@article {pmid41783924,
year = {2026},
author = {Luo, S and Lou, F and Yang, P and Zhang, Y and Yan, L and Dong, Y and Yang, B and Wang, H and Liu, Y and Pu, J and Cannon, RD and Xie, P and Ji, P and Jin, X},
title = {Dysregulation of Oral Microbial Eicosapentaenoic Acid Induced by Chronic Restraint Stress Exacerbates Periodontitis via M1 Macrophage Polarization.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e21346},
doi = {10.1002/advs.202521346},
pmid = {41783924},
issn = {2198-3844},
support = {82370968//National Natural Science Foundation of China/ ; 2026MSXM055//Chongqing medical scientific research project (Joint project of the Chongqing Health Commission and the Science and Technology Bureau)/ ; CSTB2022NSCQ-MSX1148//Natural Science Foundation of Chongqing/ ; 2025JYJ099//Project of Luzhou Science and Technology Bureau/ ; },
abstract = {The intricate interplay between chronic psychological stress and periodontitis, mediated by oral microbiota and macrophage polarization, remains largely enigmatic. Here, we demonstrate that chronic restraint stress (CRS) exacerbates periodontitis by inducing oral microbial dysbiosis and a consequential shift in host metabolism. Clinical observations reveal a significant correlation between depressive symptoms and the severity of periodontitis, which is underpinned by a distinct oral microbiome. Crucially, fecal microbiota transplantation from CRS-exposed mice into germ-free mice was sufficient to transmit the heightened periodontitis phenotype, establishing a causal role for the stress-altered microbiota. Metabolomic profiling identified a depletion of eicosapentaenoic acid (EPA) in stressed, ligature-induced periodontitis mice. Mechanistically, supplementation with EPA ameliorates periodontitis by suppressing the NF-κB signaling pathway, thereby inhibiting the pro-inflammatory M1 polarization of macrophages. Our findings unveil a novel gut-oral axis mediated by microbiota and metabolites under stress, and position the omega-3 fatty acid EPA as a promising therapeutic agent for mitigating stress-aggravated inflammatory disorders.},
}

@article {pmid41782495,
year = {2026},
author = {Loublier, C and Taminiau, B and Seidel, L and Moula, N and Tano, C and Cesarini, C and Costa, M and Lecoq, L and Daube, G and Amory, H},
title = {Survey on Faecal Microbiota Transplantation and Probiotic Use in Equine Practice in France and Belgium.},
journal = {Veterinary medicine and science},
volume = {12},
number = {2},
pages = {e70854},
doi = {10.1002/vms3.70854},
pmid = {41782495},
issn = {2053-1095},
support = {40005849//Fonds De La Recherche Scientifique - FNRS/ ; },
abstract = {BACKGROUND: Faecal microbiota transplantation (FMT) and probiotics are used in equine practice. Understanding veterinarians' perceptions and practices is crucial for effective implementation.

OBJECTIVE: (1) Evaluate the prevalence, usage patterns and perceived effectiveness of probiotics and FMT among equine veterinarians in France and Belgium. (2) Assess their knowledge, practices and influencing factors across demographics and settings. (3) Explore links between FMT protocols and treatment satisfaction.

STUDY DESIGN: Cross-sectional survey.

METHODS: An online survey collected demographic data and responses on the use of probiotics and FMT. Analyses included descriptive statistics, chi-square tests and logistic regression models.

RESULTS: Ninety-six equine veterinarians participated, practicing in Belgium (52.1%), France (39.6%) or both (8.3%). Probiotic use was reported by 82.1%, more frequent in field than clinical practice (odds ratio [OR] = 3.61, 95% CI [1.09, 12.02], p = 0.036) and in France than Belgium (OR = 5.08, 95% CI [1.44, 17.94], p = 0.012). Probiotics were used for chronic diarrhoea (88.0%), acute diarrhoea (67.6%) and inflammatory bowel diseases (45.9%). Most veterinarians (83.3%) defined probiotics well, but 16.7% misidentified non-probiotic products. FMT was used by 76.0%, mainly occasionally and therapeutically, more in clinical than field practice (OR = 4.79, 95% CI [1.03, 22.27], p = 0.046). In theory, 58.3% prioritized infection-free donors, but only 22.5% tested donors before FMT, mostly using coprology (93.8%). Those who tested donors reported higher perceived efficacy (p = 0.0029).

MAIN LIMITATIONS: Potential selection bias, as participation was voluntary. Generalizability might be limited by focus on France and Belgium. Sample size, while informative, should be expanded.

CONCLUSION: Probiotics and FMT were commonly used therapeutically by equine veterinarians in France and Belgium. Although probiotic use was widespread, some misunderstandings remained. FMT protocols varied, with donor faeces often untested. Treatment satisfaction was generally positive but estimated success rates varied. Standardized FMT protocols are needed to improve outcomes and consistency.},
}

@article {pmid41780918,
year = {2026},
author = {Patel, RK and Teja, R and Hermann, K and Franz, R and Wong, K and Kao, D},
title = {Engaging Patient and Caregiver Partners in Codeveloping a Patient Educational Video for Improving Clostridioides difficile Infection Education: Participatory Co-Design Study.},
journal = {JMIR formative research},
volume = {10},
number = {},
pages = {e81643},
doi = {10.2196/81643},
pmid = {41780918},
issn = {2561-326X},
abstract = {BACKGROUND: Patients with recurrent Clostridioides difficile infection (rCDI) and their caregivers often face considerable uncertainty regarding medical management, including the use of fecal microbiota transplantation (FMT), largely due to the scarcity of accessible and credible educational resources. Codeveloping educational materials with patients and caregivers offers a structured way to address these gaps and ensure that resources reflect the informational, psychological, and emotional needs of patients.

OBJECTIVE: The study team sought to cocreate an educational resource through an iterative process including patient and caregiver partners with lived experience of rCDI to improve C difficile infection education.

METHODS: This study examined the cocreation process of a patient-centered educational resource between the study team and patient or caregiver participants through a series of focus group (FG) sessions. Five participants took part in 3 serial FG sessions (3-5 participants each) over 13 months. Each FG session was audio recorded, transcribed, and analyzed using the NVivo (version 14) quantitative analysis software. A semantic thematic analysis framework was applied to interpret the results. Key areas of concern and preferred formats were identified following the first FG session. The first version of the educational resource was developed by the study team to address areas of concern and was iteratively refined following feedback from subsequent FG sessions with the study participants.

RESULTS: Participants expressed concerns about the lack of credible information on treatment options and their associated risks, especially with regard to FMT. They noted inadequate coverage of C difficile infection recurrence and its physical, psychological, and emotional impacts. Participants expressed a preference for educational resources in video format. On the basis of further feedback, refinements were made to improve pacing, consistency of animation, and narration, incorporating emotional and mental health considerations. The codeveloped video was well received and valued for its clear language, messaging, step-by-step guidance, and overall accessibility and clarity.

CONCLUSIONS: Our study demonstrated the feasibility and utility of patient and caregiver involvement in cocreating an educational resource on the management of rCDI, with FMT being a treatment option. Despite efforts to address knowledge gaps and preferences expressed for a video format, uncertainties remain regarding the most effective educational resource format. The integration of patient, caregiver, and study team perspectives contributed to a codeveloped video that addresses unmet needs and is patient centered. However, diverse patient experiences remain underrepresented. Future research should consider including more diverse participants as well as evaluating the effectiveness of knowledge improvement through various educational resource formats and patient health care experiences and levels of satisfaction.},
}

@article {pmid41780589,
year = {2026},
author = {Sowulewski, O and Leszkowicz, J and Sakowska, M and Spychalski, P and Szlagatys-Sidorkiewicz, A},
title = {Definitive surgery for Hirschsprung Disease between 3 and 12 months achieves best outcomes: A Systematic Review with Meta-Analysis.},
journal = {Journal of pediatric surgery},
volume = {},
number = {},
pages = {163039},
doi = {10.1016/j.jpedsurg.2026.163039},
pmid = {41780589},
issn = {1531-5037},
abstract = {INTRODUCTION: Optimal age for definitive pull-through in Hirschsprung disease (HD) is debated. Both early and delayed interventions may influence short- and long-term outcomes, but current guidelines do not provide a clear recommendation.

METHODS: A systematic review was conducted following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Nineteen studies published between 1998 and 2025, including 3,980 pediatric patients with HD undergoing definitive pull-through surgery, were included. Age at surgery was stratified using predefined thresholds (neonatal, <3 months, <6 months, <12 months, <4 years, and above). Short- and long-term outcomes were extracted and synthesized. Risk of bias was assessed using the Newcastle-Ottawa Scale.

RESULTS: Short-term outcomes were reported in 15 studies. Hirschsprung-associated enterocolitis (HAEC) was the most frequently reported complication (0-69.1%), occurring more often in neonates than in non-neonates (22.4%, 78/348 vs. 15.5%, 125/808) and in patients operated before 3 months of age compared with those operated later (20.7%, 68/328 vs. 13.6%, 60/442). Neonatal surgery was also associated with higher rates of anastomotic leakage (7.1%, 10/140 vs. 1.5%, 6/412). Long-term outcomes were assessed in 14 studies. Patients operated during the neonatal period had higher rates of fecal incontinence (30.0%, 55/183 vs. 17.8%, 56/314) and constipation (25.2%, 39/155 vs. 12.8%, 43/336). Similarly, surgery performed before 3 months of age was associated with increased rates of fecal incontinence (18.0%, 36/200 vs. 8.6%, 20/232) and constipation (23.5%, 47/200 vs. 13.8%, 32/232) at long-term follow-up.

CONCLUSIONS: Timing of definitive surgery in Hirschsprung disease is associated with differences in postoperative outcomes. Neonatal surgery and surgery performed during early infancy (<3 months) were more often associated with higher complication rates, whereas procedures performed during infancy showed more balanced results.},
}

@article {pmid41780914,
year = {2026},
author = {Cheng, M and Zhi, S and Zheng, M and Zhang, S and Hong, J},
title = {Gut Microbiota-Induced CTLA4 Expression on CD8[+] T Cells Impairs Antitumor Immunity and Promotes Colorectal Cancer Progression.},
journal = {Immunology},
volume = {},
number = {},
pages = {},
doi = {10.1111/imm.70128},
pmid = {41780914},
issn = {1365-2567},
support = {25A180025//The Key Scientific Research Project Plan of Higher Education Institutions in Henan Province/ ; 252300423545//The Youth Fund of Natural Science Foundation of Henan Province/ ; },
abstract = {This study reveals a novel gut microbiota-CD8[+] T cell axis driving immunosuppression in colorectal cancer. Analysis of 16S rRNA sequencing identified significant gut dysbiosis in CRC patients, with marked enrichment of Phocaeicola and Bacteroides. Single-cell transcriptomics uncovered substantial T cell depletion and elevated CTLA4[+]PD1[+] immune cells within the tumour microenvironment. Critically, spatial transcriptomics demonstrated co-localization of CTLA4[+]CD8[+] T cells with tumour cells, indicating direct immunosuppressive interactions. Functional validation confirmed CTLA4 overexpression impairs CD8[+] T cell effector capacity, accelerating CRC cell proliferation and invasion. In vivo models demonstrated that faecal microbiota transplantation (FMT) promoted CTL activation, reduced Bacteroides abundance, decreased the formation of CD8[+]CTLA4[+] T cells and ameliorated CRC symptoms. Additionally, CTLA4 knockdown inhibited tumour growth and metastasis. These findings establish a mechanistic pathway: gut dysbiosis induces chronic inflammation, triggering CTLA4 upregulation on CD8[+] T cells to promote T cell exhaustion and tumour immune evasion. The study provides immunological evidence for targeting the microbiota-CTLA4 axis in CRC immunotherapy.},
}

@article {pmid41780895,
year = {2026},
author = {Ma, X and Xu, Y and Nian, Y and Luo, R and Chen, T and Su, K and Li, T and Shen, C and Xie, B and Dai, H and Zhao, J and Ma, Y},
title = {Dietary carboxymethylcellulose metabolite promotes heart allograft rejection through induction of pro-inflammatory macrophages via lysophosphatidic acid.},
journal = {American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ajt.2026.02.030},
pmid = {41780895},
issn = {1600-6143},
abstract = {Carboxymethylcellulose (CMC), a common food emulsifier, induces microbiota dysbiosis and systemic inflammation; however, its impact on transplant immunity remains unclear. Allogenic heart rejection was observed in CMC-fed recipient mice, with increased abundance of lysophosphatidic acid (LPA)-producing bacteria and increased serum LPA concentration. CMC-induced transplant rejection was caused by the gut microbiota, as confirmed by fecal microbiota transplantation and gut microbiota depletion. Furthermore, LPA-treated macrophages demonstrated a pro-inflammatory ability to accelerate allograft rejection in cytotoxic T lymphocyte-associated protein 4 immunoglobulin-induced allograft survival by upregulating glycolysis. Conversely, the administrated of a glycolysis inhibitor resulted in allograft survival and abrogated the detrimental effect of LPA. Mass spectrometry and single-cell RNA sequencing confirmed that human transplant rejection patients showed significantly elevated serum LPA levels and LPAR6 expression in graft-infiltrate macrophages. Mechanistically, LPA preferentially promoted LPAR6 expression, which interacted with Rho-associated protein kinase 2 to activate the mTOR/HIF-1α pathway, thereby enhancing glycolysis and inducing pro-inflammatory macrophage polarization. Treatment with Ki16425, an LPAR antagonist, prolonged allograft survival in CMC-fed recipients. Our findings reveal a major detrimental effect of CMC on macrophage physiology and suggest that controlling LPAR6 expression or glycolysis in macrophage may improve allograft survival in transplant recipients.},
}

@article {pmid41778780,
year = {2026},
author = {Mambuque, E and Del Amo-de Palacios, A and Huete, SG and Marsh, CC and Theron, G and García-Basteiro, AL and Serrano-Villar, S},
title = {Beyond bacilli: integrating the microbiome into the TB research agenda.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2638004},
doi = {10.1080/19490976.2026.2638004},
pmid = {41778780},
issn = {1949-0984},
abstract = {Tuberculosis (TB) remains a leading infectious killer, with growing evidence that the human microbiome-particularly in the gut and lungs-shapes susceptibility, progression, and treatment outcomes. Over the past decade, studies have reported that TB-associated dysbiosis, which is more common in the gut than in the lung, is often marked by the loss of short-chain fatty acid-producing taxa and the expansion of opportunistic microbes. However, findings are frequently confounded by diet, antibiotic exposure, comorbidities, geography, and methodological variability. Most research has relied on compositional profiling, offering limited insight into functional mechanisms. This narrative review synthesizes recent evidence, emphasizing the need to integrate multiomics approaches-metagenomics, metatranscriptomics, and metabolomics-and experimental validation to uncover causal links between microbiome alterations and TB pathogenesis or therapy response. We discuss potential clinical applications, including microbiome-based diagnostics (such as stool-based microbial or metabolite signatures for TB risk stratification), prognostic indicators (such as gut microbiome recovery predicting immune normalization during therapy), and adjunctive interventions (including microbiome-derived products to reduce drug-induced liver injury or fecal microbiota transplantation, which has been shown to be safe in people with HIV on stable ART) to mitigate drug toxicity or enhance immune recovery. Key priorities include methodological standardization, confounder control, mechanistic studies, and the inclusion of high-burden settings. By moving beyond descriptive surveys toward functional, translational research, integrating insights from different microbiome methods into TB prevention, diagnosis, and treatment could redefine the clinical research agenda and open new avenues for precision medicine in this global disease.},
}

@article {pmid41778620,
year = {2026},
author = {Wang, Y and OuYang, J and Zhang, H and Shen, Y and Guo, Z and Lv, W},
title = {The Efficacy of Gut Microbiome-Modulating Therapies on Liver Cirrhosis: A Systematic Review and Network Meta-Analysis.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001010},
pmid = {41778620},
issn = {2155-384X},
abstract = {OBJECTIVE: Gut microbiome-modulating therapies are potential strategies for managing liver cirrhosis (LC), yet head-to-head comparisons to determine the optimal intervention are lacking. This study aimed to evaluate and rank the therapeutic efficacy of these therapies on liver function and disease progression in patients with LC.

METHODS: We searched major databases (PubMed, Web of Science, Embase, Cochrane Library) for randomized controlled trials (RCTs) published from January 1, 2000, to December 30, 2024. Interventions included probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) versus placebo or standard care. Primary outcomes were hepatic function indicators; secondary outcomes included inflammatory markers. Data were analyzed using random-effects frequentist network meta-analyses. The study was registered on PROSPERO (CRD420251000506).

RESULTS: Seventeen studies comprising 1051 individuals were included. Synbiotics demonstrated the most significant efficacy among all interventions, showing superior reduction in blood ammonia levels compared to placebo (Mean Difference (MD): -5.57), probiotics, and prebiotics. Prebiotics showed significant differences in lowering endotoxin levels compared to placebo (MD: -3.29) and probiotics. Furthermore, relative to placebo, prebiotics significantly reduced tumor necrosis factor-alpha (MD: -2.30) and interleukin-6 levels (MD: -4.60).

CONCLUSIONS: This network meta-analysis advances current knowledge by establishing an evidence-based hierarchy of efficacy. Synbiotics are most effective for reducing blood ammonia, whereas prebiotics demonstrate superior efficacy in lowering endotoxin and inflammatory markers. These results support a personalized therapeutic approach: prioritizing synbiotics for patients with hyperammonemia, and prebiotics for those characterized by systemic inflammation. Future high-quality RCTs are needed to standardize specific strain combinations.},
}

@article {pmid41778022,
year = {2026},
author = {Tan, Z and Young, E and Rajagopalan, A},
title = {Push Enteroscopic Jejunal and Ileoscopic Delivery of Fecomicrobiota Transplantation (FMT) for Treatment of Clostridioides difficile Enteritis in a Patient With a Total Colectomy and Ileal Pouch-Anal Anastomosis (IPAA): A Case Report.},
journal = {JGH open : an open access journal of gastroenterology and hepatology},
volume = {10},
number = {3},
pages = {e70381},
pmid = {41778022},
issn = {2397-9070},
abstract = {Clostridioides difficile infection (CDI) is recognized as the leading cause of antibiotic-associated diarrhea. There are several case reports of C. difficile enteritis in patients who have undergone colectomy and end ileostomy or ileal pouch-anal anastomosis. This case report describes a unique case of recurrent C. difficile enteritis following proctocolectomy and ileoanal pouch, treated successfully with faecal microbiota transplantation (FMT) via anterograde and retrograde delivery into the small bowel.},
}

@article {pmid41777702,
year = {2026},
author = {Zhang, YW and Li, RY and Wu, Y and Wang, P and Zhou, QR and Su, JC},
title = {Gut microbiota and bone aging: Focusing on the gut-X axis modes.},
journal = {Journal of orthopaedic translation},
volume = {57},
number = {},
pages = {101064},
pmid = {41777702},
issn = {2214-031X},
abstract = {UNLABELLED: As studies have continuously advanced, cross-linking interplay between various organs in aging individuals have continuously emerged as research hotspots. The role of gut microbiota in bone aging-related diseases, including osteoporosis, osteoarthritis, and intervertebral disc degeneration, has been extensively probed. This review first summarized the inseparable association between gut microbiota and osteoporosis, osteoarthritis, and intervertebral disc degeneration, which then explored potential mechanisms of gut-X axis through neuromodulation (microbiota-gut-brain-bone axis), immunomodulation (Th17 and Treg balance), endocrine regulation (gut-derived hormones and 5-HT), metabolite-mediated regulation (SCFAs), bacterial extracellular vesicles, and changes in microbial niche and gut microbiome-associated biomarkers. Moreover, potential intervention strategies including diet, probiotics, fecal microbiota transplantation, and physical activity were summarized to enhance clinical translation applicability. This review creatively exhibited integrated concept of "gut-X axis" to explore common, patterned mechanisms underlying "gut-bone axis", "gut-joint axis", and "gut-disc axis". Furthermore, it delves into potential mechanisms by which this shared pattern regulates bone aging-related diseases and prospectively outlines therapeutic strategies for bone aging based on this axis.

