment for mood-related disturbances.},
}

@article {pmid41601294,
year = {2026},
author = {Song, CH and Kim, N and Nam, RH and Choi, H and Jin, I and Kim, EH and Ha, S and Kang, K and Lee, W and Choi, H and Kim, YR and Seok, YJ and Lee, HK and Shin, CM and Lee, DH},
title = {Sex-Dependent Microbial and Host Profiles Following Fecal Microbiota and Bifidobacterium longum Treatment in Stress-Induced Gut Dysbiosis.},
journal = {Gut and liver},
volume = {},
number = {},
pages = {},
doi = {10.5009/gnl250440},
pmid = {41601294},
issn = {2005-1212},
abstract = {BACKGROUND/AIMS: Irritable bowel syndrome (IBS) is a chronic functional gastrointestinal disorder influenced by stress, microbial dysbiosis, and immune activation. Microbiota-directed therapies, including fecal microbiota transplantation and probiotics, show promise, but their sex-specific effects remain unclear. We compared the therapeutic effects of lyophilized fecal microbiota (LFM) with Bifidobacterium longum BBH016 in male and female Wistar rats subjected to repeated water avoidance stress.

METHODS: Fecal pellet output (FPO), colonic mast cell infiltration, and fecal short-chain fatty acids were measured. Gut microbial composition and function were analyzed by 16S rRNA sequencing and Kyoto Encyclopedia of Genes and Genomes pathway prediction.

RESULTS: Both interventions significantly reduced FPO and mast cell infiltration in males but had less pronounced effects in females. Microbiota analyses revealed sex-dependent responses, with distinct microbial trajectories in each treatment group. Using linear discriminant analysis effect size, we identified seven key taxa with treatment- or sex-specific enrichment. Alistipes onderdonkii and Bacteroides uniformis consistently increased in both LFM- and B. longum-treated groups, regardless of sex. Bacteroides finegoldii and Barnesiella intestinihominis were specifically enriched in the LFM group. In males, Blautia faecis and Fusicatenibacter saccharivorans were enriched following the interventions, whereas Parabacteroides goldsteinii appeared exclusively in stressed males. Functional predictions revealed the enrichment of estrogen signaling and bile acid pathways in males and the attenuation of proinflammatory pathways in females following LFM. Correlations between microbial taxa and host outcomes were predominantly observed in male rats.

CONCLUSIONS: These findings highlight sex-specific microbial and host responses to microbiota-targeted therapies in a stress-induced IBS model, emphasizing sex as a biological variable in designing personalized microbiome-based treatments.},
}

@article {pmid41599902,
year = {2026},
author = {Plaza-Diaz, J and Herrera-Quintana, L and Olivares-Arancibia, J and Vázquez-Lorente, H},
title = {Personalized Nutrition Through the Gut Microbiome in Metabolic Syndrome and Related Comorbidities.},
journal = {Nutrients},
volume = {18},
number = {2},
pages = {},
doi = {10.3390/nu18020290},
pmid = {41599902},
issn = {2072-6643},
mesh = {Humans ; *Metabolic Syndrome/microbiology/prevention & control/diet therapy/therapy ; *Gastrointestinal Microbiome/physiology ; Exercise ; *Precision Medicine/methods ; Comorbidity ; Diet ; },
abstract = {Background: Metabolic syndrome, a clinical condition defined by central obesity, impaired glucose regulation, elevated blood pressure, hypertriglyceridemia, and low high-density lipoprotein cholesterol across the lifespan, is now a major public health issue typically managed with lifestyle, behavioral, and dietary recommendations. However, "one-size-fits-all" recommendations often yield modest, heterogeneous responses and poor long-term adherence, creating a clinical need for more targeted and implementable preventive and therapeutic strategies. Objective: To synthesize evidence on how the gut microbiome can inform precision nutrition and exercise approaches for metabolic syndrome prevention and management, and to evaluate readiness for clinical translation. Key findings: The gut microbiome may influence cardiometabolic risk through microbe-derived metabolites and pathways involving short-chain fatty acids, bile acid signaling, gut barrier integrity, and low-grade systemic inflammation. Diet quality (e.g., Mediterranean-style patterns, higher fermentable fiber, or lower ultra-processed food intake) consistently relates to more favorable microbial functions, and intervention studies show that high-fiber/prebiotic strategies can improve glycemic control alongside microbiome shifts. Physical exercise can also modulate microbial diversity and metabolic outputs, although effects are typically subtle and may depend on baseline adiposity and sustained adherence. Emerging "microbiome-informed" personalization, especially algorithms predicting postprandial glycemic responses, has improved short-term glycemic outcomes compared with standard advice in controlled trials. Targeted microbiome-directed approaches (e.g., Akkermansia muciniphila-based supplementation and fecal microbiota transplantation) provide proof-of-concept signals, but durability and scalability remain key limitations. Conclusions: Microbiome-informed personalization is a promising next step beyond generic guidelines, with potential to improve adherence and durable metabolic outcomes. Clinical implementation will require standardized measurement, rigorous external validation on clinically meaningful endpoints, interpretable decision support, and equity-focused evaluation across diverse populations.},
}

Humans
*Metabolic Syndrome/microbiology/prevention & control/diet therapy/therapy
*Gastrointestinal Microbiome/physiology
Exercise
*Precision Medicine/methods
Comorbidity
Diet

@article {pmid41599716,
year = {2026},
author = {Krynicka, P and Cortegoso Valdivia, P and Morawski, M and Marlicz, W and Skonieczna-Żydecka, K and Koulaouzidis, A},
title = {Microbiota-Driven Strategies for Managing IBD-Associated Risks: From Infections to Mental Health.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {19},
number = {1},
pages = {},
doi = {10.3390/ph19010118},
pmid = {41599716},
issn = {1424-8247},
abstract = {Inflammatory bowel diseases (IBD) are increasingly acknowledged not merely as confined gastrointestinal disorders but as systemic immunometabolic syndromes. Central to this paradigm is the gut microbiota including non-bacterial components such as the virome, whose functional disruption marked by reduced short-chain fatty acids (SCFAs), increasingly implicated in pathogenic processes extending beyond intestinal mucosa. This review outlines how these alternations compromise the epithelial barrier and immune regulation, increasing the risk of recurrent Clostridioides difficile infections to anemia, neuropsychiatric comorbidities, and extraintestinal manifestations. We critically evaluate emerging microbiota-targeted strategies, including fecal microbiota transplantation (FMT), live biotherapeutic products (LBPs), and precision postbiotics, positioning them as potential adjuncts to conventional immunosuppression. Finally, we discuss the current barriers to clinical translation, such as safety and heterogeneity, and propose a future framework for personalized, functionally integrated IBD care aimed at restoring long-term microbiota homeostasis.},
}

@article {pmid41599127,
year = {2025},
author = {Zhou, Y and Zhang, Y and Li, Y and Chen, Y and Chi, X and You, Z and Zhang, H and Li, Y and Wu, L},
title = {Bile Derivative T3K Ameliorates Colitis by Regulating the Intestinal Microbiota-Bile Acid Axis.},
journal = {Pharmaceutics},
volume = {18},
number = {1},
pages = {},
doi = {10.3390/pharmaceutics18010020},
pmid = {41599127},
issn = {1999-4923},
support = {2023-I2M-2-009//CAMS Innovation Fund for Medical Sciences/ ; },
abstract = {Background/Objectives: The pathogenesis of ulcerative colitis (UC) is complex, and there is an urgent need for effective therapeutic agents with low side effects. Recent studies highlight the critical roles of abnormal bile acid (BA) metabolism and gut microbiota dysbiosis in UC progression. However, there is a significant knowledge gap about the relation between BA and gut microbiota. The BA derivative T3K exerts good anti-UC effect, and its mechanism is still unknown. In this study, we investigate how its anti-UC mechanism is involved in the modulation of the gut microbiota-BA axis and BA metabolism. Methods: Gene expression microarray GSE92415 of UC from the Gene Expression Omnibus was used to analyze BA metabolism. DSS-induced colitis mouse model, Caco-2 and IEC6 cells were used to confirm the anti-UC of T3K using intestinal permeability assay with FITC, Western-blot, immunohistochemical staining, immunofluorescenc and so on in vitro and in vivo. The changes in bile acid and microbiota were measured by 16S rRNA sequencing and bile acid analysis combined with pseudo-germ-free (PGF) models and fecal microbiota transplantation (FMT). Results: T3K demonstrated strong therapeutic effects, including reduced weight loss, lower disease activity index (DAI), and increased colon length. T3K also enhanced the expression of Occludin and Mucin2, and restored gut barrier integrity. Furthermore, T3K improved intestinal dysbiosis and abnormal BA metabolism in colitis mice. Through PGF models and FMT, we confirmed that T3K modulates BA metabolism via the gut microbiota. T3K specifically promotes the growth of beneficial bacteria, such as Akkermansia muciniphila, increases levels of hydrophilic BAs like muricholic acid (MCA), lithocholic acid (LCA) and its derivatives isoLCA and then repairs damaged intestinal mucosa. Conclusions: Bile acid derivative T3K, as a potential anti-UC candidate, effectively restores gut barrier integrity and then ameliorates colitis by improving gut microbiota composition and regulating BA metabolism, including increasing hydrophilic BAs.},
}