This review presents crucial role and regulatory significance of gut-X axis modes in common bone-aging related diseases. By anchoring the gut-X axis as intervention targets, the thinking of gut microbiota and its related metabolites in basic studies and clinical prevention and treatment of bone aging-related diseases might be expanded, and its clinical application transformation and development could be innovated.},
}

@article {pmid41776845,
year = {2026},
author = {Cai, Y and Sun, J and Chen, S and Wang, D and Jing, Y and Jin, X and Li, Z and Li, C and Ban, X},
title = {Agarotriose Alleviates Colitis by Promoting Akkermansia muciniphila-Derived Spermidine Production to Suppress PI3K/AKT/NF-κB Signaling.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c16297},
pmid = {41776845},
issn = {1520-5118},
abstract = {Agarotriose (A3), a marine-derived oligosaccharide from agar, has shown anti-inflammatory potential, yet the involvement of gut microbiota remains incompletely understood. Using a dextran sulfate sodium-induced colitis mouse model combined with antibiotic depletion and fecal microbiota transplantation, we found that the protective effects of A3 were largely dependent on the gut microbiota. Integrated multiomics analyses indicated that A3 preferentially enriched Akkermansia muciniphila and was associated with increased intraluminal spermidine levels. Spermidine abundance correlated with A. muciniphila enrichment and improvement of colitis-related phenotypes. In vitro, A3 promoted the growth of A. muciniphila and enhanced spermidine production. Transcriptomic and cellular analyses further suggested that spermidine attenuated inflammatory responses, at least in part, through modulation of the PI3K/AKT/NF-κB signaling pathway. Collectively, these results support a potential "A3-A. muciniphila-spermidine-host signaling" axis and suggest that A3 may serve as a promising marine-derived prebiotic for intestinal health.},
}

@article {pmid41677988,
year = {2026},
author = {Feng, R and Yang, Z and Zhou, Y and Zhao, H},
title = {The Gut-Brain-Immune Axis in Glioma: Emerging Mechanisms and Therapeutic Opportunities.},
journal = {Cellular and molecular neurobiology},
volume = {46},
number = {1},
pages = {},
pmid = {41677988},
issn = {1573-6830},
support = {ZR2022QH372//Science and Technology Development Plan of Shandong Province/ ; },
abstract = {Gliomas, particularly glioblastomas, represent some of the most treatment-resistant cancers due to their profoundly immunosuppressive tumor microenvironment (TME) and the restrictive nature of the blood–brain barrier. While recent advances in immunotherapy have transformed the treatment landscape for peripheral tumors, success in gliomas remains limited. Emerging evidence suggests that the gut microbiota—through the gut-brain-immune axis—may play a significant role in shaping systemic and central immune responses. Gut-derived microbial metabolites, immune cell modulation, and neuro-immune signaling pathways have been shown to influence microglial activation, T cell infiltration, and even response to immune checkpoint inhibitors (ICIs) such as PD-1 and emerging targets like TIM-3, LAG-3, and TIGIT. Furthermore, the efficacy and persistence of CAR-T and CAR-NK therapies may also be impacted by microbial composition, offering a novel avenue for therapeutic optimization. This review explores the biological underpinnings of the gut-brain-immune axis in glioma, summarizes key preclinical and clinical findings, and highlights the potential of gut microbiota modulation—via probiotics, engineered microbes, or fecal microbiota transplantation (FMT)—as an adjunct to immunotherapy. We also discuss technical and translational challenges, including interindividual variability and mechanistic uncertainty. Understanding the dynamic crosstalk between the gut and the glioma immune microenvironment may unlock new therapeutic strategies and improve outcomes in this highly lethal disease.},
}

@article {pmid41776699,
year = {2026},
author = {Song, Y and Wen, S and Guan, LL},
title = {Unraveling the dynamic changes in the intestinal microbiome: impacts on pre-weaning calf health and productivity.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {41776699},
issn = {1674-9782},
abstract = {The early life gut microbial colonization in pre-weaning calves plays a pivotal role in shaping their health, growth, and productivity. This review delves into the dynamic changes of intestinal microbiota during early life, emphasizing key factors such as colostrum management, feeding strategies, roughage supplementation, and microbial interventions including probiotics, prebiotics, and fecal microbiota transplantation (FMT), and non-nutritional stressors that can shape the early life microbial colonization. We highlight the microbiota's critical functions in nutrient metabolism, immune development, gut barrier integrity, and gut-brain axis regulation. Additionally, the consequences of microbial dysbiosis on calf health and its long-term effects on production performance in beef and dairy cattle are discussed. While current research has provided valuable insights, understanding causal mechanisms remains a challenge. This review aims to guide practical strategies for targeted microbial management, offering a pathway to optimize early-life interventions for improved calf health and productivity.},
}

@article {pmid41776310,
year = {2026},
author = {Kim, M and Wang, J and Pilley, SE and Lu, RJ and Xu, A and Kim, Y and Liu, M and Fu, X and Booth, SL and Mullen, PJ and Benayoun, BA},
title = {Estropausal gut microbiota transplant improves measures of ovarian function in adult mice.},
journal = {Nature aging},
volume = {},
number = {},
pages = {},
pmid = {41776310},
issn = {2662-8465},
support = {#00034120//Pew Charitable Trusts/ ; T32 AG052374/AG/NIA NIH HHS/United States ; No. 58-1950-7-707//United States Department of Agriculture | Agricultural Research Service (USDA Agricultural Research Service)/ ; },
abstract = {The decline in ovarian function with age affects fertility and is associated with increased risk of age-related diseases, including osteoporosis and dementia. Notably, earlier menopause is linked to shorter lifespan, yet the molecular mechanisms underlying ovarian aging remain poorly understood. Recent evidence suggests the gut microbiota may influence ovarian health. Here we show that ovarian aging is associated with distinct gut microbial profiles in female mice and that the gut microbiome can directly influence ovarian health. Using fecal microbiota transplantation from young or estropausal female mice, we demonstrate that heterochronic microbiota transfer remodels the ovarian transcriptome, reduces inflammation-related gene expression and induces transcriptional features consistent with ovarian rejuvenation. These molecular changes are accompanied by enhanced ovarian health and increased fertility. Integrating metagenomics-based causal mediation analyses with serum untargeted metabolomics, we identify candidate microbial species and metabolites that may contribute to the observed effects. Our findings reveal a direct link between the gut microbiota and ovarian health.},
}

@article {pmid41776098,
year = {2026},
author = {Xiang, X and Zhu, J and Jiang, J and Ding, P and Zhu, Y and Cheng, K and Ming, Y},
title = {Unique gut microbiota and metabolomic profiling as biomarker of post-transplant recovery in acute-on-chronic liver failure after liver transplantation.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13774-5},
pmid = {41776098},
issn = {1432-0614},
support = {81771722 and 82570782//National Natural Science Foundation of China/ ; },
abstract = {Acute-on-chronic liver failure (ACLF) is a severe condition arising from chronic liver disease, characterized by acute decompensation, organ failure, and high short-term mortality. Poor outcomes have also been observed in patients with ACLF after liver transplantation (LT). Emerging evidence, including a study from our center, suggests that gut microbiota plays an important role in ACLF. Patients who underwent LT at our center between October 2022 and June 2024 were included. Fecal samples were collected within 1 month post-LT for 16S rRNA and untargeted metabolomic sequencing. In this study, 144 samples from 69 patients with ACLF, cirrhosis, or hepatocellular carcinoma (HCC) were analyzed. Distinct microbiota and metabolic profiles were observed among the groups. ACLF patients exhibited significantly altered beta diversity, with notable depletion of g__Anaerostipes. Metabolomic analysis revealed substantial differences, including enrichment of tangeritin and depletion of candesartan in the ACLF group. Network analysis identified g__Anaerostipes as a key node linking differential taxa and metabolites. A random forest model based on these features effectively distinguished patient groups, with the highest classification accuracy observed in HCC. Multi-omic signatures were also associated with early allograft dysfunction (EAD), particularly g__Lachnoclostridium. Several microbial and metabolic features, including g__Lachnoclostridium, showed significant correlations with clinical indicators. The gut microbiome after LT is closely associated with ACLF. This study offers valuable insights for further investigation into the pathogenesis and post-LT prognosis. KEY POINTS: • ACLF patients have a unique gut microbiota and metabolic profile after LT • g__Anaerostipes is the prominent biomarker of ACLF's multi-omics signature • g__Lachnoclostridium is a promising indicator of recovery after LT.},
}

@article {pmid41774771,
year = {2026},
author = {Han, X and Yu, H and Gao, Q and Wang, X and Zhang, L and Zhao, Q and Yu, L and Zhang, Y and Sui, M and Li, Y},
title = {Gut Microbiota Dysbiosis Promotes CKD-associated Atrial Fibrillation Through Activation of the NLRP3 Inflammasome.},
journal = {Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology},
volume = {},
number = {},
pages = {},
doi = {10.1093/europace/euag037},
pmid = {41774771},
issn = {1532-2092},
abstract = {BACKGROUND: Chronic kidney disease (CKD) significantly increases the risk of atrial fibrillation (AF). Although alterations in the gut microbiota have been linked to CKD progression, its exact involvement in CKD-associated AF remians unclear. We amis to investigate the role of gut microbiota in the development of CKD-associated AF, and to uncover potential mechanisms that could serve as effective targets for prevention and treatment.

METHODS AND RESULTS: A rat model of CKD was induced by an adenine-enriched diet. 16S rRNA sequencing and fecal microbiota transplantation (FMT) were utilized to study the involvement of gut microbiota. AST-120, gut barrier protectants and mono-colonization experiments were performed to investigate potential mechanism. CKD rats exhibited gut microbiota dysbiosis and a significantly increased susceptibility to AF. FMT from CKD rats transferred this heightened AF susceptibility to healthy recipient rats, linked to the activation of the NLRP3 inflammasome. Mechanistically, gut dysbiosis in CKD patients leads to elevated IS levels, causing gut barrier dysfunction and increased circulating lipopolysaccharide (LPS). Elevated LPS activates atrial TLR4 receptors, triggering NLRP3 inflammasome activation, which contributes to AF pathogenesis. Treatment with the IS scavenger AST-120 or gut barrier protectants successfully prevented CKD-associated AF. Furthermore, supplementation with Lactobacillus gasseri reduced circulating IS levels and mitigated AF susceptibility in CKD rats.

CONCLUSION: This study demonstrates that gut dysbiosis-driven elevation of IS and subsequent activation of the atrial NLRP3 inflammasome are key mechanisms in CKD-associated AF. Modulating the gut microbiota could provide a new therapeutic strategy for CKD-associated AF.},
}

@article {pmid41772743,
year = {2026},
author = {He, J and Wang, MN and Chen, HJ and Zuo, GY and Li, JL and Yin, WF and Pan, XG and Cheng, YC and Xia, CY and Xu, JK and Zhang, WK},
title = {Muribaculum intestinale alleviates depressive-like behaviors by inhibiting Th17 cell differentiation and M1 microglia polarization.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02354-4},
pmid = {41772743},
issn = {2049-2618},
support = {ZRZC2025-KCC03//National High Level & Elite Medical Professionals Project of China-Japan Friendship Hospital/ ; 2025-NHLHCRF-JBGS-A-WZ-10; ZRJY2024-BJ01//National High Level & Elite Medical Professionals Project of China-Japan Friendship Hospital/ ; 82474100//National Natural Science Foundation of China/ ; 82474100, 82273815, 82273809, 82073731//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Gut microbiota dysbiosis has been implicated in the pathogenesis of depression. Our previous studies identified loganin as a potential antidepressant agent; however, its oral bioavailability is low. Whether loganin alleviates depression via modulation of the gut microbiota remains unclear.

METHODS: Chronic unpredictable stress mice model was used to evaluate the antidepressant-like effects of loganin. To determine the role of gut microbiota, mice were treated with an antibiotic cocktail (ABX) to deplete microbiota. Fecal microbiota transplantation (FMT) from loganin-treated donors and Muribaculum intestinale (M. intestinale) were performed to assess microbial contributions.

RESULTS: Loganin exerted antidepressant-like effects by modulating gut microbiota, as evidenced by reduced efficacy in ABX-treated mice and behavioral improvements in recipients of FMT from loganin-treated donors. Loganin modulated gut microbiota composition particularly increasing the abundance of Muribaculum, and increased short-chain fatty acids (SCFAs). M. intestinale alleviated depressive-like behaviors, prompted the butyrylation of RORγt, inhibited Th17 cells differentiation, and suppressed M1 microglia polarization. Importantly, overexpression of RORγt attenuated the behavioral benefits of M. intestinale.

CONCLUSION: Loganin exerts antidepressant-like effects by enriching Muribaculum and SCFAs, thereby inhibiting Th17 cell differentiation and M1 microglia polarization. M. intestinale may represent a promising microbial-based therapeutic strategy for depression.},
}

@article {pmid41771438,
year = {2026},
author = {Lynch, SV and Nagler, CR and Rachid, R},
title = {Microbial Therapeutics for the Prevention and Treatment of Food Allergy.},
journal = {The journal of allergy and clinical immunology. In practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jaip.2026.02.024},
pmid = {41771438},
issn = {2213-2201},
abstract = {Food allergy affects approximately 8% of children and 11% of adults in the United States. Available treatment including oral immunotherapy and anti-IgE are not known to lead to remission. There is now increasing evidence implicating the gut microbiome as a key regulator of allergic inflammation. Distinct microbial and metabolomic alterations characterize food-allergic individuals, and gnotobiotic mouse models show that fecal microbiota from food-allergic donors transfers allergic sensitization, whereas microbiota from healthy donors protects from anaphylaxis through induction of tolerogenic Foxp3[+]RORγt[+] regulatory T cells. Goblet cell-derived resistin-like molecule beta (RELM β) induces food allergy through modulation of the gut microbiome and depletion of indole-producing species. These findings have inspired the development of five microbial therapeutics approaches: probiotics, rationally defined bacterial consortia, fecal microbiota transplantation, metabolite-based approaches, and biologics targeting dysbiosis-associated pathways. Early-phase clinical studies support feasibility, yet long-term safety, durability, and reproducibility remain uncertain. Major challenges include inter-individual variability, ecological complexity, and regulatory standardization. Microbiome-directed therapeutics hold promise to transform food allergy management from temporary desensitization toward remission and durable immune tolerance. The application of systems biology approaches integrating metabolomics, transcriptomics, and immune phenotyping will be essential to unravel the complex host-microbial interactions that underlie the efficacy of these approaches.},
}

@article {pmid41769611,
year = {2026},
author = {Li, X and Xu, S and Li, Y and Wang, R and Qin, C and Wang, X},
title = {Research Progress on the Mechanisms of Gut Microbiota Dysbiosis Associated With Idiopathic Pulmonary Fibrosis: A Review.},
journal = {Cureus},
volume = {18},
number = {1},
pages = {e102429},
pmid = {41769611},
issn = {2168-8184},
abstract = {Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive fibrotic interstitial lung disease with an incompletely understood pathogenesis. In recent years, growing evidence has highlighted the critical role of gut microbiota dysbiosis in the onset and progression of IPF. This review comprehensively summarizes the characteristics of gut microbiota alterations associated with IPF, explores the underlying mechanisms driving these changes, and examines their impact on disease development. Particular emphasis is placed on the emerging concept of the "gut-lung axis," which elucidates the bidirectional communication between the intestinal microbiome and pulmonary health. The review further discusses microbial metabolites and immune modulation as key mediators linking gut dysbiosis to pulmonary fibrosis. Additionally, current advances in microbiota-targeted therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation, are analyzed for their potential in IPF management. By systematically integrating recent findings, this article aims to deepen the understanding of IPF pathophysiology and provide a theoretical foundation for novel treatment targets centered on gut microbiota regulation.},
}

@article {pmid41769404,
year = {2026},
author = {Zhao, Y and Chen, D and Qi, K},
title = {The role of gut microbiota in Hirschsprung's disease: from pathogenic mechanisms to microbiota-targeted therapies.},
journal = {PeerJ},
volume = {14},
number = {},
pages = {e20854},
pmid = {41769404},
issn = {2167-8359},
abstract = {Hirschsprung's disease (HSCR) is a common congenital disorder characterized by abnormal enteric nervous system development. Recent studies have demonstrated that gut microbiota and their metabolites play a significant role in the pathogenesis of HSCR. This review systematically examines the interplay between gut dysbiosis and pathophysiological alterations in HSCR, including disruptions in microbial composition, aberrant metabolite profiles, impaired intestinal barrier function, and dysregulated neuro-immune modulation. Research indicates that HSCR patients exhibit a characteristic gut microbial imbalance, which may influence the development and function of the enteric nervous system by altering the intestinal microenvironment, including metabolic profiles and immune status. Furthermore, this review explores the potential therapeutic value of microbiota-targeted interventions, such as probiotics and fecal microbiota transplantation (FMT), in HSCR treatment, providing a theoretical foundation for novel therapeutic strategies. These findings not only enhance the understanding of HSCR pathogenesis but also offer new perspectives for clinical prevention and treatment.},
}

@article {pmid41762317,
year = {2026},
author = {Altan, ZB and Ihlamur, M},
title = {The relationship between gut microbiota and neurodegenerative diseases: a genetic and epigenetic perspective.},
journal = {Metabolic brain disease},
volume = {41},
number = {1},
pages = {},
pmid = {41762317},
issn = {1573-7365},
abstract = {UNLABELLED: Gut microbiota (GM) is a complex and dynamic structure that can have a wide range of effects on human health. Studies in recent years have shown that microbiota is not only related to the gastrointestinal tract (GIT) but also to the immune and endocrine systems. It causes various effects on host physiology, especially through genetic and epigenetic mechanisms. It shows that microbiota-derived metabolites can play a role in the development of neurological diseases by changing gene expression. In this review article, the relationship between GM and neurodegenerative diseases (NDs) is explained in terms of genetics and epigenetics. In terms of the gut–brain axis (GBA); the role of systems such as short-chain fatty acids (SCFA), vagus nerve, inflammatory responses and intestinal permeability in the pathogenesis of NDs such as Alzheimer's (AD), Parkinson's (PD), Huntington's (HD) and Multiple Sclerosis (MS) is discussed. In addition, experimental studies have drawn attention to the effects of changes in microbiota on neuroinflammation and cognitive impairment. In terms of treatment strategies; Probiotics, prebiotics, synbiotics, fecal microbiota transplantation (FMT) and nutritional interventions targeting microbiota seem to be promising strategies. However, the fact that microbiota structure varies between individuals indicates that studies in this area should be conducted in a more personalized manner. This article aims to provide a basis for future research by approaching the relationship between microbiota and NDs in a holistic manner.

GRAPHICAL ABSTRACT: [Image: see text]},
}

@article {pmid41764851,
year = {2026},
author = {Guo, Q and He, Y and Cao, T and Lin, C and Deng, M and Wu, R and Cai, H},
title = {Tryptophan-kynurenine metabolism: A link between the gut microbiota dysbiosis and cognitive impairment.},
journal = {Microbiological research},
volume = {307},
number = {},
pages = {128481},
doi = {10.1016/j.micres.2026.128481},
pmid = {41764851},
issn = {1618-0623},
abstract = {Cognitive impairment is a central feature of neuropsychiatric and neurodegenerative disorders, significantly diminishing patients' quality of life. Emerging evidence underscores the role of gut microbiota dysbiosis in the progression of cognitive decline. The gut microbiota influences brain function through various mechanisms, with the kynurenine pathway standing out as a key biochemical route linking peripheral metabolism to central nervous system function, thereby impacting cognitive performance. Dysregulation of the kynurenine pathway has been closely associated with neurotransmitter imbalances, exacerbated neuroinflammation, and metabolic dysfunction, all of which contribute to the onset and progression of cognitive impairment. Recent studies suggest that interventions targeting the gut microbiota, such as probiotics, antibiotics, and fecal microbiota transplantation, may improve cognitive function by modulating the kynurenine pathway. This review examines the complex relationship between gut microbiota, the kynurenine pathway, and cognition, highlighting the potential of targeting kynurenine pathway-related enzymes and microbiota modulation as therapeutic strategies. Despite promising findings, the precise mechanisms and therapeutic potential of these interventions remain under investigation, offering new avenues for the treatment of cognitive disorders.},
}

@article {pmid41764528,
year = {2026},
author = {Zhang, W and Su, Q and Shi, H and Sun, Y and Li, X and Li, M and Wang, H and Yu, J and Wong, N and Chan, FKL and Zhang, J and Ng, SC},
title = {Discovery and characterization of Christensenella hongkongensis as a novel bacterium in the adenoma-carcinoma progression.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07886-9},
pmid = {41764528},
issn = {1479-5876},
}

@article {pmid41763794,
year = {2026},
author = {Wei, K and Peng, L and Wei, Q and Wei, Y and Wang, L and Zhu, Y and Wei, Y and Wei, X},
title = {Amelioration of colitis by donor microbiota modulated with tea active ingredients: A fecal microbiota transplantation study.},
journal = {Food research international (Ottawa, Ont.)},
volume = {229},
number = {},
pages = {118473},
doi = {10.1016/j.foodres.2026.118473},
pmid = {41763794},
issn = {1873-7145},
abstract = {Fecal microbiota transplantation (FMT) using donor microbiota modulated by tea represents an emerging approach to ameliorate ulcerative colitis (UC). This study aims to demonstrate the amelioration of dextran sulfate sodium (DSS)-induced colitis by donor microbiota modulated with tea-derived bioactive ingredients-tea polyphenols (TPP), tea polysaccharides (TPS), or theabrownin (TB). Following transplantation of fecal microbiota modulated by TPP, TPS, or TB from donors into colitis mice, significant reductions in Disease Activity Index (DAI) were observed, alongside attenuated intestinal histopathological damage. Additionally, gut barrier integrity was enhanced, as indicated by upregulated expression of occludin and Muc2. Fecal microbiota modulated by TPP and TPS showed superior efficacy in alleviating colitis compared with TB-modulated microbiota. The mechanism involved that marked enrichment of beneficial genera, including Akkermansia (TPP-enriched) and Allobaculum/Lactobacillus (TPS-enriched), which promoted the biosynthesis of short-chain fatty acids (SCFAs) and secondary bile acids, while reducing primary bile acids levels. These metabolic changes enhanced intestinal barrier function and suppressed suppressing pro-inflammatory cytokines through the modulation of TLR4/NF-κB p65 and Nrf2/ARE signaling pathways. This study not only elucidates the mechanism of tea bioactive ingredients-modulated donor microbiota alleviates colitis through regulation of the gut-microbiota-metabolite axis, but also provides a foundation for FMT-based strategies in colitis intervention.},
}

@article {pmid41763137,
year = {2026},
author = {Zhou, S and Su, F and Gao, Q and Wang, M and Duan, J and Li, J},
title = {Cordyceps cicadae polysaccharides ameliorate ulcerative colitis by modulating the gut microbiota and regulating the bile acid/FXR/NF-κB signaling pathway.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {153},
number = {},
pages = {158007},
doi = {10.1016/j.phymed.2026.158007},
pmid = {41763137},
issn = {1618-095X},
abstract = {BACKGROUND: Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease, closely linked to dysbiosis of the intestinal microbiota and abnormal bile acid homeostasis. Polysaccharides derived from Paecilomyces cicadae (CCP) exhibit immunomodulatory and anti-inflammatory effects. However, their therapeutic potential and underlying mechanisms in UC remain poorly elucidated.

PURPOSE: This research seeks to evaluate the therapeutic efficacy of CCP in the treatment of UC and utilizing the "microbiota-bile acid metabolism-immunity" axis, elucidates the mechanisms by which CCP enhances intestinal barrier integrity and ameliorates inflammation via modulation of the gut microbiota-mediated farnesoid X receptor (FXR)/NF-κB signaling pathway.

METHODS: The physicochemical properties of CCP were characterized by FTIR spectroscopy, HPLC, and SEM analyses. A dextran sulfate sodium (DSS)-induced colitis mouse model was used to evaluate the ameliorative effects of CCP. Gut microbial alterations were profiled by 16S rDNA sequencing, while targeted metabolomics enabled comprehensive quantification of bile acid profiles in serum and fecal samples. Fecal microbiota transplantation (FMT) was conducted to validate the microbiota-mediated actions of CCP. Downstream molecular mechanisms were examined using Western blotting and immunofluorescence assays to assess modulation along the microbiota-bile acid axis.

RESULTS: CCP is primarily composed of glucose, mannose, and galactose, exhibiting a characteristic polysaccharide structure with a uniform molecular weight distribution. Treatment with CCP significantly ameliorated DSS-induced colitis in mice, as evidenced by reduced weight loss, preserved colon length, and decreased histopathological damage. 16S rDNA analysis demonstrated CCP-driven restoration of intestinal microbial diversity and a marked increase in Clostridium Kas107-2 (cluster XIVa). Metabolomics revealed normalization of bile acid metabolism, with elevated synthesis of secondary bile acids (deoxycholic acid, lithocholic acid, 12-keto LCA) and reduced levels of primary bile acids (α/β-MCA). Mechanistically, CCP activated FXR signaling, suppressed IκBα phosphorylation, downregulated NF-κB signaling, and reduced production of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6). Enhanced expression of tight junction proteins (ZO-1, Occludin, Claudin-1) indicated improved epithelial barrier function. Notably, FMT from CCP-treated donors replicated these protective effects, confirming colitis attenuation, bile acid restoration, and inhibition of FXR/NF-κB signaling.

CONCLUSIONS: CCP ameliorate experimental UC by promoting the proliferation of Clostridium cluster XIVa, modulating bile acid metabolism to facilitate secondary bile acid biosynthesis, activating FXR pathways, and suppressing NF-κB-driven inflammatory responses, thereby reinforcing intestinal epithelial barrier integrity.},
}

@article {pmid41763136,
year = {2026},
author = {Guo, Y and Xu, X and Han, A and Song, F and Zhang, Y and Jiang, X and Yu, W},
title = {Isorhamnetin alleviates diet induced MASLD in mice by modulating gut microbiota and bile acid metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {153},
number = {},
pages = {157987},
doi = {10.1016/j.phymed.2026.157987},
pmid = {41763136},
issn = {1618-095X},
abstract = {BACKGROUND: With the increasing prevalence of sedentary lifestyles and high-fat, high-sugar diets, the incidence of metabolic dysfunction-associated steatotic liver disease (MASLD) has continued to rise. Although the natural flavonoid compound isorhamnetin (ISO) has been shown to improve dyslipidemia in MASLD mice, its mechanism of action in regulating lipid metabolism via the gut microbiota and its metabolites remains unclear.

OBJECTIVE: This study investigates whether ISO can ameliorate high-fat diet-induced MASLD in mice in a dose-dependent manner and explores the mediating role of the gut microbiota in this process.

METHODS: Physiological monitoring, biochemical markers assessment, tissue section analysis, 16S rRNA sequencing, bile acid (BA) targeted metabolomics, and molecular analysis were performed on mouse tissues. In addition, fecal microbiota transplantation (FMT) from mice fed a high-dose of ISO further validated the regulatory role of the gut microbiota in MASLD mice. Molecular dynamics simulations and in vitro assays were performed to evaluate the interaction between ISO and FXR.

RESULTS: ISO dose-dependently reduced body weight and hepatic lipid content, inhibited lipid synthesis and promoted lipid oxidation. ISO reshaped the gut microbiota, increasing the relative abundance of Lachnospiraceae, Oscillospiraceae, and Ruminococcaceae. These changes altered the BA pool composition by increasing the proportion of primary and conjugated BAs, activated the hepatic-ileal Farnesoid X Receptor (FXR) signaling axis, accelerated enterohepatic BA circulation, and reduced dietary fat absorption. Concurrently, ISO enhanced intestinal barrier integrity and alleviated hepatic inflammation. Fecal microbiota transplantation from ISO-treated mice partially reproduced these metabolic benefits. Molecular dynamics simulations and in vitro experiments further verified that ISO interacts with FXR and consequently enhances FXR signaling.

CONCLUSION: ISO alleviates MASLD by synergistically regulating gut microbiota and FXR signaling, highlighting its potential as a mild, multi-target natural therapeutic candidate for MASLD therapy.},
}

@article {pmid41762381,
year = {2026},
author = {Sasidharan Pillai, S and Ashraf, AP},
title = {Gut Microbiota and Metabolic Health: From Dysbiosis to Therapeutics.},
journal = {Diabetes therapy : research, treatment and education of diabetes and related disorders},
volume = {},
number = {},
pages = {},
pmid = {41762381},
issn = {1869-6953},
abstract = {The gut microbiota (GM) is a pivotal regulator of host metabolism and a contributor to the pathophysiology of obesity, type 2 diabetes (T2D), and metabolic syndrome (MS). Disruptions in GM composition and function are collectively termed dysbiosis. This review synthesizes current evidence on GM dysbiosis, moving beyond simple taxonomic associations, to examine functional drivers of metabolic dysfunction. Dysbiosis impairs metabolic health through several interconnected pathways: enhanced dietary energy extraction, compromised intestinal barrier integrity leading to metabolic endotoxemia, chronic low-grade "meta-inflammation," and the disruption of circadian rhythms and neuro-immune signaling. Beyond bacteria, dysbiosis of the gut virome and mycobiota may further modulate metabolic risk. Animal and emerging human studies indicate that reduced virome diversity and altered phage-bacteria interactions can amplify dysbiosis, promote inflammatory signaling, and impair metabolic homeostasis. Recognition of GM dysbiosis as a contributor to metabolic disease has prompted development of therapeutic strategies aimed at restoring microbial balance and function. These interventions span a spectrum from established clinical approaches with indirect microbiota effects to experimental therapies designed to directly manipulate microbial composition or activity. We evaluate the clinical readiness of GM-targeted therapies, including dietary patterns, prebiotics, probiotics, and fecal microbiota transplantation. While established metabolic treatments such as glucagon-like peptide-1 (GLP-1) receptor agonists and bariatric surgery significantly reshape the GM, direct microbial manipulations often yield variable results in human trials. We conclude that the future of metabolic management lies in personalized microbiomics, utilizing artificial intelligence and precision-based interventions to restore specific functional microbial deficits tailored to the individual host profile.},
}

@article {pmid41761979,
year = {2026},
author = {Guo, Z and Gao, Z and Zhao, Y and Ni, X and Zhang, W and Li, L and Ren, S and Li, Q and Guo, D and Yue, L and Liu, Y and Lin, L and Fan, S and Hai, X},
title = {Administering Bifidobacterium pseudolongum With Arsenic Trioxide Attenuates Acute Promyelocytic Leukemia in Mice by Restoring Immune Microenvironment and Intestinal Homeostasis.},
journal = {Frontiers in bioscience (Landmark edition)},
volume = {31},
number = {2},
pages = {48584},
doi = {10.31083/FBL48584},
pmid = {41761979},
issn = {2768-6698},
support = {82274028//National Natural Science Foundation of China/ ; 2022ZX02C09//Heilongjiang Key R&D Program/ ; //Fundamental Research Funds for the Provincial Universities in Heilongjiang Province (2025)/ ; JJ2025PL0189//Natural Science Foundation of Heilongjiang Province/ ; 2024M10//Innovation Fund of the First Affiliated Hospital of Harbin Medical University/ ; 2024M25//Innovation Fund of the First Affiliated Hospital of Harbin Medical University/ ; 230000253533210000086//2025 Central Government Fiscal Subsidy Fund for Medical Care Compliance and Capacity Enhancement (Traditional Chinese Medicine Undertakings and Inheritance and Development Component)/ ; },
abstract = {OBJECTIVE: Arsenic trioxide (ATO) is a cornerstone of acute promyelocytic leukemia (APL) therapy but induces severe gut microbiota dysbiosis, limiting its efficacy and safety. This study investigated whether adjunctive Bifidobacterium pseudolongum (BP) could mitigate these adverse effects and enhance therapeutic outcomes.

METHODS: 16S rRNA gene sequencing data of gut microbiota were obtained from a cohort of 22 APL patients treated with ATO-based regimens (20 of 22 data were obtained and analysis further), accessible under BioProject ID PRJNA935705. To evaluate the within-sample microbial community richness and evenness, alpha and beta diversity indices were calculated. Using a murine APL model, we compared ATO monotherapy with ATO+BP co-treatment. Analyses included fecal metagenomic sequencing, single-cell RNA sequencing (sc-RNA-seq), flow cytometric immune profiling, and assessment of intestinal tight junction proteins (claudin-1, occludin, and ZO-1) via immunofluorescence.

RESULTS: ATO treatment significantly reduced gut microbial diversity and depleted beneficial taxa. Sc-RNA-seq data showed that ATO could orchestrate the APL immune microenvironment mainly through functional activation of CD8+ T cells and monocytes. BP supplementation restored microbial homeostasis and synergistically enhanced ATO's antileukemic effect, reducing the leukemic burden in peripheral blood by 72% and in bone marrow by 64% compared to ATO alone. Mechanistically, BP preserved intestinal barrier integrity by upregulating tight junction protein expression and modulated anti-tumor immunity, notably increasing bone marrow CD8+ T cells by 2.21-fold.

CONCLUSIONS: BP is an effective adjunct to ATO therapy, counteracting gut dysbiosis, intestinal damage, and the immune microenvironment while synergistically improving antileukemic efficacy. Targeting the gut-leukemia axis with BP represents a promising strategy for improving the precision and safety of APL treatment.},
}

@article {pmid41761700,
year = {2026},
author = {Pepke, ML and Hansen, SB and Limborg, MT},
title = {The ageing holobiont: crosstalk between telomere dynamics, oxidative stress and the gut microbiome.},
journal = {Biological reviews of the Cambridge Philosophical Society},
volume = {},
number = {},
pages = {},
doi = {10.1002/brv.70152},
pmid = {41761700},
issn = {1469-185X},
support = {DNRF143//Danmarks Grundforskningsfond/ ; CF21-0356//Carlsbergfondet/ ; },
abstract = {The gut tissue is at the frontline of early onset of ageing. It exhibits high cell turnover rates and rapid telomere shortening, which can have systemic effects on the developing or senescing organism. We conducted a literature review of studies on the crosstalk between telomere length dynamics, telomerase activity, oxidative stress, and gut microbiota composition and activity in animals. Studies mainly on humans and animal models include correlations between telomere dynamics and gut microbiome components, particularly under pathogenic conditions, but also manipulations of either the gut microbiome through faecal microbiota transplantations or of telomere dynamics using telomerase knockout models. This synthesis reveals that components of the gut microbiome including microbial metabolites and pathogenic bacteria can affect telomere dynamics through oxidative-stress-inducing processes, and that telomere maintenance is critical in maintaining gut barrier and tissue integrity, which link inflammation and gut dysbiosis. Some of the interactions between the gut microbiome and host telomere dynamics are bidirectional and important in maintaining intestinal homeostasis. However, many of the causal molecular or cellular mechanisms - and how they translate into organismal senescence - remain to be identified. Furthermore, we highlight how recent advances in whole genome sequencing capacities and bioinformatic tools represent an often-unexploited resource for measuring telomere lengths and may be particularly valuable tools within the hologenomic framework outlined here. Investigating the role of telomere dynamics in mediating gut microbiota-host interactions in different species will improve our understanding of how crosstalk between these hallmarks of ageing shape holobiont physiology in general and the ageing phenotype in particular.},
}

@article {pmid41761646,
year = {2026},
author = {Chen, Y and Jie, W and Xu, Y and Chen, X and Zhu, S and Ma, Y and Hu, L and Chen, C and Liu, B and Xu, D and Cai, D and Liu, Z},
title = {Correlation study between gut microbiota and intestinal permeability in cerebral small vessel disease.},
journal = {Journal of Alzheimer's disease : JAD},
volume = {},
number = {},
pages = {13872877261418554},
doi = {10.1177/13872877261418554},
pmid = {41761646},
issn = {1875-8908},
abstract = {BackgroundDysbiosis of gut microbiota and increased intestinal permeability are associated with various diseases, and their relationship with cognitive dysfunction such as cerebral small vessel disease (CSVD) and Alzheimer's disease remains to be elucidated.ObjectiveThis study investigates the role of gut microbiota dysbiosis and its relationship with intestinal permeability in patients with cognitive impairment associated with CSVD (CSVD-CI).MethodsIntestinal permeability was detected in 21 patients with CSVD-CI and 20 healthy controls by testing urine lactulose/mannitol, and correlation analysis was performed between the test results and cognitive function assessment. 16S rRNA sequencing was used to analyze the different combination of gut microbiota. Feces of the patients or controls were gavaged into C57 mice, and gut barrier function, behavior, and metabolites were assessed.ResultsPatients with CSVD-CI have a higher incidence of hypertension, higher homocysteine levels, higher scores for white matter hyperintensities, and worse cognitive function. Their urinary mannitol recovery rate is higher, which is correlated with lower scores of cognitive function assessment. Alterations in the gut microbiota involve a reduction in Prevotella-9 alongside increases in Proteobacteria and Fusobacteria. Fecal microbiota transplantation (FMT) from patients with CSVD-CI increases intestinal permeability in mice, but does not change their cognitive function; meanwhile, fecal metabolomics analysis has identified alterations in bile acids and vitamins, which are associated with shifts in the gut microbiota.ConclusionsPatients with CSVD-CI have gut microbiota imbalance and increased intestinal permeability, which are associated with cognitive decline. FMT from these patients can cause intestinal leakage and the production of harmful metabolites in mice.},
}

@article {pmid41761296,
year = {2026},
author = {Ye, H and Yang, X and Zheng, M and Dong, W and Chen, X and Chen, J and Hu, M and Zhou, M and Zheng, P and Shen, L and Wu, Y and Zheng, K and Huang, XF and Yu, Y},
title = {Early risperidone exposure impairs cognitive function by perturbation of the gut microbiome and bile acids/tyrosine-PTP1B axis.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02358-0},
pmid = {41761296},
issn = {2049-2618},
abstract = {BACKGROUND: Second-generation antipsychotics (SGAs) are increasingly being utilized in children and adolescents. Risperidone, one of the most commonly prescribed SGAs in this population, has been found to adversely affect cognitive function; however, limited knowledge exists regarding the impact of risperidone on the gut microbiome-brain axis. We hypothesized that the cognitive impairment induced by risperidone is mediated by alterations in the gut microbiome and its metabolites.

RESULTS: In this study, we found that early-life risperidone exposure impaired cognition in mice, including deficits in behavior tests and hippocampal dendritic architecture. The risperidone-exposed mice also exhibited gut microbiota dysbiosis along with damage to the intestinal barrier. Fecal microbiota transplantation (FMT) from treated donors to recipients demonstrated the causal role of the gut microbiome in risperidone-induced cognitive deficits. Of note, risperidone increased the abundance of species Escherichia coli, Eggerthella lenta, Ruminococcus gnavus, Clostridium perfringens, Clostridium difficile, and Blautia hydrogenotrophica. These altered species are identified to encode 7α-HSDH, 3β/α-HSDH, TyrB, and porA, the key enzymes in secondary bile acid metabolism and tyrosine metabolism. Furthermore, a significant reduction in tauroursodeoxycholic acid (TUDCA, the metabolite of bile acid metabolism) and accumulation of p-cresol (the metabolite of tyrosine metabolism) were observed in the brains of mice exposed to risperidone. Mechanically, TUDCA prevented cognitive impairment and endoplasmic reticulum (ER) stress in the hippocampus induced by risperidone, while p-cresol induced neuronal ER stress. Knockout of protein tyrosine phosphatase 1B (PTP1B, ER stress-associated protein) in neurons ameliorated cognitive impairment and neurological damage induced by risperidone.