@article {pmid41597735,
year = {2026},
author = {Moser, K and Ballif, A and Pillonel, T and Concu, M and Montenegro-Borbolla, E and Nickel, B and Stampfli, C and Ruf, MT and Audry, M and Kapel, N and Gerber, S and Jacot, D and Bertelli, C and Galpérine, T},
title = {Fecal Microbiota Transplantation Donor Screening: Is Dientamoeba fragilis a Valid Criterion for Donor Exclusion? A Longitudinal Study of a Swiss Cohort.},
journal = {Microorganisms},
volume = {14},
number = {1},
pages = {},
doi = {10.3390/microorganisms14010217},
pmid = {41597735},
issn = {2076-2607},
support = {//internal funding at the Lausanne University Hospital (CHUV)/ ; grant number 51NF40 180575//he salaries of K.M. and E.M.-B. were supported as a part of NCCR Microbiomes, a National Centre of Competence in Research, funded by the Swiss National Science Foundation/ ; },
abstract = {Dientamoeba fragilis is a protozoan of the human digestive tract, yet its transmission and pathogenic role remain poorly understood. This study aimed to evaluate its impact on the efficacy and safety of fecal microbiota transplantation (FMT) in treating recurrent Clostridioides difficile infection (rCDI). This longitudinal cohort study analyzed stool samples from FMT donors and recipients pre-treatment and at 2 and 8 weeks post-FMT. All samples were retrospectively tested using real-time PCR. Shotgun metagenomics was also performed on selected donor-recipient pairs to explore transmission. CDI cure rates, gastrointestinal adverse events (AEs), and serious adverse events (SAEs) were assessed prospectively. A total of 53 FMT were analyzed (179 samples), with 23 (43%) derived from D. fragilis-positive donor stool (4 of 10 donors, 40%). Four of 52 recipients (18.2%), initially negative and who received treatment from positive donors, tested positive post-FMT. Shotgun metagenomics could not definitely confirm transmission due to the lack of a good reference genome. No significant differences in efficacy, AE, or SAE were observed between FMT from D. fragilis-positive versus -negative donors, even in immunocompromised patients. No SAEs were attributed to FMT. D. fragilis may be transmitted via FMT without evidence of short-term clinical impact. Consequently, RT-PCR detection should be interpreted cautiously in the context of donor exclusion decisions.},
}

@article {pmid41597728,
year = {2026},
author = {de Groen, P and Gouw, SC and Hanssen, NMJ and Nieuwdorp, M and Rampanelli, E},
title = {Early-Life Gut Microbiota: Education of the Immune System and Links to Autoimmune Diseases.},
journal = {Microorganisms},
volume = {14},
number = {1},
pages = {},
doi = {10.3390/microorganisms14010210},
pmid = {41597728},
issn = {2076-2607},
support = {09150182010020//NWO-VICI grant 2020/ ; 101141346//ERC Advanced grant/ ; 4-SRA-2025-1766-M-B//BREAKTHROUGH T1D Grant/ ; 09150172210050//ZonMw-VIDI grant 2023/ ; },
abstract = {Early life is a critical window for immune system development, during which the gut microbiome shapes innate immunity, antigen presentation, and adaptive immune maturation. Disruptions in microbial colonization-driven by factors such as cesarean delivery, antibiotic exposure, and formula feeding-deplete beneficial early-life taxa (e.g., Bifidobacterium, Bacteroides, and Enterococcus) and impair key microbial functions, including short-chain fatty acid (SCFA) production by these keystone species, alongside regulatory T cell induction. These dysbiosis patterns are associated with an increased risk of pediatric autoimmune diseases, notably type 1 diabetes, inflammatory bowel disease, celiac disease, and juvenile idiopathic arthritis. This review synthesizes current evidence on how the early-life microbiota influences immune maturation, with potential effects on the development of autoimmune diseases later in life. We specifically focus on human observational and intervention studies, where treatments with probiotics, synbiotics, vaginal microbial transfer, or maternal fecal microbiota transplantations have been shown to partially restore a disrupted microbiome. While restoration of the gut microbiome composition and function is the main reported outcome of these studies, to date, no reports have disclosed direct prevention of autoimmune disease development by targeting the early-life gut microbiome. In this regard, a better understanding of the early-life microbiome-immune axis is essential for developing targeted preventive strategies. Future research must prioritize longitudinal evaluation of autoimmune outcomes after microbiome modulation to reduce the burden of chronic immune-mediated diseases.},
}

@article {pmid41597349,
year = {2025},
author = {Varnas, D and Kunevičius, A and Burokas, A and Urbonas, V},
title = {Fecal Microbiota Transplantation for Autism Spectrum Disorder in Children: Results from a Prospective Open-Label Controlled Observational Study.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {62},
number = {1},
pages = {},
doi = {10.3390/medicina62010065},
pmid = {41597349},
issn = {1648-9144},
support = {01.2.2-LMT-K-718-03-0099//Lietuvos Mokslo Taryba/ ; },
mesh = {Humans ; *Autism Spectrum Disorder/therapy/complications ; Male ; Female ; Prospective Studies ; *Fecal Microbiota Transplantation/methods/standards ; Child ; Child, Preschool ; Treatment Outcome ; },
abstract = {Background and Objectives: Autism spectrum disorder (ASD) is a prevalent neurodevelopmental disorder with an increasing global incidence. Gut microbiota dysbiosis is believed to be playing a role in ASD pathogenesis. Fecal microbiota transplantation (FMT) is emerging as a potential therapeutic strategy to alleviate ASD-related and gastrointestinal symptoms, but data in pediatric ASD populations remain limited. Materials and Methods: We conducted a prospective, single-center, open-label controlled study to evaluate the efficacy of colonoscopic FMT in children with ASD. Participants were allocated to two groups: an intervention group that underwent a single FMT procedure and a control group. Gastrointestinal Symptoms Rating Scale (GSRS), Autism Diagnostic Observation Schedule (ADOS), Childhood Autism Rating Scale (CARS), Child Behavior Checklist (CBCL), and Parent Global Impression (PGI-R) scales were assessed for both groups at baseline and at set time points. Results: 30 participants were enrolled, with 15 in each group. At 8 weeks, no significant between-group differences were observed for the prespecified primary endpoint, change in ADOS scores. The intervention group showed significantly greater improvements in CARS (p < 0.001), PGI-R (p < 0.001), CBCL Internalizing Problems (p = 0.001), and GSRS (p = 0.037) compared with controls; CARS and PGI-R improvements persisted at 6 months. Within the intervention group, sustained improvements were noted in CARS, GSRS, and PGI-R up to 18 months. No serious adverse events were observed; three mild, self-limited adverse events were recorded following FMT. Conclusions: Colonoscopic FMT was associated with significant short-term improvements in gastrointestinal and caregiver-reported ASD symptoms (CARS), but not in ADOS scores. Some effects persisted long-term. However, due to a lack of blinding and possible selection bias, these findings should be interpreted as exploratory. Larger randomized controlled trials are needed to confirm efficacy and optimize protocols.},
}

Humans
*Autism Spectrum Disorder/therapy/complications
Male
Female
Prospective Studies
*Fecal Microbiota Transplantation/methods/standards
Child
Child, Preschool
Treatment Outcome