CONCLUSIONS: This study, for the first time, reveals that early risperidone exposure induces gut microbiome dysbiosis and disturbs the bile acids/tyrosine-PTP1B axis to impair cognitive function. These findings alert the risk of gut and neurological side effects of SGAs treatment and highlight that it is crucial to maintain gut homeostasis during the brain developmental phases of children and adolescents with SGAs exposure. Video Abstract.},
}

@article {pmid41761083,
year = {2026},
author = {Mo, C and Shao, R and Shi, Z and Lou, X and Xue, J and Ning, D and Liu, Y and Jiang, W and Wei, X and Xiao, J and Wang, F and Chen, G},
title = {Fecal microbiota transplantation reduces susceptibility to post-antibiotic CLP-induced sepsis by modulating the gut microbiota and its metabolites.},
journal = {BMC microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12866-026-04858-3},
pmid = {41761083},
issn = {1471-2180},
support = {202401AS070017//Yunnan Provincial Basic Research Program/ ; 202302AA310042//The Yunnan Provincial Major Program in Biomedicine/ ; 8256080235//National Natural Science Foundation of China/ ; },
abstract = {Sepsis remains a leading cause of mortality in intensive care units, and antibiotics continue to serve as the cornerstone of treatment. However, their potentially detrimental effects on gut health are often overlooked. Although antibiotic exposure may increase susceptibility to disease, its contribution to the progression of sepsis has not been fully elucidated. In this study, we investigated the effects of antibiotics on the gut microbiota, microbial metabolites, and intestinal barrier integrity in healthy mice, and further evaluated their impact on subsequent sepsis outcomes. Using a cecal ligation and puncture (CLP)-induced sepsis model, we demonstrated that antibiotic-induced gut dysbiosis exacerbated intestinal barrier damage and significantly increased mortality. In contrast, fecal microbiota transplantation (FMT) markedly improved survival and restored intestinal barrier function. Mechanistically, the protective effects of FMT were associated with modulation of the Hippo signaling pathway, which was accompanied by reduced intestinal permeability. Collectively, these findings highlight the critical role of antibiotic-induced gut dysbiosis in the pathogenesis of sepsis and support FMT as a potential therapeutic strategy to alleviate intestinal barrier damage and improve survival in sepsis.},
}

@article {pmid41760447,
year = {2026},
author = {Martin, M and Nguyen, VM and Puyade, M and Broca, F and Roblot, P},
title = {Faecal incontinence in systemic sclerosis: A narrative review.},
journal = {La Revue de medecine interne},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.revmed.2026.02.001},
pmid = {41760447},
issn = {1768-3122},
abstract = {Although associated with impaired health-related quality of life, faecal incontinence (FI) is underscreened in cases of systemic sclerosis (SSc). Its pathophysiology is complex and multifactorial, encompassing vasculopathy, fibrosis and probably (autoimmune) neuropathy. FI prevalence in SSc seems to be 5-6-fold higher than in the age- and sex-matched general population and is severe in nearly 15% of cases. FI is associated with diarrhoea, small intestinal bacterial overgrowth, constipation, urinary incontinence, anticentromere positivity and some features of vasculopathy. FI should be regularly screened in all SSc patients. Simple self-questionnaires are useful tools, completed by meticulous digital rectal exam for anal and puborectalis tone and by neurological examination. In case of unexplained chronic constipation or diarrhoea, endoscopic explorations are mandatory first to search for organic cause. Anorectal manometry is recommended in case of suspected anorectal dysfunction. Management should be multidisciplinary and, in general, follows the recommendations applied to the general population. It consists mainly in diet and lifestyle modifications and biofeedback therapy. Loperamide or laxative/transanal irrigation could be proposed as options in case of chronic diarrhoea or terminal constipation respectively. Nerve stimulation and faecal microbiota transplantation require further studies before conclusions can be drawn.},
}

@article {pmid41759744,
year = {2026},
author = {Waghmare, PV and Kolekar, KA and Bashir, B and Kumbhar, PS and Patil, KS and Gupta, G and Prasher, P and Jha, SK and Disouza, J and Gurav, SS and Dua, K and Singh, SK},
title = {Advocating gut-retina connection and microbiota mediated pathways in management of age-related macular degeneration: Preclinical to clinical perspective.},
journal = {Ageing research reviews},
volume = {117},
number = {},
pages = {103071},
doi = {10.1016/j.arr.2026.103071},
pmid = {41759744},
issn = {1872-9649},
abstract = {Age-related macular degeneration (ARMD) is the primary manifestation of permanent vision loss internationally. Different factors that contribute to ARMD involve ageing, genetic predisposition, oxidative stress, immunological imbalances, aberrations in the breakdown of lipids, and persistent inflammation. Gut microbiota has emerged as the significant cause of ARMD by disrupting systemic immune and inflammatory responses and metabolic homeostasis. Age-related changes in gut microbiota (dysbiosis) cause lowered microbial diversity, enhanced gut permeability, and pro-inflammatory species, leading to macular damage. The healthy gut microbiota containing Lactobacillus casei, Lactobacillus plantarum, Lactobacillus rhamnosus, Bifidobacterium bifidum, Bifidobacterium breve, Bifidobacterium longum, and Faecalibacterium prausnitzii, are responsible for maintaining gut homeostasis, protecting the retina, and preventing ARMD progression. In contrast, the elevated population of pathogenic species such as Escherichia coli, Prevotella, Desulfovibrio, Enterococcus faecalis, and Streptococcus salivarius in gut dysbiosis is involved in ARMD progression. This review explores gut microbiota and their dynamics in ageing. The age-dependent gut microbiota variations and potential biological implications for the progression of ARMD are discussed. The review also discusses observations from experimental animals and explores potential microbiome-centered treatment avenues, covering probiotics, synbiotics, dietary remedies, metabolite-based treatment, and fecal microbiota transplantation for managing ARMD. Furthermore, various challenges in the management of gut microbiota-driven ARMD are also briefed with future directions. Thus, a gut microbiota-focused paradigm can offer novel choices for ARMD prevention and treatment.},
}

@article {pmid41759374,
year = {2026},
author = {Zhou, H and Huang, Y and Chen, C and Song, M and Hylemon, PB},
title = {Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.},
journal = {Pharmacological reviews},
volume = {78},
number = {2},
pages = {100120},
doi = {10.1016/j.pharmr.2026.100120},
pmid = {41759374},
issn = {1521-0081},
abstract = {The intricate interplay between the gut microbiome and bile acid metabolism via the gut-liver axis is fundamental to hepatic homeostasis. Perturbations in this axis are increasingly implicated in the pathogenesis of diverse liver diseases, including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic liver diseases, and hepatocellular carcinoma. This review integrates current understanding of hepatic bile acid synthesis, enterohepatic circulation, and gut microbial bile acid transformations, detailing how bile acids function as signaling molecules through nuclear receptors including farnesoid X receptor, pregnane X receptor, vitamin D receptor, constitutive androstane receptor, and G-protein-coupled receptors; G protein-coupled bile acid receptor 1 (also known as Takeda G protein-coupled receptor 5), and sphingosine-1-phosphate receptor 2. We explore disease-specific alterations in gut microbiota composition and bile acid profiles in metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic liver diseases, and liver cancers, focusing on mechanisms linking gut dysbiosis, impaired intestinal barrier function, altered bile acid signaling, inflammation, and immune modulation to liver injury and progression. Furthermore, we discuss the clinical implications, highlighting the potential of microbiome signatures and bile acid profiles as diagnostic and prognostic biomarkers. Therapeutic strategies targeting the gut-liver axis, including probiotics, fecal microbiota transplantation, farnesoid X receptor agonists, and fibroblast growth factor 19 analogs, are reviewed. Finally, we address current challenges and future directions, emphasizing the need for multiomics integration, functional studies, and personalized medicine approaches to leverage the gut-liver axis for improved liver disease management. SIGNIFICANCE STATEMENT: Disruption of the gut microbiome-bile acid-liver axis is now recognized as a unifying mechanism driving multiple liver diseases, including metabolic dysfunction-associated steatotic liver disease, alcohol-associated liver disease, cholestatic liver diseases, and hepatocellular carcinoma. Unraveling the molecular and microbial interactions within this axis offers fundamental insights into disease pathogenesis and reveals novel therapeutic opportunities. Integrating multiomics technologies with artificial intelligence-based analytics will accelerate the discovery of predictive biomarkers and personalized interventions, advancing the field toward precision-based liver disease treatment protocols.},
}

@article {pmid41759265,
year = {2026},
author = {Qu, Y and Wang, P and Wang, D and Li, B and Yang, F},
title = {Intermittent fasting protects MPTP-induced Parkinson's disease mouse model through regulating gut microbiota dysbiosis.},
journal = {International immunopharmacology},
volume = {175},
number = {},
pages = {116447},
doi = {10.1016/j.intimp.2026.116447},
pmid = {41759265},
issn = {1878-1705},
abstract = {Parkinson's disease (PD) is a neurodegenerative disorder characterized by gut microbiota dysbiosis and excessive inflammatory responses. Intermittent fasting (IF) exerts neuroprotective effects on neurodegenerative diseases. However, the impact of IF on PD and its mechanisms still need to be elucidated. In the present study, we found that 13-week IF regimen (designed as alternate-day fasting) mitigated motor impairment, α-synuclein aggregation, and loss of dopaminergic neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. Meanwhile, IF attenuated intestinal dysfunctions, intestinal pro-inflammatory cytokines (tumor necrosis factor-αlphα (TNF-α) and interleukin-1 beta (IL-1β)) levels, and gut barrier destruction. Furthermore, IF alleviated brain barrier impairment and suppressed the activation of astrocytes and microglia. Mechanistic studies revealed that IF suppressed the toll-like receptor 4 (TLR4)/NF-κB signaling pathway both in the colon and substantia nigra. 16S rRNA sequencing demonstrated that IF alleviated MPTP-induced microbiota dysbiosis, decreasing harmful bacteria abundances (Proteobacteria, Burkholderiales, Sutterellaceae, Parasutterella, Burkholderiales_bacterium, and Desulfovibrio_fairfieldensis) while increasing probiotic bacteria abundances (Oscillospirales, Rikenellaceae, and Lactobacillus_murinus), which were significantly correlated with the anti-inflammatory effects of IF. Gas chromatography-mass spectrometry (GC-MS) revealed that IF induced the levels of fecal short chain fatty acids (SCFAs). Antibiotics intervention abolished the beneficial effects of IF, suggesting that gut microbiota contributed to the neuroprotection of IF for PD. These findings suggest that IF regimen may serve as a novel therapeutic strategy for PD, likely linked to its regulation of gut microbiota to inhibit gut-brain axis inflammation.},
}

@article {pmid41757041,
year = {2026},
author = {Tschang, MA and Vuong, RD and Eilers, B and Chac, D and Waalkes, A and Penewit, K and Easton, A and Schuessler, B and Daniels, R and Weil, AA and Salipante, SJ and Gibbons, SM and Schindler, AG},
title = {If you give a mouse a poopsicle: a novel fecal microbiota transplant method for exploring the role of the gut microbiome in stress-related outcomes in mice.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.02.16.705192},
pmid = {41757041},
issn = {2692-8205},
abstract = {The microbiome-gut-brain axis is a mediator of stress-related disorders. The number of preclinical studies exploring the potential causal mechanism of this connection using fecal microbiota transplantation (FMT) is growing. However, the most common method for delivering fecal transplants in rodent models is still oral gavage, which creates an adverse experience that may confound stress-related outcomes. Here, we establish an alternative methodology for FMT that decreases stress induced by traditional experimental procedures. We first used preference and anxiety behavior assays to identify antibiotic therapies having maximal tolerability and minimal anxiolytic properties. We then collected feces from donor mice and homogenized them with a microbe-stabilizing buffer to create a slurry, which was frozen into pellets ("poopsicles") for subsequent FMT. Recipient mice voluntarily consumed the pellets, and blood was collected to compare corticosterone levels relative to traditional gavage FMT. Plasma corticosterone levels were found to be significantly lower in mice receiving FMT via pellets compared to oral gavage. Furthermore, relative to gavage FMT, microbial signatures of mice receiving FMT via pellets were more similar to those of the donor pellets at one week following final FMT and were sustained for up to six weeks, as assessed by comparing Bray-Curtis beta-diversity distances. Together, these results establish effective antibiotic and FMT methods that minimize treatment-induced stress, while effectively transplanting fecal microbes between murine conspecifics.},
}

@article {pmid41754939,
year = {2026},
author = {Cosimato, I and Brescia, A and Franci, G and Casolaro, V and Folliero, V},
title = {Emerging Therapeutic Approaches for Modulating the Intestinal Microbiota.},
journal = {Pharmaceutics},
volume = {18},
number = {2},
pages = {},
pmid = {41754939},
issn = {1999-4923},
abstract = {Background/Objectives: The gut microbiota is increasingly recognized as a key determinant of human health, playing a vital role in metabolism, immunity, and disease susceptibility. Dysbiosis, or microbial imbalance, is associated with gastrointestinal disorders such as irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and Clostridioides difficile infection (CDI), as well as extraintestinal conditions, including obesity, cardiovascular disease, and neuropsychiatric disorders. This review aims to provide an updated overview of emerging therapeutic strategies to modulate the gut microbiota to restore eubiosis and improve health outcomes. Methods: A narrative review of recent literature was conducted, focusing on preclinical and clinical studies investigating microbiota-targeted therapies. The review primarily covers innovative interventional approaches, including fecal microbiota transplantation (FMT), bacterial consortium transplantation (BCT), bacteriophage therapy and outer membrane vesicles (OMVs). Results: Evidence supports the role of probiotics, prebiotics, and synbiotics in remodeling microbial communities and improving host health, although their effects may be strain- and context-dependent. FMT has demonstrated high efficacy in the treatment of recurrent Clostridium difficile infections and is being studied for IBD, IBS and extraintestinal diseases, following the recent Food and Drug Administration approval of the first commercial FMT products. BCT offers a standardized alternative to donor-derived material, with early clinical successes such as FDA-approved SER-109. Phage therapy and OMVs represent promising frontiers, offering targeted microbial modulation and interactions with the immune system, although clinical data remain limited. Conclusions: Emerging gut microbiota modulation strategies offer new perspectives for precision medicine and could transform the prevention and treatment of many diseases, but further studies are needed to ensure their safety, standardization, and clinical application.},
}

@article {pmid41754110,
year = {2026},
author = {Singh, N and Hosein, E and Virkud, YV and Keet, C and Kulis, M},
title = {The Gut Microbiome in the IgE-Mediated Food-Allergic Patient-A Narrative Review.},
journal = {Nutrients},
volume = {18},
number = {4},
pages = {},
pmid = {41754110},
issn = {2072-6643},
abstract = {Food allergies (FA) are a major public health concern in both children and adults. Immunoglobulin E (IgE)-mediated FA is characterized by allergic reactions driven by allergen-specific IgE and the subsequent degranulation of mast cells and basophils. Current FA management primarily involves avoidance of allergen-containing food, and more recently, therapies such as oral immunotherapy (OIT), sublingual immunotherapy (SLIT), and the anti-IgE biologic omalizumab. However, these interventions are not curative. The gut microbiome has been implicated in the development and regulation of oral tolerance to food antigens. This narrative review explores the role of probiotics, fecal microbiota transplantation (FMT), dietary interventions, and the interaction between the microbiome and OIT as potential strategies to manage established FA. We also explore barriers to their proliferation as part of regular clinical care. We conclude that future research should (1) address how the microbiome interacts with immunotherapies other than OIT, (2) explore the role of novel microbiome-based treatments like FMT as potential adjuvants to existing food allergy therapeutics, and (3) focus on developing standardized protocols and endpoints for microbiome-based therapeutics.},
}

@article {pmid41754077,
year = {2026},
author = {Ashkanani, G and Rob, M and Yousef, M and Ashkanani, A and Al-Najjar, YA and Laws, S and Chaari, A},
title = {The Effects of Microbiome Modulating Therapies on Inflammatory Markers in Autoimmune Disease: A Systematic Review and Meta-Analysis.},
journal = {Nutrients},
volume = {18},
number = {4},
pages = {},
pmid = {41754077},
issn = {2072-6643},
abstract = {BACKGROUND: Autoimmune diseases (ADs) are a growing global health burden, driven by chronic inflammation and immune dysregulation. The gut-immune axis plays a central role in their pathogenesis, with dysbiosis linked to several conditions. This has prompted investigation into nutraceuticals such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation as adjunctive therapies.

METHODS: We conducted a systematic review and meta-analysis following PRISMA guidelines, searching PubMed, Embase, and Web of Science for randomized controlled trials evaluating these interventions in autoimmune diseases.

RESULTS: Twenty-eight randomized control trials (RCTs) involving 2002 patients across 11 countries met inclusion criteria. Across the included RCTs, pooled analyses demonstrated significant reductions in c-reactive protein (CRP) (SMD -0.67, 95% CI -1.00 to -0.33; I[2] = 80.8%) and Tumor necrosis factor-alpha (TNF-α) (SMD -1.81, 95% CI -2.67 to -0.94; I[2] = 96%), a significant increase in Interleukin-10 (IL-10) (SMD 2.65, 95% CI 0.64 to 4.66; I[2] = 98%), and no overall significant effect on Interleukin-6 (IL-6) (SMD -0.89, 95% CI -1.99 to 0.22; p = 0.12). The strongest evidence of benefit was observed in rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease. Pooled effects are limited by extreme between-study heterogeneity (I[2] 80-98%), leaving interpretation as exploratory rather than definitive. More limited or inconsistent findings were reported for systemic lupus erythematosus, hypothyroidism, axial spondylarthritis, and juvenile idiopathic arthritis. Heterogeneity in study design, probiotic strain selection, dosage, and treatment duration limited comparability across trials.

CONCLUSIONS: Overall, microbiome-targeted nutraceuticals appear promising for attenuating systemic inflammation in select autoimmune conditions, but results remain mixed. Larger, rigorously designed RCTs with standardized endpoints are needed to clarify efficacy, identify optimal formulations, and define patient populations most likely to benefit.},
}

@article {pmid41753607,
year = {2026},
author = {Yuan, H and Yi, L and Jia, H and Song, G and Cheng, W and Xie, Y and Zhu, J and Zhao, S},
title = {Gut Microbiota-Derived Metabolites to Regulate Intramuscular Fat Deposition in Pigs.},
journal = {Microorganisms},
volume = {14},
number = {2},
pages = {},
pmid = {41753607},
issn = {2076-2607},
support = {2024YFD1800404//National Key Research and Development Program of China/ ; 32360808//National Natural Science Foundation of China/ ; 31760645//National Natural Science Foundation of China/ ; 31260592//National Natural Science Foundation of China/ ; 31060331//National Natural Science Foundation of China/ ; 32560790//National Natural Science Foundation of China/ ; 202202AE090032//Major Science and Technology Project of Yunnan Province/ ; 202501AS070086//Major Science and Technology Projects of Yunnan Province/ ; },
abstract = {Intramuscular fat (IMF) is a crucial determinant of pork quality, influencing tenderness, flavor, and consumer preferences, yet selective breeding has reduced its levels in modern pigs. This review explores the molecular and cellular mechanisms of IMF deposition, including progenitor cell differentiation via pathways like Wnt/β-catenin and PPARγ, and advances in non-invasive detection methods such as hyperspectral imaging and Raman spectroscopy. It highlights correlations and causal links between the gut microbiota composition and IMF, established through omics analyses, fecal microbiota transplantation, and germ-free models. Key microbial metabolites, including short-chain fatty acids (SCFAs) and bile acids, modulate lipid metabolism bidirectionally via signaling receptors like GPR43, FXR, and TGR5. Future research should integrate multi-omics and develop probiotics to enhance IMF efficiency for sustainable pork production.},
}

@article {pmid41752141,
year = {2026},
author = {Wu, Y and Wong, OWH and Chen, S and Wang, Y and Zhang, G and Gao, Y and Chan, FKL and Ng, SC and Su, Q},
title = {Gut Microbiome Mediates the Causal Link Between Autism Spectrum Disorder and Dietary Preferences: A Mendelian Randomization Study.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41752141},
issn = {1422-0067},
abstract = {Autism spectrum disorder (ASD) frequently co-occurs with malnutrition and gut dysbiosis, yet the underlying mechanisms remain poorly understood. Herein, this cross-sectional study first profiles dietary intake differences using dietary records from 210,874 participants (ASD = 232; non-ASD = 210,642; median age = 56.18) from the UK Biobank (UKB). Second, a bi-directional Mendelian Randomization (MR) approach serves to dissect relationships between ASD genetic susceptibility and dietary preferences by leveraging genome-wide association metadata from the iPSYCH-PGC (ASD) and UKB (dietary intake/food-liking traits). The same strategy is implemented to identify ASD-associated gut microbial species. Mediation analyses further assess the role of gut microbiota in the association between ASD and dietary preferences. Subjects with ASD exhibit higher consumption of cheese, processed meat, and oily fish, alongside lower intake of fruits, and demonstrate a preference for high-fat/salt and energy-dense foods. Additionally, the depletion of Turicibacter, Streptococcus, and Lachnospiraceae NK4A136 was causally related with ASD (all false discovery rate < 0.05; β = -0.15, β = -0.10, β = -0.093, respectively), which significantly mediates the ASD-associated elevated preference for high-fat/salt foods. In conclusion, ASD is associated with specific dietary preferences, likely mediated via gut microbiota, highlighting the future potential of gut microbiome-based therapeutics to modify eating disorders for ASD.},
}

@article {pmid41752122,
year = {2026},
author = {Wang, SJ and Nian, HY and Chen, ZH and Cui, L},
title = {Human Microbiota-Associated Pig Models for Translational Microbiome Research: A Scoping Review.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41752122},
issn = {1422-0067},
support = {23141900100//Science and Technology Commission of Shanghai Municipality/ ; },
abstract = {The human microbiota-associated (HMA) pig model provides a physiologically relevant platform that bridges preclinical and translational research. However, its use remains limited, with existing studies showing considerable variation in establishment methods. This scoping review systematically evaluates methodological frameworks, engraftment outcomes, and research applications of HMA pig models. Additionally, it highlights their strengths, limitations, and implications for future studies. We conducted a comprehensive literature search in PubMed, Web of Science, Scopus, and Directory of Open Access Journals, following PRISMA guidelines for Scoping Reviews. The review examines the methodological foundations of HMA pig model generation and proposes a minimal reporting framework to promote standardization. It synthesizes studies on human microbiota engraftment in pigs, identifying factors that influence colonization efficiency. Finally, it summarizes current applications, discusses persistent limitations and translational challenges, and outlines opportunities for future research. Overall, these integrated insights aim to foster standardized, reproducible protocols for HMA pig model preparation and guide advancements in the field.},
}

@article {pmid41752118,
year = {2026},
author = {Kurdi, MA and Alotaibi, H and Alkhuraymi, AT and Aldahery, LN and Alhawaj, AF and Aldali, HJ},
title = {Amyotrophic Lateral Sclerosis (ALS) Genetics and Microbiota: A Comprehensive Review.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41752118},
issn = {1422-0067},
abstract = {Amyotrophic Lateral Sclerosis (ALS) is a severe, progressive neurodegenerative disorder characterized by the loss of upper and lower motor neurons, affecting 0.5 to 2.6 per 100,000 people, with a median survival of 2 to 5 years. It is increasingly seen as a multisystem disorder, sharing essential clinicopathological features with Frontotemporal Dementia (FTD). This convergence arises from overlapping molecular processes, including severe oxidative stress, glutamate-mediated excitotoxicity, mitochondrial dysfunction, and widespread aggregated TDP-43 proteinopathy in both sporadic and familial cases. Several key genetic factors have been identified, particularly mutations in C9orf72, SOD1, TARDBP, and FUS, which serve as important targets for novel treatments, such as Tofersen, a recently approved SOD1-specific antisense oligonucleotide (ASO) gene therapy. Additionally, there is increasing evidence of the gut-brain connection. Dysbiosis, involving species such as Akkermansia muciniphila, and lower levels of neuroprotective metabolites, such as nicotinamide, may affect the course of the disease. As a result, treatment strategies are shifting toward a personalized approach. This includes using gene therapy, ranging from ASOs and RNA interference (RNAi) to new CRISPR-based genome editing. It also involves exploring microbiome-modulating treatments, such as specific probiotics and Fecal Microbiota Transplantation (FMT). While microbiome and gene therapies remain largely experimental, their potential is promising, as highlighted by the recent approval of Tofersen. These novel approaches could be further enhanced and guided by more robust diagnostic criteria and by investigating early multimodal treatment strategies to slow the progression of this complex disease.},
}

@article {pmid41751793,
year = {2026},
author = {Ptáček, O and Musil, Z and Guarnieri, G and Vrbacká, A and Moudrá, P and Zlámalová, A and Röszlerová, P and Tonhajzer, M and Musil, V and Morelli, A and Zach, P},
title = {Amyotrophic Lateral Sclerosis: The State of the Art on Treatments and the Therapeutic Role of the Intestinal Microbiome in Human Studies.},
journal = {International journal of molecular sciences},
volume = {27},
number = {4},
pages = {},
pmid = {41751793},
issn = {1422-0067},
support = {Cooperatio 39 - Oncology and Haematology//Charles University/ ; Cooperatio 33-Intensive Care Medicine//Charles University/ ; Cooperatio 36-Medical Diagnostics and Basic Medical Sciences//Charles University/ ; #NEXTGENERATIONEU//European Commission/ ; MNESYS (PE0000006) - A Multiscale integrated approach to the study of the nervous system in health and disease (DR. 1553 11.10.2022)//Ministry of University and Research (MUR), National Recovery and Resilience Plan (NRRP)/ ; },
abstract = {Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disorder; to date, there is no long-term effective treatment. Recently, a relationship has been discovered between the human intestinal microbiome and the pathogenesis of ALS, on which basis faecal microbiota transplantation (FMT) has been proposed as a potential treatment for ALS. In this review, we compare three existing case studies examining the effect of FMT on the course of ALS, highlighting differences in methodology and results. In two of the studies, a halt in the progression of ALS symptoms was observed following FMT, accompanied by improvement in patient health. However, in the third and largest study, no significant effect of FMT was observed. The possible explanation for this discrepancy may be the intentional depletion of intestinal microorganisms using antibiotics prior to FMT in the third study. Future studies and/or completion of the ongoing clinical studies will help clarify the therapeutic effectiveness of FMT in ALS patients.},
}

@article {pmid41749649,
year = {2026},
author = {Pawłowski, P and Zaj, N and Iwaniszczuk, K and Grzelka, I and Makuch, W and Samardakiewicz-Kirol, E and Kościołek, A and Samardakiewicz, M},
title = {Personalizing Nutritional Therapy in Pediatric Oncology: The Role of Gut Microbiome Profiling and Metabolomics in Mitigating Mucositis and Enhancing Immune Response to Chemotherapy.},
journal = {Children (Basel, Switzerland)},
volume = {13},
number = {2},
pages = {},
pmid = {41749649},
issn = {2227-9067},
abstract = {INTRODUCTION: Intensive chemotherapy protocols and hematopoietic stem cell transplantation (HSCT) in children with cancer frequently lead to severe complications, such as mucositis and immune dysfunction. A growing body of evidence indicates that these complications are closely associated with the patient's nutritional status and the composition of the gut microbiome, which becomes profoundly destabilized as a result of cytotoxic therapy and antibiotic use.

BACKGROUND: The aim of this review is to critically evaluate the current state of knowledge on the interplay between gut dysbiosis, metabolomic profiles-with particular emphasis on short-chain fatty acids (SCFAs)-and treatment-related toxicity in pediatric patients, as well as to delineate pathways toward personalized nutritional therapy.

METHODS: A narrative review was conducted, including clinical and preclinical studies published between January 2015 and October 2025. PubMed/MEDLINE, Embase, Cochrane Library, and other databases were searched, focusing on changes in microbiome composition, correlations between gut-derived metabolites and the severity of complications (sepsis, graft-versus-host disease [GvHD], mucositis), and the effects of targeted nutritional interventions (probiotics, prebiotics, postbiotics, and fecal microbiota transplantation [FMT]) on microbiome modulation during anticancer therapy.

RESULTS: The analysis demonstrates that pediatric oncologic treatment leads to a marked reduction in microbial diversity, including the loss of protective Clostridiales taxa (e.g., Faecalibacterium), accompanied by an overgrowth of Proteobacteria pathobionts. Metabolomic profiling indicates that low SCFA levels (e.g., butyrate < 20-50 µmol/g) are a strong predictor of severe mucositis, prolonged neutropenia, and an increased risk of sepsis. Interventions aimed at restoring eubiosis and enhancing SCFA production show potential in strengthening the intestinal barrier, modulating immune responses, and enabling maintenance of the planned relative dose intensity (RDI) of chemotherapy by reducing treatment-related toxicity.

CONCLUSIONS: Gut microbiome profiling and fecal metabolomics represent promising prognostic tools in pediatric oncology. There is an urgent need for further research employing "omics"-based approaches to develop precise, individually tailored nutritional protocols. Such strategies, including postbiotics and FMT, may minimize treatment-related adverse effects and improve long-term clinical outcomes in pediatric patients.},
}

@article {pmid41749264,
year = {2026},
author = {Li, L and Cai, F and Liu, Z and Mo, W and Zhang, J and Qin, J and Liang, C and Xu, H and Liu, S and Tang, S and Peng, P and Liang, J and Ruan, H and Qin, R and Luo, F and Xiong, G and Yang, C and Zou, J and Liu, S and Geng, Y and Huang, J},
title = {Cross-kingdom microbial interactions in the gut during inflammatory bowel disease.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07692-3},
pmid = {41749264},
issn = {1479-5876},
abstract = {BACKGROUND: Inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC), is characterized by chronic, relapsing inflammation of the gastrointestinal tract. Recent studies emphasize the importance of gut microbiome dysbiosis in IBD pathogenesis, where interactions among bacteria, fungi, protozoa, and viruses contribute to inflammation, immune modulation, and epithelial barrier disruption.

METHODS: A comprehensive narrative literature review was conducted, focusing on human data and preclinical studies. Biomedical databases were searched for research related to microbial communities and their role in IBD development, specifically targeting microbial metabolites, gut fungi, protozoa, and viruses. Relevant studies were analyzed to assess their impact on immune pathways and microbial interactions.

RESULTS: The review reveals how different microbial kingdoms collaborate through bacteria-fungi, bacteria-protozoa, and phage-bacteria interactions, influencing metabolite production and immune system function. Specific microbial metabolites like short-chain fatty acids (SCFAs), indoles, bile acids, and others play significant roles in regulating mucosal immunity and barrier function. Disruptions in these interactions lead to chronic inflammation and contribute to disease progression. Multi-kingdom therapies, including probiotics, yeast-based treatments, and fecal microbiota transplantation (FMT), show promise but face challenges due to clinical variability.

CONCLUSION: Understanding IBD as a disruption of microbial ecosystems enables the development of personalized treatment strategies. Multi-omics studies and microbiome-based interventions targeting specific microbial interactions hold potential for more effective, individualized therapies in IBD management. However, further research and larger clinical trials are necessary for translating these findings into routine clinical practice.},
}

@article {pmid41747917,
year = {2026},
author = {Liu, X and Wang, Y and Medina, AA and Liu, D and Liu, J and Tang, W and Wang, M and Chen, X and Huang, K and Liu, M and Wang, C and Liu, Y},
title = {Probiotic-derived extracellular vesicles attenuate cholestatic liver damage via gut-liver axis.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {108152},
doi = {10.1016/j.phrs.2026.108152},
pmid = {41747917},
issn = {1096-1186},
abstract = {Gut-liver axis disturbance is the unifying pathogenesis of cholestatic liver diseases. The purpose of this study was to explore the underlying mechanisms of the probiotic Lactobacillus amylovorus (LA) and its secreted extracellular vesicles (EVs) on liver damage and fibrosis in 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC)-fed and multidrug resistance protein 2 knockout (Mdr2[-/-]) mice. Direct replenishment of LA is sufficient to correct the DDC-fed and Mdr2[-/-]-induced liver damage and fibrosis. Mechanistic studies show that the secretion of EVs is required for the LA-induced liver protective effects. RNA sequencing results demonstrated that the enrichment of differentially expressed genes was associated with glutathione metabolism, microbial metabolism in diverse environments and inflammatory mediator regulation of TRP channels in DDC-fed mice. Our findings revealed that LAEVs reshaped the gut microbiota, which was associated with increased bile acids (BAs) deconjugation and fecal BAs excretion, repaired gut barrier function, activated intestinal Farnesoid X receptor/Fibroblast growth factor 15 (FXR/FGF-15) axis, reduced liver BAs and oxidative stress level, which ultimately mitigated liver damage and fibrosis in both DDC-fed and Mdr2[-/-] mice. Notably, LAEVs did not ameliorate DDC-induced liver damage or fibrosis in antibiotic-treated mice. Furthermore, LAEVs provided protection against DDC-induced liver injury and fibrosis in fecal microbiota transplantation mice. LAEVs did not ameliorate DDC-induced liver damage or fibrosis in BSH inhibitor (CAPE)-treated mice. LAEVs also failed to improve liver damage and fibrosis in DDC-induced intestinal epithelial cell-specific FXR knockout (Fxr[△IE]) mice. This study revealed that LAEVs mitigated cholestatic liver fibrosis via regulating gut microbiota-bile acid-ROS axis in mice.},
}

@article {pmid41747877,
year = {2026},
author = {Waghmare, A and Rahangadale, S and Khare, K and Taksande, B and Umekar, M and Mangrulkar, S},
title = {Interweaving microglial senescence and gut microbiome dynamics in Alzheimer's disease - Mechanisms and therapeutic frontiers.},
journal = {Molecular and cellular neurosciences},
volume = {},
number = {},
pages = {104075},
doi = {10.1016/j.mcn.2026.104075},
pmid = {41747877},
issn = {1095-9327},
abstract = {Alzheimer's disease (AD), a prevalent neurodegenerative disorder characterized by cognitive impairment and neuronal degeneration, is increasingly recognized as being driven not only by the traditional amyloid-beta and tau pathologies but also by persistent neuroinflammation and systemic immune dysregulation. Emerging evidence implicates microglia senescence and gut microbiota dysbiosis is critical contributors to the neuroinflammatory landscape. Senescent microglia marked by reduced phagocytic ability and a pro-inflammatory secretory profile, are unable to clear pathogenic stimuli, thereby intensifying neuronal damage. Simultaneously, gut dysbiosis, characterized by a reduction in beneficial bacteria and an increase in endotoxin-producing species, elevates systemic inflammation and compromises the intestinal and blood brain barrier. Microbial metabolites, such as short-chain fatty acids (SCFAs) and lipopolysaccharides (LPS), affect microglial activation through the gut-brain axis, primarily via the TLR4/NF-κB and NLRP3 inflammasome pathways, thus promoting microglial senescence and exacerbating AD pathology. Therapeutic approaches that target these interacting pathways are rejuvenation of microglia with senolytics and stimulation of TREM2; regulation of gut microbiota with probiotics, prebiotics, lifestyle modification, dietary intervention; and fecal microbiota transplantation. Precision medicine approaches incorporating microbiome profiling and immunogenetic analysis will enhance these treatments. This review combines mechanistic insight into microglial aging and gut-brain interaction, emphasizes their synergistic role in AD pathogenesis, and delineates integrated therapeutic strategies. Dissection of the gut-microglia axis can reveal novel targets for early intervention to counteract neuroinflammation, improve cognitive function, and slow disease progression in AD.},
}

@article {pmid41747725,
year = {2026},
author = {Chen, K and Liu, Y and Rong, J and Dai, N and Xu, C and Li, H and Zhong, L and Wang, B and Ji, Z and Xie, S and Xu, Y and Yang, F and Wang, J and Li, D and Gu, Y and Zhou, X and Li, Y and Chen, M and Chen, Y and Li, W and Tang, Z and Cai, J and Xu, J and Xia, S and Zhan, Q and Zhou, Z},
title = {Strain-level genetic heterogeneity and colonization dynamics drive microbiome therapeutic efficacy.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.02.002},
pmid = {41747725},
issn = {1934-6069},
abstract = {Fecal microbiota transplantation (FMT) has shown immunotherapeutic promise, yet its efficacy in non-small-cell lung cancer (NSCLC) remains unclear. We demonstrate that FMT improves anti-PD-1 efficacy and progression-free survival in a single-arm trial of advanced PD-L1-negative NSCLC. Analyzing over 2,000 metagenomes from diverse disease cohorts and healthy controls via a high-resolution strain-tracking framework, we reveal that phylogenetically distinct strains within identical species exert opposing therapeutic effects, resolving prior inconsistencies. We identify conserved ecological principles where engraftment relies on species-intrinsic metabolic and immune evasion traits. Crucially, successful colonization by specific beneficial strain variants correlates with positive clinical outcomes. Finally, we identify 38 priority species with robust engraftment potential and significant heterogeneity as candidates for precision therapeutics. These findings establish a strain-function-efficacy paradigm, elucidating the mechanistic basis of variable outcomes and guiding next-generation microbiome drug development.},
}

@article {pmid41746975,
year = {2026},
author = {Wang, G and Liu, L and Zhang, H and Mao, P and Lu, S and Zhang, X and Li, X and Song, C},
title = {Effects of tacrolimus treatment on the gut microbiota and metabolites in liver transplant recipients.},
journal = {PloS one},
volume = {21},
number = {2},
pages = {e0343817},
pmid = {41746975},
issn = {1932-6203},
abstract = {BACKGROUND: Liver transplantation (LT) is an effective treatment for patients with end-stage liver disease. In recent years, more and more evidence has supported the association between gut microbiota dysbiosis and the pathogenesis and progression of liver diseases.

METHODS: The study included 36 patients who received tacrolimus treatment after liver transplantation. Patients were stratified into subgroups according to three key variables: tacrolimus treatment duration, whole-blood tacrolimus concentration, and tacrolimus concentration-to-dose (C/D) ratio. Fecal samples and whole-blood specimens were collected from all participants. The Illumina HiSeq X platform was used to detect the gut metagenome, analyzing the composition and characteristics of the gut microbiota. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) technology was employed to detect metabolites of the gut microbiota, revealing their metabolic profiles.

RESULTS: As the duration of tacrolimus use increased, the diversity of the gut microbiota also increased, and the abundance of Escherichia coli_D and Bacteroides stercoris rose. Additionally, the abundance of Brunovirus and Uetakevirus tended to decrease. The abundance of gene functions related to chemical carcinogenesis and bacterial invasion of epithelial cells significantly decreased. In the gut microbiota metabolites, 16 substances like Astragaloside A and Acetyl-L-carnitine significantly increased, while 108 substances like Capsaicin and TLK significantly decreased. Within a certain range, as the concentration of tacrolimus in whole blood increased, the diversity of the gut microbiota increased. The abundance of Phocaeicola and Klebsiella increased, and the abundance of Peduovirus among viruses also rose. However, excessively high concentrations may lead to a decrease in the diversity of the gut microbiota and a decrease in the abundance of Phocaeicola. With respect to the C/D ratio, increased ratios were linked to significantly higher levels of 57 fecal metabolites (e.g., PC 34:2, 5-Methyl-2'-deoxycytidine), whereas 13 metabolites (e.g., FAHFA 2:0/16:0) showed substantial declines.

CONCLUSIONS: Tacrolimus treatment is associated with distinct alterations in gut microbiota and metabolites among LT recipients. These findings provide a preliminary framework for future investigations aimed at optimizing immunosuppressive regimens, although their clinical translational potential requires validation in larger-scale, prospective cohort studies.},
}

@article {pmid41745976,
year = {2026},
author = {Németh, K and Tóth, I and Lányi, K and Schilling-Tóth, BM and Csorba, S and Žura Žaja, I and Sterczer, Á},
title = {The Collaborative Collapse: Bile Acid Dysmetabolism as a Central Pathogenic Driver in Canine and Feline Multi-Systemic Disorders-From Mechanisms to Precision Therapeutics.},
journal = {Veterinary sciences},
volume = {13},
number = {2},
pages = {},
pmid = {41745976},
issn = {2306-7381},
support = {SRF-003//University of Veterinary Medicine Budapest/ ; 2025-2.1.1-EKÖP-2025-00022//Ministry of Culture and Innovation of Hungary from the National Research, Development and Innovation Fund/ ; },
abstract = {Veterinary metabolomics has redefined bile acids (BAs) from simple digestive surfactants to systemic endocrine signals within a microbial-host metabolic axis. This review aims to evaluate how BA dysmetabolism acts as a central pathogenic factor in canine and feline disease. We analyze the BA pool's integrity, which depends on a specialized functional guild, primarily Peptacetobacter hiranonis, responsible for 7α-dehydroxylation. We delineate two principal pathological profiles: (1) microbial collapse, characterized by secondary bile acid (SBA) depletion and compromised farnesoid X receptor (FXR) and Takeda G protein-coupled receptor 5 (TGR5) signaling, which exacerbates inflammation in chronic enteropathy (CE), protein-losing enteropathy (PLE), and exocrine pancreatic insufficiency (EPI); and (2) hepato-biliary spillover, wherein host-induced dysfunction results in primary bile acid (PBA) excess. Recent data have linked these disruptions to skeletal health, feline renal fibrosis, cardiac remodeling in myxomatous mitral valve disease (MMVD), and neuroinflammation in epilepsy and hepatic encephalopathy. The discovery of microbially conjugated bile acids (MCBAs) and microbial extracellular vesicles (MEVs) reveals highly specific, vesicle-mediated communication pathways impacting systemic health. Diagnostic protocols should prioritize functional profiling, including the dysbiosis index (DI), serum conjugated BA analysis, and SBA/PBA ratios. Clinical management is moving beyond empirical fecal microbiota transplantation (FMT), towards precision synthetic microbial consortia (SynComs), neuroprotective BAs like tauroursodeoxycholic acid (TUDCA), and molecular postbiotics to restore the collaborative metabolome.},
}