@article {pmid41596802,
year = {2026},
author = {Qin, T and Wei, Y and Zheng, W and Li, S and Song, S and Ai, C},
title = {Bacteroidesfinegoldii and Parabacteroides goldsteinii Mediate Fucoidan-Induced Attenuation of Intestinal Inflammation in Mice Through Betaine- and Spermidine-Related Pathways.},
journal = {Foods (Basel, Switzerland)},
volume = {15},
number = {2},
pages = {},
doi = {10.3390/foods15020203},
pmid = {41596802},
issn = {2304-8158},
abstract = {Fucoidan improves host health by enriching beneficial taxa such as Bacteroides and Parabacteroides, yet the underlying mechanisms remain unclear. This study validated the association between these two genera and fucoidan-mediated mitigation of intestinal inflammation in mice. Subsequently, the effects of Parabacteroides goldsteinii and Bacteroides finegoldii were evaluated in colitis mice, and the contributions of microbiota-associated metabolites spermidine and betaine were investigated in vitro. Both strains reduced IL-6 (32-36%), TNF-α (30-37%), and IL-1β (40-45%) levels and increased levels of catalase (25-35%) and glutathione peroxidase (31-45%) in the colon. Mechanically, these strains suppressed activation of the NF-κB and MAPK pathways and preserved tight junction integrity by inhibiting myosin light chain kinase activation. These effects were associated with alterations of gut microbiota, characterized by decreased Proteobacteria and increased Bacteroidota, resulting in increased betaine (45-60%) and spermidine (90-112%). In vitro, betaine and spermidine alleviated LPS-induced inflammation and oxidative damage by regulating macrophage polarization. These results suggest that Bacteroides and Parabacteroides contribute to fucoidan-induced improvement of host health through betaine- and spermidine-related pathways. Future studies should clarify the origins of key metabolites and validate their causality and translational relevance using approaches such as fecal microbiota transplantation, metabolite tracing, and human-relevant systems.},
}

@article {pmid41595645,
year = {2026},
author = {Rusu, M and Ichim, C and Anderco, P and Pălăștea, A and Boicean, A},
title = {Gut-Kidney Axis: Unraveling the Role of the Microbiome in Chronic Kidney Disease.},
journal = {Biomedicines},
volume = {14},
number = {1},
pages = {},
doi = {10.3390/biomedicines14010109},
pmid = {41595645},
issn = {2227-9059},
abstract = {Chronic kidney disease (CKD), which affects over 850 million individuals globally, is increasingly regarded as a systemic condition in which the gut microbiota represents a key pathogenic node. This review provides an integrated overview of mechanistic, translational and clinical data implicating the gut-kidney axis in CKD. The CKD-associated microbiota displays a characteristic dysbiosis, marked by depletion of short-chain fatty acid-producing commensals, overgrowth of proteolytic and urease-expressing taxa and disruption of epithelial barrier integrity. These disturbances favor the generation and systemic accumulation of gut-derived uremic toxins, most notably indoxyl sulfate, p-cresyl sulfate, indole-3-acetic acid and trimethylamine-N-oxide, which promote endothelial dysfunction, vascular calcification, fibrosis and chronic inflammation, thereby hastening renal function loss and heightening cardiovascular risk. Microbiome-directed interventions, including dietary modification, prebiotics, probiotics, synbiotics, intestinal dialysis, fecal microbiota transplantation, gut-acting sorbents and nephroprotective phytochemicals, are summarized with emphasis on their effects on uremic toxin burden and clinical surrogates. System-level implications of the gut-kidney axis for cardiovascular disease, immunosenescence and sarcopenia are discussed, together with future priorities for integrating multi-omics profiling and precision microbiome-based strategies into nephrology practice.},
}

@article {pmid41594368,
year = {2026},
author = {Han, L and Zhou, F and Zhang, C and Li, H and Zheng, Y and Tian, Y and Liu, Y and Yin, J and Huang, X},
title = {Lean DLY Pig-Derived Fecal Microbiota Promotes Growth Performance by Modulating Gut Microbiota: Serum Metabolic Profiles in Obese Ningxiang Pigs.},
journal = {Animals : an open access journal from MDPI},
volume = {16},
number = {2},
pages = {},
doi = {10.3390/ani16020177},
pmid = {41594368},
issn = {2076-2615},
support = {U20A2055//National Natural Science Foundation of China/ ; CX20230714//Graduate Research Innovation Project of Hunan Province/ ; },
abstract = {Fecal microbiota transplantation (FMT) has demonstrated potential in reshaping gut microbiota to improve animal phenotypes, yet its application in lean-type to obese-type pigs like Ningxiang (NX) pigs remains unclear. To address this, we investigated the effects of Lean Duroc × Landrace × Yorkshire (DLY) pig-derived fecal microbiota on the growth, gut microbiota composition, and serum metabolism of obese NX pigs. Thirty-six 50-day-old castrated male NX pigs of similar initial body weight were randomly assigned to either a control group or FMT group. The trial lasted for 35 days. Results indicated that FMT significantly improved the average daily gain and increased nutrient digestibility. Serum biochemical analysis revealed elevated levels of globulin and total protein and reduced low-density lipoprotein cholesterol in the FMT group. In addition, 16S rRNA sequencing demonstrated that FMT modified gut microbiota composition and diversity, enriching beneficial genera such as Blautia, Agathobacter, Faecalibacterium, and Eubacterium_coprostanoligenes_group. Untargeted serum metabolomics further revealed altered metabolite profiles linked to lipid and amino acid metabolism. Correlation analysis further revealed a link between these enriched bacteria and metabolites changes. Overall, these findings demonstrate that transplantation of the fecal microbiota from lean DLY pigs significantly improved the growth performance of obese NX pigs by improving nutrient digestibility and modulating the gut microbiota-host metabolic axis.},
}

@article {pmid41593440,
year = {2026},
author = {Lv, J and Liu, R and Sun, Z and Zhang, J and Zhang, Y and Zhao, X and Liu, J and Zhou, X and Zhang, M and Liu, Q and Gao, F},
title = {Gut Microbiota as Neuroimmune Modulators in Myasthenia Gravis: Mechanistic Insights from the Gut-Brain Axis to Therapeutic Innovations.},
journal = {The American journal of Chinese medicine},
volume = {},
number = {},
pages = {1-21},
doi = {10.1142/S0192415X26500023},
pmid = {41593440},
issn = {1793-6853},
abstract = {Myasthenia gravis (MG) is a chronic autoimmune disorder characterized by an immune-mediated attack on neuromuscular junction acetylcholine receptors (AChRs), and its pathogenesis is closely linked to immune dysregulation. Emerging evidence has highlighted the pivotal role of the gut microbiota in the pathophysiology of MG through immunomodulation, microbial metabolite signaling, and gut-brain axis interactions. This review combines 16S rRNA sequencing, metagenomic, and metabolomic data to reveal distinct gut microbial signatures in patients with MG. These signatures include reduced α-diversity, depletion of beneficial taxa like Bacteroides and Bifidobacterium, enrichment of pathobionts such as Escherichia and Enterococcus, and diminished levels of the short-chain fatty acids (SCFA), which were inversely correlated with disease severity. Experimental models have demonstrated that fecal microbiota transplantation (FMT) and probiotic supplementation with strains like Bifidobacterium ameliorate symptoms by restoring Th17/Treg equilibrium, suppressing the expression of pro-inflammatory cytokines including IL-6 and TNF-α, and enhancing intestinal barrier integrity. Mechanistically, gut dysbiosis exacerbates autoimmunity via NF-αB pathway activation, disrupts tryptophan metabolism and impairs gut-brain signaling. While existing studies have established microbiota-MG associations, further causal validation, personalized therapeutic strategies, and multi-omics integration remain critical priorities. Microbiota-targeted interventions, including precision FMT and metabolite delivery, hold translational potential, but their validation via large-scale randomized controlled trials and interdisciplinary approaches like AI-driven microbiota profiling is essential if they are to advance precision medicine for MG management.},
}

@article {pmid41589673,
year = {2026},
author = {Rosa, A and Gargari, M and Martelli, M},
title = {Gut-Brain-Jaw Axis: The Emerging Role of Gut Microbiota in Temporomandibular Disorders and Orofacial Pain-A Narrative Review.},
journal = {Journal of oral rehabilitation},
volume = {},
number = {},
pages = {},
doi = {10.1111/joor.70156},
pmid = {41589673},
issn = {1365-2842},
abstract = {BACKGROUND: Temporomandibular disorders (TMDs) and chronic orofacial pain are multifactorial conditions influenced by complex neurobiological and systemic mechanisms. Recent findings emphasise the gut-brain axis as a central modulator of pain, neuroinflammation, and immune signalling. Nevertheless, the role of the gut microbiota in TMD pathogenesis and oral rehabilitation remains insufficiently characterised.

METHODS: A structured literature search was conducted in PubMed/MEDLINE, Scopus, and Web of Science up to December 2024 using combinations of keywords including "gut microbiota," "temporomandibular disorder," and "orofacial pain." Eligible publications included clinical studies, systematic and narrative reviews, meta-analyses, and theoretical works addressing microbiota-pain relationships.

RESULTS: Recent Mendelian randomization studies reveal causal associations between specific bacterial genera and TMD risk. Experimental models demonstrate that gut dysbiosis exacerbates temporomandibular joint inflammation and neuroinflammatory responses, while restoring microbial balance through probiotics or faecal microbiota transplantation alleviates pain hypersensitivity. Mechanistic studies suggest that microbial metabolites such as short-chain fatty acids, GABA, and serotonin modulate trigeminal pain pathways via vagal and immune signalling.

CONCLUSION: Current evidence supports a bidirectional gut-brain-jaw communication system influencing both peripheral and central pain mechanisms. Incorporating microbiome-targeted approaches-such as dietary modulation, probiotics, and microbial therapy-may enhance TMD management and promote a more holistic, personalised model of oral rehabilitation.},
}

@article {pmid41589431,
year = {2025},
author = {Şahin, N and Salbaş, E},
title = {The Gut-Joint Connection: Microbiome's Role in Rheumatic Disease.},
journal = {Archives of rheumatology},
volume = {40},
number = {4},
pages = {413-421},
doi = {10.5152/ArchRheumatol.2025.25192},
pmid = {41589431},
issn = {2618-6500},
abstract = {The human gut microbiome is a pivotal regulator of systemic immunity and a central factor in the pathogenesis of rheumatic diseases. An imbalance in this microbial community, known as "dysbiosis," can trigger and perpetuate autoimmune responses through the "gut-joint axis." A key mechanism underpinning this connection is increased intestinal permeability ("leaky gut"), which facilitates the translocation of microbial products like lipopolysaccharide into the systemic circulation, thereby provoking chronic inflammation. Concurrently, dysbiosis disrupts the critical homeostatic balance between pro-inflammatory Th17 cells and regulatory T cells, an immunological hallmark of conditions such as rheumatoid arthritis (RA), ankylosing spondylitis, and systemic lupus erythematosus (SLE). Specific microbial signatures, including the expansion of Prevotella copri in RA and Ruminococcus gnavus in SLE, are emerging as potential diagnostic biomarkers. This deeper understanding is paving the way for innovative therapeutic strategies. Interventions aimed at modulating the gut microbiota, such as targeted diets, probiotics, prebiotics and fecal microbiota transplantation, represent a promising frontier for the personalized management of rheumatic diseases. This review explores the foundational mechanisms linking the microbiome to autoimmunity and discusses the clinical potential of harnessing the gut-joint axis to improve patient outcomes.},
}

@article {pmid41587946,
year = {2026},
author = {Quraishi, MN and Moakes, CA and Yalchin, M and Blackwell, C and Segal, J and Ives, NJ and Magill, L and Manzoor, SE and Gerasimidis, K and McMullan, C and Mathers, J and Horniblow, R and Loi, S and Kaur, M and Loman, NJ and Sharma, N and Hawkey, P and McCune, V and Quick, J and Nicholls, S and McMurray, C and Nichols, B and Svolos, V and Raguideau, S and Kerbiriou, C and Oo, YH and Beggs, AD and Crees, N and Hansen, R and Hart, AL and Gaya, DR and Quince, C and Iqbal, TH},
title = {Mechanistic insights into FMT for the treatment of ulcerative colitis: analysis of the STOP-Colitis trial.},
journal = {Journal of Crohn's & colitis},
volume = {},
number = {},
pages = {},
doi = {10.1093/ecco-jcc/jjag006},
pmid = {41587946},
issn = {1876-4479},
abstract = {BACKGROUND AND AIMS: Faecal microbiota transplantation (FMT) is a promising therapy for ulcerative colitis, but variable responses and unclear mechanisms limit its efficacy. We aimed to compare nasogastric versus colonic FMT delivery and define the microbial and immunological changes associated with clinical response.

METHODS: In this prospective, open-label, randomised pilot trial (STOP-Colitis), 30 adults with active ulcerative colitis were randomised to receive multi-dose FMT via nasogastric tube or colonoscopy with subsequent enemas. Key endpoints were clinical outcomes at week 8 and longitudinal multi-omic analyses of stool and biopsies to define changes in microbial composition (16S rRNA and shotgun metagenomics), short-chain fatty acids, mucosal T-cells, and host gene expression.

RESULTS: Colonic FMT was superior to nasogastric delivery, with a higher clinical response rate at week 8 (75% [9/12] vs 25% [2/8]; RR 2·94, 95% CI 0·84-10·30-per protocol analysis). Response was underpinned by successful microbial engraftment, leading to significantly increased faecal microbial diversity and enrichment of SCFA-producing taxa, including Oscillospiraceae and Christensenellaceae. This correlated with reduced faecal calprotectin. Responders showed a significant increase in mucosal regulatory T cells (P = 0·01), with a concurrent decrease in Th17 (P = 0·03) and CD8 + T cells. This anti-inflammatory shift was confirmed by mucosal transcriptomics, which revealed upregulation of metabolic pathways and downregulation of proinflammatory defence pathways in responders. (Trial registration: ISRCTN13636129).

CONCLUSION: Colonic FMT is a more effective delivery route than nasogastric administration. Clinical response is driven by the engraftment of immunomodulatory bacteria that restore a healthy host-microbe dialogue, providing rationale for developing targeted microbial therapeutics.},
}

@article {pmid41586375,
year = {2025},
author = {Zhao, Z and Wu, B},
title = {Gut microbiota dysbiosis aggravates sepsis-induced lung injury by promoting neutrophil extracellular traps and suppressing host integrin defense.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1699748},
pmid = {41586375},
issn = {1664-302X},
abstract = {BACKGROUND: The gut-lung axis is central to systemic inflammatory regulation, but the mechanisms by which gut microbiota dysbiosis aggravates sepsis-induced acute lung injury (ALI), particularly through neutrophil extracellular traps (NETs) and integrin signaling, remain unclear. Given the critical need for microbiota-based therapeutic strategies, this study investigates the mechanistic link between gut microbiota, NET formation, and pulmonary endothelial barrier dysfunction.

METHODS: Using a cecal ligation and puncture (CLP) sepsis model, control, sepsis, and fecal microbiota transplantation (FMT) groups were compared. Lung injury was assessed via histopathology, wet/dry weight ratios, and bronchoalveolar lavage fluid (BALF) analysis. High-throughput RNA sequencing (GO/KEGG/PPI) identified key targets, validated by lentiviral knockdown/overexpression of ITGAM and ITGB2 in vivo and in vitro [mouse pulmonary microvascular endothelial cells (MPMECs) and neutrophil co-cultures]. NETs were quantified by MPO-DNA ELISA and immunofluorescence.

RESULTS: CLP-induced sepsis triggered severe pulmonary edema, neutrophil infiltration, and NET accumulation, alongside downregulation of ITGAM/ITGB2 and tight junction proteins (β-catenin/ZO-1/VE-cadherin). FMT reduced NETs by 58% (p < 0.001) and restored endothelial barrier integrity. Transcriptomics revealed ITGAM/ITGB2 as central nodes in neutrophil activation and integrin pathways. In vitro, NET exposure increased endothelial permeability (3.1-fold FITC-dextran flux, p < 0.01) and IL-6/TNF-α secretion, while ITGAM/ITGB2 overexpression reversed these effects. Conversely, integrin silencing abolished FMT's protection, exacerbating ALI.