@article {pmid41745910,
year = {2026},
author = {Cao, X and Zhou, L and Ding, Y and Ma, C and Chen, Q and Li, N and Ren, H and Yan, P and Jia, J},
title = {Study of Fecal Microbiota Transplantation Ameliorates Colon Morphology and Microbiota Function in High-Fat Diet Mice.},
journal = {Veterinary sciences},
volume = {13},
number = {2},
pages = {},
pmid = {41745910},
issn = {2306-7381},
support = {ZR2023MC164//the Natural Science Foundation of Shandong Province/ ; 2022KJ137//the Youth Innovation Team Project Program of Shandong Provincial Education Department/ ; },
abstract = {This study investigates whether fecal microbiota transplantation (FMT) can alleviate gut microbiota dysbiosis induced by a high-fat diet (HFD) through modulation of fatty acid metabolism, competition for nutrients, production of short-chain fatty acids (SCFAs), and restoration of mucus layer integrity. To elucidate the mechanisms by which FMT regulates colonic microbial function and host metabolic responses, 80 male Bal b/c mice were randomly assigned to four experimental groups (n = 20 per group): Normal Diet Group (NDG), High-Fat Diet Group (HDG), Restrictive Diet Group (RDG), and HDG recipients of NDG-derived fecal microbiota (FMT group). The intervention lasted for 12 weeks, during which body weight was monitored biweekly. At the end of the experiment, tissue and fecal samples were collected to assess digestive enzyme activities, intestinal histomorphology, gene expression related to gut barrier function, and gut microbiota composition via 16S rRNA gene sequencing. Results showed that mice in the HDG exhibited significantly higher final body weight and greater weight gain compared to those in the NDG and RDG (p < 0.05). Notably, FMT treatment markedly attenuated HFD-induced weight gain (p < 0.05), reducing it to levels comparable with the NDG (p > 0.05). While HFD significantly elevated the activities of α-amylase and trypsin (p < 0.05), FMT supplementation effectively suppressed these enzymatic activities (p < 0.05). Moreover, FMT ameliorated HFD-induced intestinal architectural damage, as evidenced by significant increases in villus height and the villus height-to-crypt depth ratio (V/C) (p < 0.05). At the molecular level, FMT significantly downregulated the expression of pro-inflammatory cytokines (IL-1β, IL-1α, TNF-α) and upregulated key tight junction proteins (Occludin, Claudin-1, ZO-1) and mucin-2 (MUC2) relative to the HDG (p < 0.05). 16S rRNA analysis demonstrated that FMT substantially increased the abundance of beneficial genera such as Lactobacillus and Bifidobacterium while reducing opportunistic pathogens including Romboutsia (p < 0.05). Furthermore, alpha diversity indices (Chao1 and ACE) were significantly higher in the FMT group than in all other groups (p < 0.05), indicating enhanced microbial richness and community stability. Functional prediction using PICRUSt2 revealed that FMT-enriched metabolic pathways (particularly those associated with SCFA production) and enhanced gut barrier-related functions. Collectively, this study deepens our understanding of host-microbe interactions under HFD-induced metabolic stress and provides mechanistic insights into how FMT restores gut homeostasis, highlighting its potential as a therapeutic strategy for diet-induced dysbiosis and associated metabolic disorders.},
}

@article {pmid41745224,
year = {2026},
author = {Spaggiari, L and Tedeschi, G and Benatti, G and De Benedittis, M and Franzè, MT and Pinetti, D and Pericolini, E and Ardizzoni, A},
title = {Untargeted Metabolomic Analysis of Cell-Free Supernatants (CFSs) from Different Clinical Isolates of Saccharomyces cerevisiae and Their Effects on Candida albicans Virulence.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {12},
number = {2},
pages = {},
pmid = {41745224},
issn = {2309-608X},
support = {not applicable//FAR Dipartimentale 2024 (Ardizzoni) and FAR Dipartimentale 2025 (Pericolini)/ ; },
abstract = {Saccharomyces cerevisiae probiotic properties are effective for the treatment of infections by the opportunistic pathogen Candida albicans. Here, we assessed the anti-Candida effect of cell-free supernatants (CFSs) from three different fecal isolates and one ATCC strain of S. cerevisiae. We evaluated C. albicans growth inhibition through CFUs, and the impairment of virulence factors (adhesion, biofilm formation, and metabolic activity) by crystal violet and XTT assays. An untargeted metabolomic analysis of the CFSs was also performed. The CFSs moderately reduced C. albicans growth, but they could impair C. albicans virulence by reducing its capacity to adhere and to form a biofilm, and by decreasing the metabolic activity of biofilm-embedded fungal cells. The untargeted metabolomic analysis indicated an overexpression of N-acetyl-DL-tryptophan and other molecules derived from its metabolism (kynurenic acid and indole-3-acrylic acid), the dipeptides glycyl-L-leucine, prolyl-leucine, and γ-L-glutamyl-L-leucine, and the unconventional nucleotide inosine in the CFSs from fecal isolates, as compared to the reference strain. Further studies are warranted to better characterize the metabolome of these CFSs. Should the effects described here also be confirmed in vivo, the possible future employment of S. cerevisiae CFSs as a postbiotic aid to the current antifungal therapy may be considered.},
}

@article {pmid41745080,
year = {2026},
author = {Kumar, S and Himanshu, and Gaur, P and Ahmad, S and Puri, P and Raj, VS and Pandey, RP},
title = {Microbiota Transplantation as a Future Novel Therapeutic Strategy Approach.},
journal = {Diseases (Basel, Switzerland)},
volume = {14},
number = {2},
pages = {},
pmid = {41745080},
issn = {2079-9721},
abstract = {Bacterial vaginosis (BV) is a leading cause of genital discomfort among women globally, and it arises from dysbiosis of the vaginal ecosystem characterized by the overgrowth of pathogenic bacteria. Current therapeutic strategies primarily rely on antibiotics and/or probiotics, which demonstrate clinical efficacy but are frequently associated with limitations such as antimicrobial resistance, high recurrence rates, and incomplete restoration of a healthy vaginal microbiota. Inspired by the success of fecal microbiota transplantation in gastrointestinal disorders, vaginal microbiome transplantation (VMT) from healthy donors has emerged as a potential alternative therapeutic approach for BV. However, experimental and early clinical studies indicate that VMT efficacy is not uniform across individuals, with considerable inter-individual variability in treatment outcomes. Host genetic factors, baseline vaginal microbial composition, immune status, and environmental influences are likely to modulate therapeutic success, underscoring the need for personalized interventions. This article critically evaluates the shortcomings of existing standardized treatments, highlights the potential advantages and challenges of VMT, and discusses emerging, precision-based therapeutic strategies for BV in light of recent research advances and ongoing clinical trials worldwide.},
}

@article {pmid41744425,
year = {2026},
author = {Sandeep, G and Pahari, S and Nayak, V and Gundamaraju, R and Mishra, P and Misra, A},
title = {The Gut-Prostate Axis: Decoding the Interplay of Environmental Factors, Microbial Metabolites, and Hormonal Regulation in Prostate Cancer Pathogenesis.},
journal = {Technology in cancer research & treatment},
volume = {25},
number = {},
pages = {15330338261424322},
pmid = {41744425},
issn = {1533-0338},
abstract = {Prostate cancer remains one of the most common malignancies in men, with its progression strongly influenced by androgen signaling. While genetic alterations are well-documented in prostate cancer, growing evidence highlights the contribution of environmental factors, particularly diet and the gut microbiome, in modulating disease risk and therapy response. The gut microbiota plays a crucial role in regulating host metabolism, immune responses, and hormone activity. Recent findings suggest that specific microbial communities influence androgen biosynthesis and metabolism through enzymes such as β-glucuronidase, altering systemic androgen availability and imp acting tumor progression. Additionally, microbial metabolites, including short-chain fatty acids, secondary bile acids, and bacterial genotoxins, can affect inflammatory pathways and cellular signaling relevant to prostate tumorigenesis. Experimental studies also indicate that modifying the gut microbiota through dietary interventions, probiotics, or fecal microbiota transplantation can influence tumor growth and improve responses to immunotherapy and hormone-based treatments. In this review we present the current knowledge on gut-prostate axis, examine the mechanistic links between microbial activity and prostate cancer biology, and discuss emerging microbiome-based strategies as potential therapies. A deeper understanding of this bidirectional crosstalk could pave the way for microbiome-informed approaches to prevention, diagnosis, and personalized treatment of prostate cancer.},
}

@article {pmid41743894,
year = {2026},
author = {Jayathilaka, NS and Wijekoon, KJ and Sachinthani, SDD and Weththasinghe, AV and Ganamurali, N and Sabarathinam, S},
title = {Enteroendocrine hormones and gut microbiota in obesity: a systematic review from mechanistic insight to precision metabolic care.},
journal = {Journal of diabetes and metabolic disorders},
volume = {25},
number = {1},
pages = {73},
pmid = {41743894},
issn = {2251-6581},
abstract = {PURPOSE: This systematic review aims to synthesize current evidence on enteroendocrine cell alterations in obesity, elucidate the mechanisms by which gut microbial taxa and metabolites regulate gut hormone release, and assess therapeutic innovations targeting the microbiota-enteroendocrine axis for precision metabolic care.

METHODS: A systematic search of PubMed, Web of Science, Scopus, and Embase was conducted from January 2015 to July 2025 following Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines. Studies examining enteroendocrine cell function, gut microbiota composition, and their metabolic interactions in human obesity, animal models, and cellular systems were included. Data were extracted on gut hormone levels, microbial community structure, short-chain fatty acid production, and therapeutic interventions. Quality assessment was performed using the Cochrane Risk of Bias tool for randomized controlled trials and Newcastle-Ottawa Scale for observational studies.

RESULTS: Microbial dysbiosis characterized by depletion of short-chain fatty acid-producing bacteria is associated with impaired gut hormone release and altered free fatty acid receptor signaling. Therapeutic strategies including glucagon-like peptide-1 receptor agonists are associated with substantial weight loss, whereas probiotics, prebiotics, and fecal microbiota transplantation show variable and generally modest metabolic effects in human studies.

CONCLUSION: The microbiota-enteroendocrine axis represents a promising therapeutic target for obesity management, supported by mechanistic and associative evidence.Multi-modal precision approaches integrating hormonal pharmacotherapy with microbiota modulation may enable more durable metabolic benefits and personalized obesity treatment.},
}

@article {pmid41743795,
year = {2026},
author = {Zhang, J and Ji, J and Dai, X and Li, B and Liu, T and Zhang, S and Yu, Y},
title = {Microplastics and Nanoplastics Cause Thyroid Dysfunction in Adolescent Mice through the Intestinal Microbiota-Mediated Hypothalamus-Pituitary-Thyroid Axis.},
journal = {Environment & health (Washington, D.C.)},
volume = {4},
number = {2},
pages = {313-323},
pmid = {41743795},
issn = {2833-8278},
abstract = {Polypropylene (PP) and poly-(ethylene terephthalate) (PET) plastic products are widely used in diet packaging and may generate microplastics (MPs) and nanoplastics (NPs) during use. However, their effects and mechanisms on causing endocrine system diseases remain unclear. Here, we established a dietary exposure mouse model using micro and nanoplastics (MNPs) and found that MNPs caused a decrease in thyroid function in adolescent mice. Fecal microbiota transplantation (FMT) was used to reconstruct the intestinal microbiota of mice to reveal the mechanisms of thyroid dysfunction. The abundance of Bacteroides in the intestinal tract significantly changed after FMT. PP-MPs and NPs affected the levels of lysophosphatidylethanolamine and fatty acid esters of hydroxy fatty acids, respectively, which competitively bound to thyrotropin receptor (TSHR) on the thyroid gland, thus affecting the thyroid function. PET-MNPs affected the level of 4-hydroxy-3-methoxyphenylglycol sulfate, which regulated the activity of sympathetic nervous system by acting on the thyrotropin-releasing hormone receptor and TSHR in mice, thereby interfering with the regulatory function of the hypothalamus-pituitary-thyroid (HPT) axis on the synthesis and secretion of thyroid hormones. This study emphasizes the key role of intestinal microbiota-mediated HPT axis in thyroid dysfunction caused by MNP exposure and provides theoretical basis for the prevention of endocrine-related diseases during adolescence caused by MNPs.},
}

@article {pmid41743374,
year = {2026},
author = {Marasco, G and Meacci, D and Sarnelli, G and Tosetti, C and Cremon, C and Savarino, EV and Barbara, G},
title = {Diarrhea management: from pathophysiology to microbiota modulation.},
journal = {Therapeutic advances in gastroenterology},
volume = {19},
number = {},
pages = {17562848261424324},
pmid = {41743374},
issn = {1756-283X},
abstract = {Diarrhea, whether acute or chronic, is a common clinical condition with numerous causes that collectively impose significant health, economic, social, and psychological burdens worldwide. Based on its duration, diarrhea is classified as acute when lasting less than 2 weeks and chronic when persisting for more than 4 weeks. From a pathophysiological standpoint, diarrhea can be categorized into four main types: osmotic, secretory, inflammatory, and motility-related. Acute diarrhea is most commonly caused by infectious gastroenteritis and tends to have a self-limited course. In contrast, chronic diarrhea presents a more complex diagnostic challenge due to its varied etiologies and clinical presentations. A shared feature among many causes of both acute and chronic diarrhea is an alteration in the gut microbiota, a condition referred to as dysbiosis. While acute infections often result in temporary microbial imbalance, chronic conditions such as irritable bowel syndrome and symptomatic uncomplicated diverticular disease are associated with persistent dysbiosis. This review aims to explore the most prevalent causes and underlying mechanisms of acute and chronic diarrhea, with a particular focus on the role of the gut microbiota. It will also examine the principal therapeutic strategies aimed at modulating intestinal microbiota, including prebiotics, probiotics, antibiotics, and fecal microbiota transplantation.},
}

@article {pmid41743065,
year = {2026},
author = {Ren, D and Chai, X and Xiang, C and Zhao, Y and Sun, P and Wang, M and Li, J and Wu, J and Yi, C and Chen, S and Li, E and Zhao, S},
title = {Acer truncatum Bunge seed oil attenuates learning and memory impairment in AD mouse model via modulating gut microbiota and metabolism.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1757330},
pmid = {41743065},
issn = {2296-861X},
abstract = {This study aimed to clarify the neuroprotective effect of Acer truncatum Bunge seed oil (ASO) and its interactions with the gut microbiota in transgenic mice with 5 × Familial Alzheimer's disease (5 × FAD). The AD-transgenic mice were fed with standard diet supplemented with 4% ASO from one to six months of age. The result show that ASO intervention can alleviate learning and memory impairment, enhance motor coordination and endurance, and reduce Aβ deposition in the brains. It also inhibit the proliferation of microglia and astrocytes, decrease the levels of IL-1β, IL-6, and TNF-α in the hippocampus and serum. Then, ASO could increase the Chao1 index and Shannon index, alter the gut microbiota composition, specifically, enhance the growth of gut bacteria correlated with the production of SCFAs, including Ruminococcaceae, Butyricicoccus, Sutterella and others, particularly those related to butyrate production. Additionally, ASO can increase the concentrations of SCFAs in fresh feces and serum, particularly butyric acid. ASO could primarily modulate the biosynthesis of unsaturated fatty acids, glycerophospholipid metabolism, and sphingolipids metabolism in serum. At the same time, Fecal microbiota transplantation (FMT) could reduce Aβ deposition, enhance learning and memory. Finally, Supplementation of sodium Buty also mitigate learning and memory impairments. This study highlights the gut microbiota might be a potential therapeutic target for AD and provides a scientific foundation for developing novel pharmaceuticals or nutraceuticals.},
}

@article {pmid41741396,
year = {2026},
author = {Garcia-Guevara, F and Resink, T and Clasen, F and Uhlén, M and Achour, A and Shoaie, S},
title = {Temporal dynamics of gut biosynthetic gene clusters link persistent colonization and engraftment in fecal microbiota transplantation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2634469},
pmid = {41741396},
issn = {1949-0984},
abstract = {The human gut microbiome carries a large array of biosynthetic gene clusters (BGCs) that encode the production of secondary metabolites, yet their temporal dynamics and role during microbial colonization remain largely unexplored. Here, we tracked BGCs profile over time in a cohort of healthy adults, and identified two distinct groups: persistent, which are stable over time, and transient, which are more sporadic. Functional annotations indicated persistent gene clusters are enriched in antibiotic resistance mechanisms, while transient ones more frequently carry virulence-associated genes. We then examined colonization of these two groups in the context of fecal microbiome transplantation. Our results show that persistent gene clusters exhibit higher colonization rates than transient ones. These findings contribute to our understanding of how microbial metabolites influence host health, potentially guiding future therapeutic strategies targeting the microbiome.},
}

@article {pmid41738638,
year = {2026},
author = {Eriksen, LL and Støy, S and Hansen, MM and Gatten, EP and Erikstrup, C and Kelsen, J and Mullish, BH and Marchesi, JR and Thomsen, KL and Dahlerup, JF and Dahl Baumwall, SM and Hvas, CL},
title = {Dynamics in circulating immune cell subsets after faecal microbiota transplantation for recurrent Clostridioides difficile infection.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001008},
pmid = {41738638},
issn = {2155-384X},
abstract = {BACKGROUND: Faecal microbiota transplantation (FMT) is effective for recurrent Clostridioides difficile infection (rCDI). Adverse reactions to FMT occur early, and cellular immune responses after FMT may contribute to effects and reactions. We compared early changes in peripheral immune cell subsets and clinical outcomes in patients with rCDI who received either FMT and antibiotics or antibiotics alone in a randomized trial.

METHODS: Thirty-five patients with rCDI were randomized to vancomycin and FMT (n=20) or vancomycin alone (n=15). Blood samples were drawn before (wk0) and one week (wk1) after treatment. In three additional patients, blood samples were drawn before, and 24 hours and wk1 after FMT. Adaptive and innate immune cell subsets and gut-homing memory (CD45RO+integrinβ7+) and effector (CD45RO-integrinβ7+) T cells were analysed by flow cytometry.

RESULTS: FMT induced subtle changes in immune cell subsets with no clear pattern from wk0 to wk1. The Treg fraction tended to decrease after FMT, and a similar decrease at 24 hours indicated rapid Tregs dynamics. NKT cells increased during the first 24 hours and returned to baseline level at wk1. Regardless of FMT, patients with clinical resolution from rCDI had a decrease in non-classical monocytes and a shift in gut-homing memory to effector cells at wk1.

CONCLUSION: In rCDI, FMT induced subtle and transient dynamics in peripheral immune cell subsets. Tregs and NKT cells seemed responsive and should be further studied. Cure of CDI may be associated with an increase in circulating gut-homing T cells.},
}

@article {pmid41737395,
year = {2026},
author = {Wen, D and Liu, S and Wu, Y and Zhang, H and Zhang, K},
title = {Fecal microbiota transplantation improves functional constipation through the gut microbiome-bile acid-receptor axis.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1751593},
pmid = {41737395},
issn = {2296-858X},
abstract = {Functional Constipation (FC) is a prevalent gastrointestinal motility disorder worldwide that markedly impairs patients' quality of life, yet the currently available treatment options often show limited efficacy. In recent years, research has gradually revealed the critical role of the gut microbiota and bile acid metabolism in the pathogenesis of FC. Fecal Microbiota Transplantation (FMT), which restores the intestinal microecological balance by transferring gut microbiota from healthy donors, has demonstrated clinical efficacy in promoting bowel movements, improving stool consistency, and enhancing patients' quality of life. However, its underlying mechanisms remain incompletely understood. Current evidence indicates that FMT restores microbial diversity, increases beneficial taxa, and partially reconstructs the bile acids (BAs) profile, thereby modulating Farnesoid X Receptor (FXR) and Takeda G Protein-Coupled Receptor 5 (TGR5) mediated signaling pathways to enhance intestinal secretion and alleviate constipation-related symptoms. The resulting microbiota-bile acid-receptor pathway elucidates the mechanistic link between microbial remodeling and host gastrointestinal motility, thereby offering theoretical support for the therapeutic application of FMT in functional constipation.},
}

@article {pmid41736135,
year = {2026},
author = {Huang, H and Peng, S and Liu, Y and Chen, L and Wu, F},
title = {Fecal microbiota transplantation for advanced non-small cell lung cancer with secondary PD-1 resistance efficacy prognostic factors and microbiome diversity analysis.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07885-w},
pmid = {41736135},
issn = {1479-5876},
support = {2025YLCE0054//Talent Program of Ganzhou Sci-Tech and Medical Joint Program/ ; 82560474//Regional Programs of the National Natural Science Foundation of China/ ; 82560461//Regional Programs of the National Natural Science Foundation of China/ ; 82360507//Regional Programs of the National Natural Science Foundation of China/ ; },
}

@article {pmid41735123,
year = {2026},
author = {D'Arcangelo, G and Paparella, R and Gravina, A and Tarani, F and Tarani, L and Aloi, M and Petrella, C},
title = {Exploring novel biomarkers in pediatric ulcerative colitis: The role of Lipocalin-2, MMP-9, and MMP-9/LCN-2 complex.},
journal = {Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.dld.2026.01.224},
pmid = {41735123},
issn = {1878-3562},
abstract = {BACKGROUND AND AIMS: Lipocalin-2 (LCN-2), Matrix Metalloproteinase-9 (MMP-9), and the MMP-9/LCN-2 complex are emerging biomarkers for ulcerative colitis (UC). While extensively studied in adults, data in children are limited. This study aimed to evaluate their serum levels in children with newly diagnosed UC, compare them with healthy controls, and assess correlations with disease severity and extent.