CONCLUSION: We unveil a novel gut microbiota-NET-integrin axis in sepsis-induced ALI, where microbial dysbiosis promotes NET-mediated suppression of ITGAM/ITGB2, leading to endothelial barrier failure. Our findings position FMT and integrin modulation as promising strategies to mitigate pulmonary vascular dysfunction, advancing the therapeutic potential of microbiota-targeted interventions in critical care.},
}

@article {pmid41585577,
year = {2026},
author = {Benterkia, S and Blythe, J},
title = {Brief Report: Can Fecal Microbiota Transplantation Treat Depression?.},
journal = {JGH open : an open access journal of gastroenterology and hepatology},
volume = {10},
number = {1},
pages = {e70336},
pmid = {41585577},
issn = {2397-9070},
}

@article {pmid41585498,
year = {2026},
author = {Jin, X and Wei, J and Min, X and Fan, Y and Yuan, Z and Du, Z and Su, Z and Xun, T and Du, Q and Liang, T and He, X and Tang, W},
title = {Gut microbiota and Parkinson's disease: exploring pathogenesis and potential therapeutic strategies from a gut-brain axis perspective.},
journal = {iScience},
volume = {29},
number = {2},
pages = {114185},
pmid = {41585498},
issn = {2589-0042},
abstract = {Parkinson's disease (PD) is a prevalent neurodegenerative disorder with a global prevalence exceeding 1‰, posing a significant public health challenge. Although the pathogenesis of PD is not yet fully elucidated, accumulating evidence suggests that it results from the interplay between genetic and environmental factors, highlighting its multifactorial nature. With advances in translational medicine, the gut has emerged as a critical participant in PD onset and progression. This review systematically summarizes the role of the gut in PD, particularly emphasizing potential mechanisms involving neuroinflammation in the central nervous system (CNS), pathological aggregation of α-synuclein (α-syn), and mitochondrial dysfunction. Furthermore, gut-targeted therapeutic strategies for PD are discussed, including fecal microbiota transplantation (FMT), gut-directed anti-inflammatory therapies, supplementation with gut microbiota-derived metabolites such as short-chain fatty acids (SCFAs), and interventions targeting α-syn aggregation. A deeper understanding of these mechanisms not only advances the pathological knowledge of PD but also provides theoretical foundations for the early diagnosis and innovative treatment of the disease.},
}

@article {pmid41585029,
year = {2026},
author = {Hecker, MT and Rosero, C and Mendo-Lopez, R and Wilson, BM and Torres-Teran, MM and Donskey, CJ},
title = {Long-Term Follow-Up After Fecal Microbiota Transplantation via Freeze-Dried Capsules for Recurrent Clostridioides difficile Infection.},
journal = {Pathogens & immunity},
volume = {11},
number = {1},
pages = {1-13},
pmid = {41585029},
issn = {2469-2964},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is a standard therapy for recurrent Clostridioides difficile infection (CDI). Limited information is available on the durability of response after FMT via freeze-dried oral capsules and on whether patients who fail an initial FMT can be successfully managed with repeated FMT.

METHODS: We conducted a retrospective cohort study of all patients undergoing initial FMT for recurrent CDI via freeze-dried capsules from March 2015 through June 2022 at 2 acute-care hospitals. Information on response to FMT during the initial management period (ie, 3 months after the initial FMT) and long-term durability of response was collected through direct communication with patients and medical record review. Episodes occurring within 90 days of the initial FMT were defined as recurrences, whereas those occurring more than 90 days after the initial FMT were defined as additional CDI episodes.

RESULTS: Of 129 patients with recurrent CDI treated with FMT via freeze-dried capsules, 114 (89%) had experienced 3 or more prior episodes of CDI. At 3 months after the initial FMT, 103 (80%) patients had no recurrence, 26 (20%) patients had 1 or more recurrences managed with 1 (n=21) or 2 (n=2) additional FMTs, and 3 (12%) were transitioned to CDI suppressive therapy. During subsequent long-term follow-up (median 182 weeks), 21 of the 126 patients (17%) who did not transition to suppressive therapy had additional episodes managed with CDI therapy only (n=9), CDI therapy and additional FMT (n=10), or suppressive CDI therapy (n=2).

CONCLUSIONS: In a real-world setting with long-term follow-up, FMT via freeze-dried capsules was effective for the management of recurrent CDI. Repeated FMT procedures were effective for the management of patients with early failure after initial FMT and with additional episodes during long-term follow-up.},
}

@article {pmid41584842,
year = {2025},
author = {Ruchko, E and Chernysheva, M and Sokolov, V and Starinnov, Z and Sabirov, M and Vasiliev, A},
title = {β-cell heterogeneity and molecular plasticity in type 2 diabetes: multi-omics perspectives and the role of gut microbiota.},
journal = {Frontiers in cell and developmental biology},
volume = {13},
number = {},
pages = {1698296},
pmid = {41584842},
issn = {2296-634X},
abstract = {Type 2 diabetes (T2D) is a complex metabolic disorder characterized by systemic insulin resistance and progressive deterioration of pancreatic β-cell function. Advances in single-cell transcriptomics, epigenomics, and spatial transcriptomics have delineated marked β-cell heterogeneity, revealing subpopulations with differential secretory capacity, stress resilience, and vulnerability to metabolic and immune-mediated insults. These high-resolution approaches have further identified disease-associated alterations in other islet endocrine cells, as well as in immune, stromal, and exocrine pancreatic compartments, highlighting the central role of intercellular signaling in T2D pathogenesis. Concurrently, microbiome research has elucidated mechanisms by which gut microbial composition and metabolic activity modulate glucose homeostasis and β-cell function through immunoregulatory pathways, maintenance of epithelial barrier integrity, and enteroendocrine signaling, notably via glucagon-like peptide-1 (GLP-1). Therapeutic strategies targeting the gut microbiota include conventional probiotics, prebiotics, and fecal microbiota transplantation, alongside emerging synthetic biology approaches employing genetically engineered probiotic strains to deliver bioactive molecules, including GLP-1, directly in the gut microenvironment. This review integrates current multi-omics and experimental evidence to provide a comprehensive framework for understanding β-cell molecular plasticity, microbiota-mediated metabolic regulation, and their intersection as potential therapeutic targets. Such integrative approaches offer prospects for the development of precision interventions aimed at preserving or restoring β-cell function in T2D.},
}

@article {pmid41584685,
year = {2026},
author = {Li, W and Wang, X and Zhang, Y and Yang, H and Wang, X and Meng, W and Hu, T and Zhang, W and Zhu, Y and Wang, J and Yang, G},
title = {Engineered Bacillus subtilis WB600/ZD reduces post-weaning diarrhea in piglets by modulating gut microbiota and aryl hydrocarbon receptor (AHR) signaling.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {24},
number = {},
pages = {46-60},
pmid = {41584685},
issn = {2405-6383},
abstract = {Post-weaning diarrhea (PWD) causes significant economic losses to the pig industry. A previous study demonstrated that engineered Bacillus subtilis WB600 expressing Zophobas atratus defensin (ZD), termed WB600/ZD, alleviates intestinal inflammation, modulates gut microbiota, and maintains redox homeostasis in Salmonella-challenged mice; however, the precise mechanisms remain unclear. In this study, a total of 50 weaned Landrace × Large White piglets at 21 d of age were assigned to four groups: healthy piglets fed standard diet (H group; 6.60 ± 0.48 kg, n = 15) or 2 × 10[9] CFU/mL WB600/ZD (H + WB600/ZD group; 6.00 ± 0.68 kg, n = 15), and diarrheic piglets fed standard diet (PWD group; 6.51 ± 1.16 kg, n = 10) or 2 × 10[9] CFU/mL WB600/ZD (PWD + WB600/ZD group; 6.91 ± 0.57 kg, n = 10). All groups received 7 d of treatment followed by 3 d of post-treatment monitoring. During the 10-d trial period, the body weight, feed intake per group, and diarrhea incidence were recorded. Results demonstrated that WB600/ZD reduced diarrhea incidence in both healthy (P < 0.001) and diarrheic piglets (P = 0.040). Additionally, WB600/ZD improved the growth performance, including final body weight (P = 0.017) and average daily gain (ADG; P = 0.007), without affecting average daily feed intake (ADFI; P = 0.907). Mechanistically, WB600/ZD increased the levels of serum glutathione peroxidase (GSH-Px; P = 0.014) and reduced myeloperoxidase (MPO; P < 0.001) and malondialdehyde (MDA; P < 0.001). Integrated fecal microbiota and metabolites showed that this protective effect of WB600/ZD was associated with gut microbiota-dependent tryptophan metabolism (P < 0.001). Furthermore, antibiotic-treated (pseudo-germ-free) mice receiving fecal microbiota transplantation (FMT) from WB600/ZD-treated piglets or administered the aryl hydrocarbon receptor (AHR) agonist 6-formylindolo[3,2-b]carbazole (FICZ) before Salmonella enterica subsp. enterica serovar Infantis (S. Infantis) challenge exhibited activation of the AHR/cytochrome P450 family 1 subfamily A member 1 (CYP1A1) signaling pathway (P = 0.022) and increased interleukin (IL)-22 secretion (P < 0.001), thereby alleviating S. Infantis infection. Overall, this study provides strong evidence that WB600/ZD is a promising antibiotic alternative for preventing PWD in newly weaned piglets.},
}

@article {pmid41584317,
year = {2026},
author = {Jawed, F and Aziz, R and Mir, SUI and Khan, SA},
title = {Gut microbiota, sarcopenia, and type 2 diabetes: a triangular pathophysiological network.},
journal = {Journal of diabetes and metabolic disorders},
volume = {25},
number = {1},
pages = {41},
pmid = {41584317},
issn = {2251-6581},
abstract = {PURPOSE: Type 2 diabetes mellitus (T2DM), sarcopenia, and gut microbiota dysbiosis are increasingly recognized as interrelated conditions. T2DM accelerates muscle wasting through insulin resistance, inflammation, and oxidative stress, while sarcopenia worsens metabolic dysfunction. This review explores the interconnected conditions of Type 2 Diabetes, sarcopenia, and gut microbiota dysbiosis, highlighting their therapeutic potential and the need for interventions targeting these conditions for metabolic and musculoskeletal health.

METHODS: An extensive literature search was performed in PubMed, EMBASE, Scopus, and Web of Science up to July 2025 using terms related to gut microbiota, sarcopenia, and T2DM. Both preclinical and human studies were included if they addressed microbial composition, metabolites, inflammation, insulin resistance, or muscle protein turnover.

RESULTS: Evidence indicates bidirectional relationships: T2DM patients show higher prevalence of sarcopenia, while reduced muscle mass increases T2DM risk. Gut dysbiosis in T2DM is characterized by depletion of SCFA-producing taxa (e.g., Faecalibacterium prausnitzii) and enrichment of endotoxin-producing bacteria, leading to systemic inflammation and impaired insulin signaling. Germ-free and antibiotic-treated rodent models demonstrate muscle atrophy, whereas probiotic or prebiotic supplementation restores muscle mass and improves glucose metabolism. Limited clinical trials suggest dietary fibre, probiotics, and fecal microbiota transplantation improve glycemic control and inflammatory markers, with potential secondary benefits on muscle function.

CONCLUSION: T2DM, sarcopenia, and gut microbiota are linked through insulin resistance, inflammation, and altered signaling. Targeting gut-muscle-metabolism axis through diet, microbiota modulation, and exercise is promising. Future longitudinal and interventional studies are needed to establish causality and develop precision microbiome-based therapies.

SUMMARY: Type 2 diabetes mellitus (T2DM), sarcopenia, and gut microbiota dysbiosis are interconnected in a triangular pathophysiological network. T2DM accelerates muscle loss through insulin resistance, inflammation, and oxidative stress, while sarcopenia worsens glycaemic control. Gut dysbiosis reduces beneficial short-chain fatty acid (SCFA) production and increases pro-inflammatory metabolites such as lipopolysaccharides, further impairing muscle metabolism and glucose regulation. Preclinical and emerging clinical evidence shows that dietary fibre, probiotics, and fecal microbiota transplantation can modulate this axis. Targeting the gut-muscle-metabolism triad offers promising integrative strategies for preventing and managing diabetic sarcopenia.},
}

@article {pmid41583842,
year = {2025},
author = {Sandblom, G and Koishibayeva, LM and Poskus, T and Koishibayev, ZM},
title = {Editorial: Microflora and bacterial translocation in intestinal obstruction.},
journal = {Frontiers in surgery},
volume = {12},
number = {},
pages = {1760588},
pmid = {41583842},
issn = {2296-875X},
}

@article {pmid41583463,
year = {2025},
author = {Zha, T and Ding, Y and Xu, X and Zhang, Y and Guo, J and Ge, H and Xu, L},
title = {The oral-gut axis in chronic atrophic gastritis: current perspectives and integrated strategies.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1699501},
pmid = {41583463},
issn = {1664-3224},
mesh = {Humans ; *Gastritis, Atrophic/microbiology/therapy/immunology/metabolism/etiology ; *Gastrointestinal Microbiome/immunology ; Helicobacter Infections/microbiology/immunology/complications ; Dysbiosis ; Helicobacter pylori ; *Mouth/microbiology/immunology ; Chronic Disease ; Animals ; },
abstract = {Chronic atrophic gastritis (CAG) is a key precursor to gastric cancer, characterized by progressive mucosal atrophy, inflammation, and microbial dysbiosis. The Correa cascade model highlights Helicobacter pylori as a primary driver, progressing from gastritis to atrophy, intestinal metaplasia (IM), dysplasia, and malignancy. However, 20%-30% of CAG cases lack H. pylori involvement, emphasizing the roles of non-H. pylori microbial dysbiosis, environmental factors, and the oral-gut axis in disease progression. Oral microbes, such as Porphyromonas gingivalis, translocate to the stomach, amplifying inflammation through NF-κB and Wnt/β-catenin pathways and altering metabolites like short-chain fatty acids and trimethylamine N-oxide. Pro-inflammatory cytokines, including IL-1β, IL-6, and IL-17, alongside Th17-driven immune dysregulation, further accelerate carcinogenesis. This perspective integrates multi-omics data to elucidate microbiome shifts, metabolic changes, and immune responses across CAG subtypes. Advanced diagnostics, such as endoscopic imaging, serum biomarkers, and oral microbiota profiling, enable precise risk stratification. Management strategies extend beyond H. pylori eradication to include probiotics, fecal microbiota transplantation, periodontal interventions, and herbal compounds, targeting the oral-gut axis to restore microbial balance and halt carcinogenesis. This framework offers novel avenues for prevention and therapy in high-burden regions.},
}

Humans
*Gastritis, Atrophic/microbiology/therapy/immunology/metabolism/etiology
*Gastrointestinal Microbiome/immunology
Helicobacter Infections/microbiology/immunology/complications
Dysbiosis
Helicobacter pylori
*Mouth/microbiology/immunology
Chronic Disease
Animals

@article {pmid41583462,
year = {2025},
author = {Bong, H and Min, J and Kim, S and Lim, W and Lim, D and Eom, H and Her, Y and Jeon, M},
title = {ATOMIC: a graph attention network for atopic dermatitis prediction using human gut microbiome.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1670993},
pmid = {41583462},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Dermatitis, Atopic/microbiology/diagnosis/etiology ; Adult ; Dysbiosis ; Female ; Computational Biology/methods ; Male ; },
abstract = {INTRODUCTION: Atopic dermatitis (AD) is a chronic inflammatory skin disease driven by complex interactions among genetic, environmental, and microbial factors; however, its etiology remains unclear. Recent studies have reported the role of gut microbiota dysbiosis in AD pathogenesis, leading to increased interest in microbiome-targeted therapeutic strategies such as probiotics and fecal microbiota transplantation. Building on these findings, recent advances in computational modeling have introduced machine learning and deep learning-based approaches to capture the nonlinear relationships between gut microbiota and diseases. However, these models focus on diseases other than AD and often fail to capture complex microbial interactions or incorporate microbial genomic information, thereby offering limited interpretability.