METHODS: In this prospective case-control study, 32 children with UC (6-18 years) and 38 healthy controls were enrolled. Baseline clinical (Pediatric Ulcerative Colitis Activity Index/ PUCAI), laboratory (albumin, hemoglobin, Erythrocyte Sedimentation Rate, C-reactive protein/CRP, fecal calprotectin), and endoscopic (extent, Ulcerative Colitis Endoscopic Index of Severity/UCEIS) data were collected. Serum LCN-2, MMP-9, and MMP-9/LCN-2 complex levels were measured by ELISA.

RESULTS: Serum LCN-2, MMP-9, and MMP-9/LCN-2 levels were significantly higher in UC patients than controls. ROC analysis indicated LCN-2 had the best diagnostic performance. Higher LCN-2 and MMP-9 levels were observed in children with more severe endoscopic disease (UCEIS > 4) or pancolitis. LCN-2 levels inversely correlated with albumin, whereas MMP-9 positively correlated with CRP and UCEIS.

CONCLUSIONS: LCN-2 and MMP-9 are promising biomarkers in pediatric UC, reflecting disease severity and extent. Their measurement may have clinical utility in monitoring disease progression and guiding management in children.},
}

@article {pmid41735080,
year = {2026},
author = {Yu, Y and Lu, L and Ji, G and Xu, H},
title = {Ecological battle of gut microbiota under drug intervention.},
journal = {Trends in microbiology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tim.2026.01.002},
pmid = {41735080},
issn = {1878-4380},
abstract = {Ecological consequences of drug exposure in the gut microbiota remain difficult to predict. In a recent Cell study, Shi et al. have demonstrated that nutrient competition and interspecies antagonism drive drug-induced microbiome restructuring. Their predictive framework advances mechanistic understanding of drug-microbiome interactions and fecal microbiota transplantation.},
}

@article {pmid41734860,
year = {2026},
author = {Wu, QL and Zhou, YR and Chen, ZR and Liu, MX and Liu, MX and Liu, YF and Li, ZS and Zhao, QR and Zhang, YQ and Zhang, GQ and Zhang, Z and Gong, YT and Tang, C and Yang, T and Du, ZC},
title = {Roles of the gut microbiota in cancer immunotherapy: Mechanistic foundations and therapeutic opportunities.},
journal = {Critical reviews in oncology/hematology},
volume = {221},
number = {},
pages = {105230},
doi = {10.1016/j.critrevonc.2026.105230},
pmid = {41734860},
issn = {1879-0461},
abstract = {Cancer immunotherapy has revolutionized oncological treatment through diverse modalities including immune checkpoint blockade, adoptive cell therapy, therapeutic vaccines, and cytokine-based approaches. Despite these advances, clinical responses remain heterogeneous, with sustained benefit limited to a minority of patients. Emerging evidence now implicates gut microbiota as a critical systemic regulator of immunotherapy efficacy across multiple treatment platforms, mechanistically linking intestinal dysbiosis to antitumor immunity through the gut-immune-tumor axis. Specific commensal taxa and their metabolites, including short-chain fatty acids and tryptophan derivatives, regulate anti-tumor immunity through effector T cell enhancement, dendritic cell activation, and regulatory T cell suppression. This review systematically examines the microbial-metabolite-immune axis, elucidating mechanisms whereby intestinal microbes and metabolites mediate immunotherapy responses. We comprehensively evaluate microbiota-targeting strategies including dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation, providing mechanistic insights and translational frameworks. We further discuss current challenges in transitioning from associative microbiome studies to mechanistic causality, standardizing intervention protocols, and integrating multi-modal microecological data, proposing future directions for engineered probiotics and precision microbial therapeutics to optimize outcomes under current immunotherapy.},
}

@article {pmid41732311,
year = {2026},
author = {Makkieh, Y and Shah, HH and Imran, SB and Pathan, SMK and Saju, AC and Majooju, M and Garg, A and Naag, T and Islam, R and Fahima, C and Ali, R},
title = {The gut-heart axis: Exploring the role of the gut microbiome in cardiovascular health - A focused systematic review.},
journal = {American heart journal plus : cardiology research and practice},
volume = {61},
number = {},
pages = {100687},
pmid = {41732311},
issn = {2666-6022},
abstract = {This focused systematic review examines the role of the gut microbiota in cardiovascular disease (CVD). The review explores mechanisms linking gut dysbiosis with CVD via microbial metabolites such as trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs), which affect inflammation, endothelial function, and lipid metabolism. Interventions including dietary modifications, probiotics, prebiotics, fecal microbiota transplantation, and pharmacological agents such as statins, rifaximin, and empagliflozin are evaluated for their impact on microbial composition and cardiovascular outcomes. Probiotic strains and fiber-rich diets demonstrated modest improvements in blood pressure, lipid profiles, and inflammatory markers. Studies revealed that gut microbiome alterations influence drug metabolism and bleeding risk in patients taking oral anticoagulants. Limited evidence suggests that modulation of the microbiota may reduce chemotherapy-induced cardiotoxicity. However, only nine eligible studies met the inclusion criteria, reflecting the early and heterogeneous nature of this research area. Consequently, these findings should be interpreted as exploratory and hypothesis-generating. The focused review emphasizes the need for large-scale trials to validate microbiome-targeted strategies in CVD prevention and management. This focused systematic review is registered with PROSPERO (ID: CRD420251022190).},
}

@article {pmid41731480,
year = {2026},
author = {Liu, P and Hu, P and Jin, M and Wan, Y and Wu, J and Sun, W and Tang, Y and Huang, L and Zhang, D and Shi, D and Xie, T and Tong, Y and Zheng, H and Wang, L and He, H and Xu, X},
title = {Gut microbiota dysbiosis contributes to diabetic nephropathy via affecting renal lipid deposition and inflammatory responses.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-07832-9},
pmid = {41731480},
issn = {1479-5876},
support = {82304948//National Natural Science Foundation of China/ ; No.2022MHCX01//School-level Project Innovation Project of Minhang Hospital Affiliated to Fudan University/ ; 24ZR1461700//Shanghai Natural Science Foundation/ ; 2024MZYS07//High-Level Specialist Physician Training Program under the Collaborative Health Service System of Medical Education and Research in Minhang District/ ; 2023MHBJ04//Minhang District Central Hospital Topnotch Project/ ; 2025MHZ035//Natural Science Research Project in Minhang District/ ; },
}

@article {pmid41729099,
year = {2026},
author = {Zhang, B and Si, Y and Liu, Y and Wei, J and Li, M and Si, D and Li, H and Wang, X and Han, P and Wang, W and Bao, J and Cheng, L and Lei, Y and Ma, H and Liu, Y},
title = {Simulated microgravity induces cerebral dysfunction by disturbing protective microbiota-metabolite-microglia signaling across the gut‒brain axis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2635820},
pmid = {41729099},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Rats ; *Weightlessness Simulation/adverse effects ; Male ; Fecal Microbiota Transplantation ; *Microglia/metabolism ; Hippocampus/metabolism ; Rats, Sprague-Dawley ; Signal Transduction ; *Brain/metabolism ; },
abstract = {Long-duration spaceflight characterized by microgravity adversely affects operator proficiency postlanding, yet the mechanisms by which microgravity induces cerebral dysfunction refractory to short-term recovery among astronauts remain poorly defined. Here, we demonstrate that simulated microgravity (SMG) leads to chronic behavior disorders and cognitive deficits via a microbiota-metabolite-brain axis. Fecal microbiota transplantation (FMT) from long-term SMG-treated donor rats to recipients (n = 5 per group) under normal gravity (NG) induces anxiety-like behaviors and spatial working memory disturbances by impairing synaptic plasticity in the hippocampus, reproducing the phenotype of SMG-exposed rats. SMG destroys intestinal barriers and alters the gut microbiota to a proinflammatory state with an increased abundance of Proteobacteria but decreased production of linoleic acid (LA) and LA-derived metabolites, which is highly associated with neuroinflammation in the hippocampus. Mechanistically, LA can be taken up by the hippocampus under NG conditions, and then block inflammatory microglial activation by interacting with signal transducer and activator of transcription 1 (STAT1) and inhibiting its phosphorylation at Tyr 701 and Ser 727. However, the Proteobacteria, especially Pseudomonas aeruginosa, tend to be the dominant phylum in gut microbiota under SMG conditions and consume large amounts of LA, breaking LA-dependent immune homeostasis in the central nervous system (CNS). Dietary supplementation with LA significantly mitigated SMG-induced neuroinflammation and cognitive impairment. Taken together, our findings in SD rats models reveal a critical role for gut microbiota dysbiosis in simulated microgravity-associated encephalopathy, offering a novel strategy for LA replenishment to improve brain function during spaceflight.},
}

Animals
*Gastrointestinal Microbiome/physiology
Rats
*Weightlessness Simulation/adverse effects
Male
Fecal Microbiota Transplantation
*Microglia/metabolism
Hippocampus/metabolism
Rats, Sprague-Dawley
Signal Transduction
*Brain/metabolism

@article {pmid41727680,
year = {2026},
author = {Su, B and Cao, Y and Ma, L and Huang, J},
title = {BMI-stratified phenotypes of polycystic ovary syndrome: advances in gut microbiota research and personalized management strategies.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1734041},
pmid = {41727680},
issn = {1664-2392},
mesh = {Humans ; *Polycystic Ovary Syndrome/microbiology/therapy/pathology ; *Gastrointestinal Microbiome/physiology ; Female ; *Body Mass Index ; *Precision Medicine/methods ; *Obesity/complications/microbiology ; Phenotype ; Dysbiosis ; },
abstract = {Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine-metabolic disorder affecting 11%-13% of women of reproductive age. Based on body mass index (BMI), patients can be phenotypically classified into obese and non-obese subgroups: the obese PCOS is characterized by insulin resistance, hyperandrogenemia, and metabolic syndrome, with more pronounced metabolic risks; non-obese PCOS primarily manifests as reproductive endocrine dysfunction. In recent years, studies have shown that the Gut microbiota plays a key role in the pathogenesis of PCOS, and dysbiosis in the obese subgroup is generally more pronounced, potentially amplifying metabolic abnormalities through pathways such as short-chain fatty acids, bile acid disturbances, and endotoxin-related low-grade inflammation. This review systematically summarizes the clinically heterogeneous features of BMI-stratified PCOS and its gut microbiota characteristics, with a focus on elucidating the mechanistic differences between obese and non-obese individuals in terms of inflammation, metabolites, and endocrine regulatory pathways. Based on current evidence, individualized intervention strategies targeting different BMI subtypes are proposed, including dietary and lifestyle modifications, interventions with probiotics/prebiotics/synbiotics, and exploration of emerging precision microbiome therapies such as fecal microbiota transplantation. The interaction between BMI and gut microbiota provides new directions for stratified management and personalized treatment of PCOS; however, high-quality longitudinal and interventional studies are still needed to clarify causal relationships and optimize microbiota-targeted strategies.},
}

Humans
*Polycystic Ovary Syndrome/microbiology/therapy/pathology
*Gastrointestinal Microbiome/physiology
Female
*Body Mass Index
*Precision Medicine/methods
*Obesity/complications/microbiology
Phenotype
Dysbiosis

@article {pmid41727556,
year = {2026},
author = {Millar, BC and Cates, MJ and Torrisi, MS and Round, AJ and Warde, A and Lowery, CJ and Moore, JE},
title = {Antimicrobial Resistance: The Answers.},
journal = {British journal of biomedical science},
volume = {83},
number = {},
pages = {15559},
pmid = {41727556},
issn = {2474-0896},
mesh = {Humans ; *Anti-Bacterial Agents/therapeutic use/pharmacology ; *Drug Resistance, Bacterial ; COVID-19/epidemiology ; SARS-CoV-2 ; },
abstract = {Antimicrobial resistance (AMR) has caused a global public health crisis, contributing to approximately five million deaths in 2019 and predicted deaths of approximately ten million annually by 2050. This equates to approximately 1.4-fold more deaths annually from AMR in 2050 than the entire COVID-19 pandemic to date. To tackle this AMR pandemic, regulatory and policy frameworks have been prepared at local, national and international levels with multi-faceted proposals and advances encompassing surveillance, diagnostics, infection prevention, antibiotic prescribing and variation of existing and novel treatment approaches. This narrative review primarily focuses on research and development which have been documented over the last five years in relation to therapeutic approaches at various stages in clinical development and the potential role that vaccines can play in the fight against AMR. This review provides an overview on antibacterial drugs, including novel classes of antibiotics, which have been recently approved, as well as combination antibiotic therapy and the potential of repurposed drugs. The potential role of novel antimicrobial, antibiofilm and quorum sensing inhibitors, such as antimicrobial peptides, nanomaterials and compounds from the extreme and natural environments, as well as ethnopharmacology including the antimicrobial effects of plants, spices, honey and venoms are explored. Novel therapeutic approaches are critically discussed in terms of their realistic clinical potential, detailing recent and ongoing trials to highlight the current interest of these approaches, including immunotherapy, bacteriophage therapy, antimicrobial photodynamic therapy (aPDT), antimicrobial sonodynamic therapy (aSDT), nitric oxide therapy and microbiome manipulation including faecal microbiota transplantation (FMT). The potential of predatory bacteria as living antimicrobial agents is also discussed. Importantly, there have been many technological developments which have enhanced bioprospecting and research and development of novel antimicrobials which this review draws attention to, including artificial intelligence, machine learning and Organ-on-a-Chip devices. Finally, key messages from the recent World Health Organization report into the role of vaccines against AMR provides an interesting perspective relating to prevention which can be of significance in tackling the AMR burden.},
}

Humans
*Anti-Bacterial Agents/therapeutic use/pharmacology
*Drug Resistance, Bacterial
COVID-19/epidemiology
SARS-CoV-2

@article {pmid41727337,
year = {2026},
author = {Toumazi, D and Charalambous, C and Constantinou, C and Nicolaou, N},
title = {From the gut to the brain: The involvement of the gut microbiota in the development and progression of glioblastoma.},
journal = {Neuro-oncology advances},
volume = {8},
number = {1},
pages = {vdaf267},
pmid = {41727337},
issn = {2632-2498},
abstract = {Glioblastoma (GB) is the most malignant tumor in the adult central nervous system (CNS), presenting substantial treatment challenges due to its infiltrative nature, heterogeneity and immunosuppressive environment it creates. Current therapeutic efforts are focused on enhancing our understanding of GB and developing effective therapies. An emerging area of interest is the bidirectional gut-brain axis, which mediates communication between gut microbiota and CNS. The gut-brain axis allows the microbiota to modulate the immune system and inflammatory pathways through microbial metabolites, such as short-chain fatty acids (SCFAs) and tryptophan derivatives, promoting or suppressing GB progression. Understanding these interactions can lead to microbiota-targeted therapies for GB patients. Novel therapies, such as fecal microbiota transplantation to enhance immunotherapy response and using bacterial toxins to cross the blood-brain barrier, show promise in improving treatment-resistant GB treatment. Additionally, the role of probiotics and antibiotics on GB prognosis is being investigated. While more research is needed to understand the gut microbiota's role in GB, recent findings suggest promising directions for future therapies. This review examines the interplay between key immune system components and the microbiota in GB development and explores how this understanding could facilitate the development of novel therapeutic interventions.},
}

@article {pmid41725847,
year = {2026},
author = {Liu, G and Chen, L and Guan, M and Xiao, N},
title = {Global trends and future perspectives in autism spectrum disorder and gut microbiota research: a comprehensive bibliometric analysis.},
journal = {Frontiers in neuroscience},
volume = {20},
number = {},
pages = {1607951},
pmid = {41725847},
issn = {1662-4548},
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is a heterogeneous neurodevelopmental condition. Increasing studies examine whether gut microbiota alterations and the gut-brain axis are linked to ASD-relevant phenotypes. As the literature expands rapidly, a quantitative mapping is needed to clarify influential work and evolving themes.

OBJECTIVE: To map global research on ASD and the gut microbiota, identify major contributors and knowledge bases, and characterize thematic evolution and emerging fronts.

METHODS: We analyzed 1,391 English-language articles and reviews indexed in the Web of Science Core Collection (1999-2024). CiteSpace, VOSviewer, and R were used to evaluate publication trends, collaboration networks, co-citation structure, keyword clustering, and burst detection.

RESULTS: Publication output increased slowly before 2010 and accelerated after 2018. The United States and China were leading contributors and key collaboration hubs. The co-citation core was anchored by landmark experimental and translational studies, including work on microbiome-to-behavior links and microbiome-targeted interventions. Keyword clustering and timeline views highlighted three prominent thematic directions: fecal microbiota transplantation, Rett syndrome, and maternal immune activation. Recurrent and burst keywords emphasized the gut-brain axis, short-chain fatty acids, gastrointestinal symptoms, and oxidative stress. Recent burst terms, including obesity, major depressive disorder, and glutamate, suggest increasing connections to metabolic and broader psychiatric dimensions.

CONCLUSION: ASD-microbiome research has shifted from descriptive comparisons toward mechanism-oriented and intervention-relevant questions. Future progress will benefit from standardized protocols, longitudinal designs, and multi-omics integration, together with rigorously designed trials to evaluate microbiome-targeted strategies.},
}

@article {pmid41724232,
year = {2026},
author = {Tang, H and Sulaiman, JE and Zhang, Y and Yang, Y and Wang, J and Zhong, W and Lei, H and Liu, Y},
title = {Cyanidin-3-O-glucoside alleviates aflatoxin B1-induced splenic immunotoxicity via gut microbiota remodeling.},
journal = {Environmental pollution (Barking, Essex : 1987)},
volume = {396},
number = {},
pages = {127856},
doi = {10.1016/j.envpol.2026.127856},
pmid = {41724232},
issn = {1873-6424},
abstract = {While the hepatotoxicity of aflatoxin B1 (AFB1) is well characterized, its immunotoxicity remains overlooked. This study investigates whether cyanidin-3-O-glucoside (C3G), a bioactive polyphenolic flavonoid, can alleviate AFB1-induced immunotoxicity. Our results demonstrated that C3G significantly ameliorated AFB1-induced splenic injury, which was associated with the suppression of the NLRP3/caspase-1/GSDMD pyroptosis pathway and reduced expression of IL-1β and IL-18. Furthermore, C3G modulated the gut microbiota by enriching specific beneficial bacteria (e.g., Alistipes and Candidatus Saccharimonas) and reversed AFB1-induced metabolic disorders. Transplantation of fecal microbiota from C3G-pretreated donor mice reproduced the protective effect of C3G in mice exposed to AFB1, whereas sterile fecal filtrate transplantation only offered partial relief, indicating that the core mechanism depends on viable microbiota. In summary, C3G alleviates AFB1-induced splenic injury by restructuring the dysbiotic gut microbiota into a more enriched community. This remodeling restores metabolic homeostasis and inhibits NLRP3-mediated pyroptosis via the gut-spleen axis. Our findings demonstrate that C3G alleviates AFB1-induced splenic immunotoxicity by remodeling the gut microbiota via the gut-spleen axis, establishing a novel microbiota-dependent strategy mediated by natural polyphenols.},
}

@article {pmid41724218,
year = {2026},
author = {Liu, J and Liu, T and Nie, L and Zhou, L and Luo, J and Guo, L and Zhang, X and Gong, M and Chen, Z and Li, X and Fan, X},
title = {Semaglutide attenuates autistic-like behaviors in BTBR mice through the shaping of gut microbiota.},
journal = {Pharmacological research},
volume = {225},
number = {},
pages = {108149},
doi = {10.1016/j.phrs.2026.108149},
pmid = {41724218},
issn = {1096-1186},
abstract = {Autism spectrum disorder (ASD) is a multifaceted neurodevelopmental condition characterized by deficits in social communication and the presence of repetitive behaviors. The significance of the gut-brain axis in the pathogenesis of ASD often points to a relationship with gut dysbiosis and metabolic disruptions in affected individuals. This study investigates the potential of the glucagon-like peptide-1 receptor agonist, semaglutide, to modulate gut microbiota, metabolic pathways, and neurodevelopmental outcomes using the BTBR T(+) Itpr3(tf)/J (BTBR) mouse model of ASD. Our findings indicate that administration of semaglutide during an early neurodevelopmental stage leads to significant improvements in social behavior, cognitive function, and repetitive behaviors in BTBR mice. This therapeutic effect is associated with the restoration of gut microbiota, as demonstrated by fecal microbiota transplantation from C57BL/6 J controls and semaglutide-treated BTBR mice, which ameliorated the ASD behaviors in BTBR mice. Metabolomic profiling identified adrenic acid (AdA) as a crucial mediator; AdA levels in BTBR mice were lower but returned to normal following semaglutide treatment. Additionally, RNA sequencing revealed that hippocampal neurogenesis is associated with semaglutide treatment, and AdA supplementation restored social behaviors and hippocampal neurogenesis. These results highlight the critical role of the gut microbiota-brain axis in the therapeutic effects of semaglutide on ASD and suggest that targeting this axis alongside AdA may represent a promising strategy for ASD.},
}

@article {pmid41723574,
year = {2026},
author = {Benedé-Ubieto, R and Estévez-Vázquez, O and Acar, R and Leal-Lassalle, H and Gutierrez, AH and Redondo-Urzainqui, A and Iborra, S and Odintsova, VE and Tyakht, A and Herranz, JM and Firat, Z and Basol, M and Korkmaz, B and Sanz-García, C and Juanola, O and Caparrós, E and Francés, R and Ciudin, A and Pericàs, JM and Gómez-Santos, B and Aspichueta, P and Treichel, N and Clavel, T and Reißing, J and Bruns, T and Bartneck, M and Mazariegos, MS and Wolters, JC and Jorquera, G and Liedtke, C and Vaquero, J and Bañares, R and Cakan-Akdogan, G and Ávila, MA and Konu, O and Cubero, FJ and Nevzorova, YA},
title = {Alcohol consumption in metabolic dysfunction-associated steatotic liver disease (MASLD): understanding the gut-liver crosstalk for clinical translation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2631834},
pmid = {41723574},
issn = {1949-0984},
mesh = {Animals ; Humans ; *Gastrointestinal Microbiome/drug effects ; Mice ; Male ; *Liver/metabolism/pathology/drug effects ; Disease Models, Animal ; *Alcohol Drinking/adverse effects ; Zebrafish ; Mice, Inbred C57BL ; Diet, High-Fat/adverse effects ; *Fatty Liver/microbiology/metabolism/etiology ; Hep G2 Cells ; Fecal Microbiota Transplantation ; Female ; Diet, Western/adverse effects ; Hepatocytes/metabolism ; Dysbiosis ; Middle Aged ; },
abstract = {OBJECTIVE: In the present study, we investigated the role of the gut-liver crosstalk in the pathogenesis of steatotic liver disease (SLD) induced by the compounding and deleterious effects of alcohol and metabolic risk factors, and explored the potential translational aspects of microbiome-based interventions.