METHODS: To address these limitations, we propose ATOMIC, an interpretable graph attention network-based model that incorporates microbial co-expression networks to predict AD. Microbial co-expression networks incorporate microbial genomic information as a node feature, thereby enhancing their ability to capture functionally relevant microbial patterns. To train and test our model, we collected and processed 99 gut microbiome samples from adult patients with AD and healthy controls at Kangwon National University Hospital (KNUH).

RESULTS: ATOMIC outperformed baseline models, achieving an AUROC of 0.810 and an AUPRC of 0.927 for KNUH dataset. Furthermore, ATOMIC identified microbes potentially associated with AD prediction and proposed candidate microbial biomarkers that may inform future therapeutic strategies.

DISCUSSION: By identifying key microbial taxa that contributed to the AD classification through its interpretable attention mechanism, ATOMIC provides a foundation for personalized microbiome-based interventions and biomarker discovery. Additionally, to facilitate future research, we publicly released a gut microbial abundance dataset from KNUH. The source code and processed abundance data are available from ATOMIC GitHub repository at https://www.github.com/KU-MedAI/ATOMIC.},
}

Humans
*Gastrointestinal Microbiome
*Dermatitis, Atopic/microbiology/diagnosis/etiology
Adult
Dysbiosis
Female
Computational Biology/methods
Male

@article {pmid41583434,
year = {2025},
author = {Zhang, Y and Zhang, H and Miao, T and Wang, X and Zuo, Y and Zhang, R and Zhang, L and Cheng, Y and Liu, D and Chen, X and Li, L and Xie, X and Li, N},
title = {Advances in the study of gut microecology and mechanisms of hyperuricemia and gouty arthritis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1738716},
pmid = {41583434},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Hyperuricemia/microbiology/immunology/therapy/metabolism/etiology ; *Arthritis, Gouty/microbiology/immunology/therapy/metabolism/etiology ; Animals ; Dysbiosis/immunology ; Uric Acid/metabolism ; Fecal Microbiota Transplantation ; },
abstract = {Gouty arthritis is a metabolic disorder caused by purine metabolism dysregulation, characterized by monosodium urate crystal deposition in and around joints, triggering acute articular inflammation via NLRP3 inflammasome activation and IL-1β-mediated inflammatory cascades. While hyperuricemia represents a critical biochemical prerequisite for gouty arthritis development, elevated serum urate levels do not invariably lead to the disease. Mounting evidence suggests a significant relationship between gut microbiota and the pathogenesis of both gouty arthritis and hyperuricemia. The gut microbial ecosystem influences host health through metabolic and immune function modulation, performing essential roles in digestion, energy harvesting, and short-chain fatty acid production. Intestinal dysbiosis can damage epithelial integrity, compromise immune tolerance, and activate immune cells, thus contributing to disease onset and progression. Elucidating the complex interactions between gut microbiota and the mechanisms underlying gouty arthritis and hyperuricemia presents promising opportunities for developing novel preventative and therapeutic interventions. This review synthesizes recent advances in understanding the gut-joint axis and evaluates emerging therapeutic strategies including probiotics, dietary interventions, and fecal microbiota transplantation.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Hyperuricemia/microbiology/immunology/therapy/metabolism/etiology
*Arthritis, Gouty/microbiology/immunology/therapy/metabolism/etiology
Animals
Dysbiosis/immunology
Uric Acid/metabolism
Fecal Microbiota Transplantation

@article {pmid41582062,
year = {2026},
author = {Hartman, V and Bracke, B and Chapelle, T and Hendrikx, B and Huysentruyt, F and Liekens, E and Roelant, E and Roeyen, E and Ysebaert, D and Roeyen, G},
title = {Comparing faecal Elastase-1 and [13]C mixed triglyceride breath test in patients undergoing pancreatic surgery.},
journal = {HPB : the official journal of the International Hepato Pancreato Biliary Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.hpb.2026.01.001},
pmid = {41582062},
issn = {1477-2574},
abstract = {BACKGROUND: The optimal test for diagnosing pancreatic exocrine insufficiency (PEI) remains debated. This study compares the diagnostic accuracy of faecal elastase-1 (FE-1) and the [13]C Mixed Triglyceride Breath Test (MTGT) in patients undergoing pancreatic surgery.

METHODS: Patients undergoing pancreatic resection at Antwerp University Hospital (2016-2023) had FE-1 and MTGT testing before and after surgery. The MTGT was used as the reference standard. Agreement between both tests was evaluated using Cohen's kappa.

RESULTS: Preoperatively, in a patient cohort of 249 patients, PEI was detected in 25.3 % using MTGT and 39.6 % using FE-1 (cutoff <200 μg/g). The sensitivity and specificity of FE-1 were 63.5 % and 68.3 %, respectively. Agreement was fair (κ = 0.27). After pancreatoduodenectomy, the prevalence of PEI increased to 60 % (MTGT) and 92.2 % (FE-1), with only slight agreement between tests (κ = 0.17). Although FE-1 demonstrated high sensitivity (98.1 %), its specificity was poor (16.7 %), resulting in an 83.5 % false-positive rate.

CONCLUSIONS: In patients undergoing pancreatic surgery, especially after pancreatoduodenectomy, the agreement between MTGT and FE-1 is substantially lower than expected. FE-1 demostrates low specificity and a high false-positive rate, resulting in overdiagnosis and unnecessary economic and patient burden.},
}

@article {pmid41580820,
year = {2026},
author = {Ding, M and Xiao, Z and Hou, X and Luo, Z and Zhang, Z and Guo, M and Xu, C and Xu, R and Shan, J and Peng, H},
title = {Targeting G-protein-coupled receptors and gut microbiota: Ge-Lian Qi-Shen decoction elevates GLP-1 to combat non-alcoholic fatty liver disease.},
journal = {Chinese medicine},
volume = {21},
number = {1},
pages = {51},
pmid = {41580820},
issn = {1749-8546},
support = {KZYY2209//Kunshan Traditional Chinese Medicine Science and Technology Development Fund Project/ ; XZR2024193//Nanjing University of Chinese Medicine Natural Science Foundation Project/ ; KS2233//Kunshan Social Development Project/ ; ZD202425//Key Projects of Jiangsu Provincial Science/ ; LCZX202229//Suzhou Clinical Key Disease Diagnosis and Treatment Project/ ; },
abstract = {BACKGROUND: Non-alcoholic fatty liver disease (NAFLD), often accompanied by insulin resistance, obesity, and hyperlipidemia, is a challenging metabolic disorder to treat. Ge-Lian Qi-Shen Decoction, a traditional Chinese herbal formula, has been clinically used to alleviate symptoms associated with NAFLD, but its underlying mechanisms remain unclear.

METHODS: A NAFLD model was established in C57BL/6J mice using a high-fat diet (HFD). The effects of 4-week GQD intervention at different doses on NAFLD-related symptoms were assessed using biochemical analyses, pathological sections, and oral glucose tolerance tests. ELISA and qPCR were employed to investigate the impact of GQD on serum GLP-1 levels and intestinal Gcg gene expression in NAFLD mice. The direct stimulatory effects of GQD on GLP-1 secretion were examined in NCI-H716 cells and HFD-fed mice. UPLC-MS/MS was used to analyze the composition of ileal contents in GQD-treated mice, and the regulatory effects of 24 identified compounds on GLP-1 secretion were evaluated. Additionally, 16S rDNA sequencing, metabolomics and fecal microbiota transplantation were utilized to explore the role of gut microbiota in GQD's anti-NAFLD effect.

RESULTS: GQD improved HFD-induced hepatic steatosis, impaired glucose tolerance, and elevated blood lipid levels in a dose-dependent manner. It increased serum GLP-1 levels, reduced energy intake, and enhanced glucose tolerance in mice. A single dose of GQD directly elevated serum GLP-1 levels in HFD-fed mice and improved glucose tolerance in a GLP-1-dependent manner. In NCI-H716 cells, GQD promoted intracellular calcium influx and GLP-1 release by activating two G-protein-coupled receptors (GPCRs): bitter taste receptors and TGR5. Compounds such as berberine, coptisine, nuciferine, liensinine, higenamine, aurantio-obtusin, and obtusifolin in GQD activated bitter taste receptors, while maslinic acid and cycloastragenol activated TGR5, facilitating GLP-1 secretion. Furthermore, GQD gavage increased the levels of Muribaculaceae and Akkermansia in mouse feces, leading to elevated concentrations of short-chain fatty acids (SCFAs) such as acetate, propionate, butyrate, and valerate. These SCFAs potentially activated fatty acid-related GPCRs, such as GPR41, in the colon, thereby enhancing colonic Gcg expression. FMT experiment showed that gut microbiota can partially mediate the effect of GQD in increasing GLP-1 levels thus alleviating NAFLD.

CONCLUSION: Some alkaloids, anthraquinones, and triterpenoids in GQD can activate GPCRs, including bitter taste receptors and TGR5, in intestinal endocrine cells, promoting GLP-1 secretion. Simultaneously, GQD regulates gut microbiota composition and metabolism, increasing SCFA levels and Gcg gene expression, leading to sustained elevation of GLP-1 levels. These combined effects contribute to the alleviation of NAFLD symptoms.},
}

@article {pmid41580778,
year = {2026},
author = {Bai, Y and Kong, X and Wang, J},
title = {Targeting microbiome-driven epigenetic modifications: a new frontier in breast cancer treatment.},
journal = {Clinical epigenetics},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13148-025-02046-0},
pmid = {41580778},
issn = {1868-7083},
abstract = {Breast cancer remains a leading cause of morbidity and mortality among women worldwide, with significant heterogeneity in its development and treatment response. Recent advances in understanding the roles of the microbiome and epigenetic regulation have opened new avenues for addressing the complexities of breast cancer progression and therapeutic resistance. This review explores the intricate relationship between the gut and intratumoral microbiomes and epigenetic modifications, such as DNA methylation, histone modifications, and non-coding RNAs. Specifically, we examine how microbial metabolites, particularly short-chain fatty acids (SCFAs), regulate gene expression via epigenetic mechanisms, influencing tumor growth, metastasis, and treatment response. The impact of metabolic diseases, including obesity and type 2 diabetes mellitus (T2DM), on breast cancer risk through microbiome-mediated epigenetic changes is also discussed. Furthermore, the review highlights emerging therapeutic strategies that integrate microbiome modulation with epigenetic therapies, including the use of probiotics, dietary interventions, and fecal microbiota transplantation (FMT), as well as DNA methyltransferase (DNMT) inhibitors and histone deacetylase (HDAC) inhibitors. These innovative approaches hold promise for overcoming treatment resistance and improving clinical outcomes in breast cancer patients. Future research should focus on elucidating the molecular pathways through which the microbiome influences epigenetic regulation and developing personalized, microbiome-targeted therapies that enhance the efficacy of existing treatments. By targeting both the genetic and epigenetic drivers of breast cancer, microbiome-based interventions represent a novel frontier in the fight against this challenging disease.},
}

@article {pmid41580690,
year = {2026},
author = {Zhu, B and Huang, J and Zhang, H and Lin, H and Chen, T and Min, L and Yang, Y and Liu, Y and Guo, S},
title = {Akkermansia muciniphila vesicles attenuate smoking-induced cognitive decline via ILA-mediated AhR-dependent microglial reprogramming.},
journal = {Journal of nanobiotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12951-026-04044-7},
pmid = {41580690},
issn = {1477-3155},
support = {A2402014//Shenzhen Medical Research Fund/ ; 2023B110008//Guangdong Provincial Clinical Research Center for Laboratory Medicine/ ; 32300761//Youth Foundation of the National Natural Science Foundation of China/ ; },
abstract = {Chronic cigarette smoking accelerates age-related cognitive decline, yet the underlying mechanism remains elusive. Here, we elucidate a pathway through which smoking-induced gut dysbiosis contributes to cognitive impairment. This dysbiosis is marked by reductions in the abundances of Akkermansia muciniphila (A. muciniphila) and its metabolite indole-3-lactic acid (ILA), which correlate with cognitive deficits in older adult smokers. Using fecal microbiota transplantation, we demonstrate that the microbiota from smoke-exposed donors recapitulates cognitive impairment and microglial dysfunction in recipient mice. Importantly, these deficits were mitigated by treatment with either A. muciniphila-derived outer membrane vesicles (OMVs) or exogenous ILA, which restore synaptic integrity. Mechanistically, we demonstrate that both OMVs and ILA exert their neuroprotective effects via aryl hydrocarbon receptor (AhR) signaling. This AhR-dependent activation reprograms microglial metabolism toward oxidative phosphorylation, thereby suppressing neuroinflammation and restoring cellular bioenergetics. These findings suggest a mechanism through which smoking influences brain function via specific gut microbial metabolites and highlight the A. muciniphila-ILA-AhR axis as a promising target for preventing cognitive decline.},
}

@article {pmid41580415,
year = {2026},
author = {Song, M and Zhou, W and Fan, J and Cai, D and Wei, H and Tao, S},
title = {Dietary fiber deficiency exacerbates intestinal inflammation via miR-6240-enriched gut extracellular vesicles.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00918-8},
pmid = {41580415},
issn = {2055-5008},
support = {2022YFA1304104//National Key Research and Development Program/ ; 32272898//National Nature Science Foundation of China/ ; },
abstract = {Emerging evidence underscores the critical role of dietary fiber in maintaining gut homeostasis. While extracellular vesicles (EVs) have recently gained attention as key mediators of host-microbe communication, their functional contribution to fiber deficiency-associated pathologies remains largely unexplored. In this study, we revealed that a fiber-free diet induces significant intestinal inflammatory damage in mice, an effect that can be faithfully reproduced through fecal microbiota transplantation. Importantly, we demonstrated that intestinal epithelial cells-derived EVs from fiber-deprived mice are sufficient to recapitulate the detrimental effects of fiber deficiency. Mechanistic studies revealed enrichment of miR-6240 in these EVs, which targeted the 3'UTR of STAT6 mRNA to suppress its expression. This impairment of STAT6 signaling inhibited M2 macrophage polarization, exacerbating intestinal inflammation. This novel pathway is further validated in primary macrophage adoptive transfer experiments. Our work unveils a previously unrecognized mechanism by which fiber deficiency exacerbates intestinal inflammation through IECs-derived EVs and miR-6240/STAT6-mediated macrophage dysfunction.},
}

@article {pmid41580145,
year = {2026},
author = {Merrick, B and Cooper, R and Davido, B and Goldenberg, S},
title = {The role of the gut microbiome in MDRO colonisation and infection.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2026.01.009},
pmid = {41580145},
issn = {1469-0691},
abstract = {BACKGROUND: Colonisation of the gastrointestinal tract by multidrug-resistant organisms (MDROs) is a precursor to endogenous infection and onward transmission. The gut microbiome provides colonisation resistance (CR) - the ability to prevent or limit the establishment of pathogens, including MDROs - through nutrient and niche competition, production of inhibitory metabolites, and immune modulation. However, its integrity is threatened by antibiotics, adverse diet, and healthcare exposures.

OBJECTIVES: To describe mechanistic, epidemiological, and interventional evidence on the role of the gut microbiome in MDRO colonisation and infection, and to highlight implications for clinical practice, policy, and research.

SOURCES: PubMed/MEDLINE, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov were searched from 1 January 2000 to 30 September 2025, supplemented by hand-searching of key international guidelines (EUCIC/ESCMID, WHO, CDC/ECDC, NICE/UKHSA) and reference lists.

CONTENT: CR is shaped by microbial and host factors, including metabolic interactions, immune responses, and environmental exposures. Antimicrobials, non-antimicrobial drugs, diet, travel, and healthcare contact can disrupt the microbiota, predisposing to MDRO acquisition and infection. Observational data link gut microbial composition to risk of colonisation and infection outcomes, but predictive models are imperfect. Interventions to preserve or restore CR - such as diet-based strategies, probiotics, and faecal microbiota transplant - show promise but require robust and repeated, context-specific evaluation.

IMPLICATIONS: Protecting the microbiome must be a clinical and policy priority. Short-course, microbiome-sparing antimicrobial regimens, microbiome-aware diagnostics, and public health measures that support microbiome resilience could reduce MDRO burden and infections. Rigorous trials of microbiota-based therapies and integration of microbiome stewardship into antimicrobial resistance strategies are essential for translating mechanistic insights into patient benefit.},
}

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

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

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

REGISTRATION: INPLASY202470112.},
}

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

GRAPHICAL ABSTRACT: [Image: see text]

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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