DESIGN: The effects of combined exposure to alcohol and a high-fat, high-cholesterol diet (HFHC) Western diet (WD) were tested in a dietary mouse DUAL model and compared to mice fed only with WD. Liver and gut phenotypes were evaluated via histochemistry, flow cytometry, gene expression, proteomic, and metabolomic analyses. The effects on the gut microbiota were studied in both DUAL mice and MASLD patients with a history of alcohol consumption. Antibiotic-induced microbiota depletion (AIMD) and microbiota modulation therapies (probiotics and fecal microbiota transplant (FMT)) were performed in mice. Primary human hepatocytes and HepG2 cells were used to study the underlying mechanisms. Zebrafish larvae exposed to alcohol and a HFHC diet were used as a validation model.

RESULTS: Alcohol in combination with WD synergistically exacerbated SLD. DUAL-diet-induced disruption of the intestinal barrier led to LPS leakage into the bloodstream and subsequent TLR4-mediated hepatic inflammation. This, together with enhanced intestinal fat absorption, and impaired intrahepatic lipid oxidation - particularly due to insufficient CPT-1 activity - contributed to prominent steatohepatitis. The DUAL-induced changes in the gut microbiota showed similarities to human dysbiosis in MASLD patients who consumed alcohol, including an increase in Bacteroides and Alistipes. AIMD improved pathology, indicating a causal role of the microbiota in the pathophysiology of DUAL steatohepatitis, whilst early microbiome modulation via FMT induced mild improvements in liver and gut physiology.

CONCLUSIONS: These results indicated that the microbiota‒gut‒liver axis plays a crucial role in the progression of SLD intensified by alcohol and concurrent metabolic risk factors, thus providing a promising translational target for potential therapeutic interventions.},
}

Animals
Humans
*Gastrointestinal Microbiome/drug effects
Mice
Male
*Liver/metabolism/pathology/drug effects
Disease Models, Animal
*Alcohol Drinking/adverse effects
Zebrafish
Mice, Inbred C57BL
Diet, High-Fat/adverse effects
*Fatty Liver/microbiology/metabolism/etiology
Hep G2 Cells
Fecal Microbiota Transplantation
Female
Diet, Western/adverse effects
Hepatocytes/metabolism
Dysbiosis
Middle Aged

@article {pmid41723572,
year = {2026},
author = {Liang, H and Ding, X and Liu, S and Tong, S and Wang, X and Zhang, Z and Wang, W and Zhang, X and Yuan, Y and Jiang, Y and Sun, T},
title = {Aging-caused the changes of the gut microbiota drive intestinal barrier dysfunction and increase sepsis susceptibility.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2630475},
pmid = {41723572},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome/physiology ; Animals ; Mice ; *Sepsis/microbiology/metabolism ; Humans ; *Aging ; Male ; Feces/microbiology ; Mice, Inbred C57BL ; Histamine/metabolism ; *Intestinal Mucosa/metabolism/microbiology ; Female ; Bacteria/classification/genetics/isolation & purification/metabolism ; Fecal Microbiota Transplantation ; Aged ; Disease Susceptibility ; Disease Models, Animal ; Middle Aged ; },
abstract = {Physiological and pathological changes associated with aging contribute to deteriorating disease prognosis in sepsis. However, the mechanisms by which these disturbances exacerbate inflammation remain underexplored. In this study, fecal samples were collected from aged and young septic patients and mice and subsequently transplanted into young pseudo-germ-free mice via fecal microbiota transplantation. Fecal, colon tissue, and blood samples were collected to be used 16S rDNA sequencing to characterize the gut microbiota, histopathological examination, enzyme-linked immunosorbent assay and FITC-dextran intestinal permeability assay to assess gut injury and gut barrier function. Additionally, nontargeted and targeted metabolomics were used to identify differential metabolites in the feces of aged and young septic mice. To further validate the roles of specific bacterial strains and their metabolites in sepsis, genetically engineered bacteria were used in both in vivo and in vitro experiments. The results showed that an increased abundance of Klebsiella aerogenes (K. aero) in aged hosts, which led to elevated histamine (HA) production and exacerbated intestinal barrier dysfunction. Importantly, K. aero strains carrying a histidine decarboxylase gene variant were identified as major HA producers. Mechanistically, HA was shown to drive intestinal barrier dysfunction by inhibiting Nlrp6 expression and its subsequent binding to LC3, thereby impairing autophagy. Treatments that modulated HA levels or overexpressed Nlrp6 ameliorated inflammation in septic mice. These findings suggest that targeting the HA-Nlrp6-LC3 axis could offer a novel therapeutic approach for managing sepsis, particularly in aged populations.},
}

*Gastrointestinal Microbiome/physiology
Animals
Mice
*Sepsis/microbiology/metabolism
Humans
*Aging
Male
Feces/microbiology
Mice, Inbred C57BL
Histamine/metabolism
*Intestinal Mucosa/metabolism/microbiology
Female
Bacteria/classification/genetics/isolation & purification/metabolism
Fecal Microbiota Transplantation
Aged
Disease Susceptibility
Disease Models, Animal
Middle Aged

@article {pmid41722712,
year = {2026},
author = {Beales, JT and Mohanty, V and Seng, MM and Tapp, ZM and Sardesai, SD and Williams, NO and Gatti-Mays, ME and Stover, DG and Sudheendra, PK and Wesolowski, R and Bailey, MT and Ni, A and Cologna, SM and Pyter, LM},
title = {Gut microbiota and metabolite disruption during breast cancer chemotherapy is associated with peripheral neuropathy sensory symptoms and pain.},
journal = {Brain, behavior, and immunity},
volume = {135},
number = {},
pages = {106489},
doi = {10.1016/j.bbi.2026.106489},
pmid = {41722712},
issn = {1090-2139},
abstract = {Chemotherapy-induced peripheral neuropathy (CIPN) is a common and serious adverse effect of chemotherapeutic agents such as taxanes, platinum compounds, and vinca alkaloids. Efforts to prevent and treat CIPN are impeded by an incomplete understanding of its pathogenesis. Recently, the gut microbiota has been causally linked to CIPN in rodent models. However, human studies exploring this connection are limited. Here, in a cohort of 70 patients with early-stage breast cancer, relationships between disruptions in the gut microbiota during chemotherapy and both participant CIPN symptoms and general pain symptoms were investigated. Study participants provided fecal samples (for 16S rRNA sequencing and targeted metabolomics), blood samples, and sensory symptom information during the three days prior to their first and their final chemotherapy (including a taxane drug) infusions. Sensory neuropathy symptoms increased during treatment, as did circulating levels of neurofilament light chain (NFL), a putative biomarker of CIPN. Decreases in microbiota alpha diversity during chemotherapy were associated with worse neuropathy symptoms during treatment, along with worsening of general pain, after controlling for pre-treatment baseline symptoms. Larger shifts in beta diversity from baseline to last infusion also coincided with more severe neuropathy symptoms. Bacterial producers of short-chain fatty acids were decreased in participants with neuropathy symptoms at the final chemotherapy infusion. Furthermore, decreases in fecal levels of short-chain fatty acids during treatment were related to worse neuropathy symptoms, suggesting a potential mechanism by which gut microbiota alterations could influence CIPN. Collectively, these findings corroborate preclinical work linking the gut microbiota to CIPN and provide evidence of potential microbiota involvement in general pain symptoms as well. Larger confirmatory studies in the future could support microbiota-targeted interventions for CIPN, such as fecal microbiota transplants or dietary interventions.},
}

@article {pmid41722699,
year = {2026},
author = {Shang, A and Shen, J},
title = {Gut microbiota and their metabolites in stroke: From mechanistic study toward therapeutic perspectives.},
journal = {Pharmacological research},
volume = {225},
number = {},
pages = {108147},
doi = {10.1016/j.phrs.2026.108147},
pmid = {41722699},
issn = {1096-1186},
abstract = {Stroke is a medical emergency with high incidence, mortality, disability rate, and multiple complications, which place a serious burden on families and society. Clinically, gastrointestinal dysfunction has been observed in a significant percentage of stroke patients, suggesting that gut microbiota may be a viable target for stroke prevention and therapy. In this review, we summarized the alterations in the intestinal environment following stroke across clinical and preclinical models, highlighting the changes in the major bacterial communities, including Bacteroidetes, Firmicutes, Proteobacteria and Actinomycetota, etc. Considering the connection between the brain-gut axis, we discussed the therapeutic potential for treating ischemic stroke by modulating the gut microbiota, including protection of the blood-brain barrier (BBB) and the intestinal barrier, as well as the application of fecal microbiota transplantation (FMT). Furthermore, we highlighted the main mechanisms of regulating gut microbiota to improve stroke outcomes, involving intestinal metabolites such as short-chain fatty acids (SCFAs), trimethylamine N-oxide (TMAO), and phenylacetylglutamine (PAGln), endotoxin, hormones, and amino acids, as well as factors related to immunity, inflammation, and oxidative stress. Finally, we summarized potential targeted therapeutic approaches, such as natural small molecules, engineered probiotics, and bile acid-nanoparticles, etc. Collectively, these insights support the gut microbiota as a promising target for mitigating stroke risk, attenuating acute injury, and enhancing recovery.},
}

@article {pmid41722622,
year = {2026},
author = {Allen, SL and Breen, L and Lord, JM and Duggal, NA},
title = {Age-related sarcopenia and the gut microbiome: mechanistic insights into the gut-muscle axis and potential microbiome based therapeutic interventions.},
journal = {Ageing research reviews},
volume = {},
number = {},
pages = {103065},
doi = {10.1016/j.arr.2026.103065},
pmid = {41722622},
issn = {1872-9649},
abstract = {Ageing is associated with a loss of skeletal muscle mass, strength and function, termed sarcopenia. The presence of sarcopenia is known to be problematic leading to an increased risk of falls, fractures and mortality. Age-related changes in the gut microbiome, characterized by reduced diversity and altered metabolite production, may compromise intestinal barrier function, leading to increased permeability. These age-associated changes in the gut microbiome led to changes in circulating microbial metabolites and toxins, such as a decrease in short-chain fatty acids, an increase in lipopolysaccharides and an imbalance in bile acid production. Together these alterations may contribute to the development of sarcopenia through impairments in muscle protein turnover. Currently, lifestyle-based approaches e.g., exercise and diet, alongside the use of pre-, pro- and post-biotics have been proposed as strategies to target the gut-muscle axis and combat the risk of sarcopenia in the expanding ageing population. However, little evidence is available to support their use within clinical settings. Several new strategies including the nutraceutical Urolithin A and faecal microbiome transplants (FMT) have been suggested to treat age-related sarcopenia. This review provides insight into the potential interactions of the gut microbiome and skeletal muscle with ageing and sarcopenia development, alongside potential new and existing countermeasures.},
}

@article {pmid41721978,
year = {2026},
author = {Mokhtari, H and Hoseini, MHM and Hashemi, SM and Tahvildari, S and Yeganeh, F},
title = {Intrarectal delivery of chitosan hydrogel-encapsulated mesenchymal stem cell-conditioned media attenuates disease severity in experimental ulcerative colitis.},
journal = {Inflammopharmacology},
volume = {},
number = {},
pages = {},
pmid = {41721978},
issn = {1568-5608},
support = {43002260//Deputy of Research, Faculty of Medicine, Shahid Beheshti University of Medical Sciences/ ; },
abstract = {BACKGROUND: Ulcerative colitis (UC) is a chronic inflammatory disease characterized by mucosal immune dysregulation and epithelial injury. While mesenchymal stem cells (MSCs) hold regenerative and immunomodulatory promise, their use entails safety and logistical challenges. MSC-derived conditioned medium (MSC-CM) may offer a safer, cell-free alternative. Here, we present a novel intrarectal delivery strategy that pairs MSC-CM with a mucoadhesive chitosan hydrogel (Cs-Hyd), aiming for localized mucosal therapy in colitis.

METHODS: Experimental colitis was induced in mice via DSS exposure. Human MSCs were cultured under standardized conditions to generate CM enriched in immunoregulatory factors. This CM was loaded into a chitosan hydrogel, validated for mucoadhesion and release kinetics, and administered intrarectally. Clinical metrics (weight loss, stool consistency, fecal blood), colon length, histopathology, cytokine profiles, and myeloperoxidase (MPO) activity were assessed. Data were analyzed via ANOVA with post hoc Tukey correction; significance was set at p < 0.05.

RESULTS: In the DSS model, 60% mortality was observed by day 10, whereas the Cs-Hyd containing MSC-CM (Cs-Hyd-CM) group achieved 100% survival (n = 4-6, log-rank p = 0.034). Cs-Hyd-CM-treated mice exhibited substantially less weight loss (- 5.2 ± 1.3% vs. - 15.1 ± 2.2%; repeated-measures ANOVA, p = 0.008), lower Disease Activity Index (DAI: 2.1 ± 0.6 vs. 8.0 ± 0.9; p = 3.2 × 10[-4]), and preserved colon length (7.5 ± 0.4 cm vs. 6.0 ± 0.3 cm; p = 6.2 × 10[-3]). Histology scores decreased by ~ 70% (4.0 ± 0.7 vs. 12.1 ± 0.8; p = 3.1 × 10[-6]), confirming mitigation of ulceration and inflammation. Treatment with Cs-Hyd-CM reduced TNF-α by ~ 40% vs DSS-only (104.5 ± 6.8 → 63.8 ± 8.7 pg/mg; p = 4.6 × 10[-4]) while restoring IL-10 toward normal levels (p = 3.0 × 10[-3]). MPO activity dropped ~ 52% (76.5 ± 3.4 → 36.8 ± 5.3 U/mg; p = 8.4 × 10[-4]). Collectively, Cs-Hyd-CM significantly attenuated disease severity and promoted mucosal healing in DSS colitis.

CONCLUSIONS: Local intrarectal delivery of MSC-CM via chitosan hydrogel substantially alleviates experimental UC. This cell-free platform leverages MSC secretome functions, immunomodulation, barrier restoration, and controlled retention, while avoiding the complexities and risks of cell transplantation.},
}

@article {pmid41720783,
year = {2026},
author = {Lee, JM and Kim, MJ and Lee, H and Hyun, Y and Nam, SW and Jeon, DG and Shin, JH and Kim, ES},
title = {Maternal gut microbial legacy shapes intestinal health and susceptibility of offspring to colitis.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00938-4},
pmid = {41720783},
issn = {2055-5008},
support = {RS-2021-NR060094//National Research Foundation of Korea/ ; 2023R1A2C2005817//National Research Foundation of Korea/ ; 2021R1A6C101A416//Ministry of Education/ ; 2021R1A6C101A416//Ministry of Education/ ; 2021R1A6C101A416//Ministry of Education/ ; },
abstract = {Maternal gut dysbiosis caused by inflammatory bowel disease during pregnancy can affect the gut health of the offspring by altering the composition of the gut microbiota, as well as immune function; however, the underlying mechanisms and potential for therapeutic intervention remain unclear. This study investigated the impact of maternal colitis on the gut health of offspring, and assessed the therapeutic potential of microbial manipulation. Offspring born to mothers with colitis exhibited gut microbial dysbiosis characterized by Lactobacillus spp. depletion, impaired barrier function, low-grade intestinal inflammation, compromised Wnt signaling, reduced crypt cell proliferation and diminished organoid-forming capacity, all of which increased their susceptibility to colitis in adulthood. Notably, early-life interventions such as fecal microbiota transplantation (FMT), targeted supplementation with Lactobacillus and cross-fostering during the postnatal period effectively reshaped the gut microbiota and reduced the risk of developing colitis later in life. These findings underscore the critical impact of the prenatal maternal gut microbial community on programming offspring intestinal barrier function and immune homeostasis, thereby influencing lifelong disease susceptibility. Moreover, the early-postnatal period represents a crucial therapeutic window in which microbial interventions like FMT can effectively mitigate gut dysbiosis and confer long-term protection against colitis.},
}

@article {pmid41719127,
year = {2026},
author = {Wang, S and Su, LY and Lan, D and Pan, H and Xiong, M and Yao, M and Deng, Y and Fan, Z and Cao, Y and Zhou, H},
title = {Adenosine signaling driven by the gut microbiota underlies chronic alcohol-induced anesthetic resistance.},
journal = {Cell reports},
volume = {45},
number = {3},
pages = {117015},
doi = {10.1016/j.celrep.2026.117015},
pmid = {41719127},
issn = {2211-1247},
abstract = {Chronic alcohol consumption increases anesthetic tolerance, yet the underlying in vivo mechanisms remain unclear. Here, we demonstrate that long-term alcohol exposure reduces anesthetic efficacy in both humans and mice, prolonging induction and shortening maintenance. Fecal microbiota transplantation from alcohol-exposed donors recapitulated this phenotype in naive mice, indicating a causal role of gut microbiome alterations. Metagenomic and metabolomic analyses identified elevated adenosine as a key microbiota-derived metabolite. Adenosine supplementation decreased anesthetic sensitivity, likely via downregulation of gamma-aminobutyric acid (GABA) receptors. Our findings reveal a gut microbiota-adenosine pathway mediating alcohol-induced anesthetic resistance.},
}

@article {pmid41718442,
year = {2026},
author = {Stafford, WH and McArthur, J and Ghafoor, S},
title = {Critical Intestinal Perforations in Pediatric Immunocompromised Patients: A Case-Based Review.},
journal = {Pediatric reports},
volume = {18},
number = {1},
pages = {},
pmid = {41718442},
issn = {2036-749X},
abstract = {As survival rates for children with cancer and immune disorders have improved, clinical focus has shifted toward managing serious treatment-related complications. Intestinal perforation remains life-threatening and is typically diagnosed by signs of peritonitis and inflammation. This report presents three high-risk pediatric patients who developed severe intestinal perforation without the usual clinical symptoms. Each patient was receiving high-dose corticosteroids and/or targeted biologic immunomodulators (ruxolitinib, anakinra, tocilizumab, eculizumab). Classic indicators such as fever, leukocytosis, hemodynamic instability, and abdominal pain were absent, despite surgical findings of fecal contamination and bowel necrosis. All three patients survived to hospital discharge. These cases demonstrate that potent immunomodulatory therapies can mask the physiological response to perforation. Relying solely on traditional clinical signs may delay diagnosis. In this population, subtle findings such as persistent gastrointestinal bleeding, feeding intolerance, or minor imaging abnormalities should prompt consideration of perforation. Early imaging and multidisciplinary review are essential for timely intervention and improved outcomes.},
}

@article {pmid41716824,
year = {2026},
author = {Ge, C and Zou, C and Lv, Y and Huang, W and Luo, X and Wu, L and Hu, Z and Zhan, S and Shen, X and Lin, G and Yu, D and Liu, B},
title = {Trace mineral sources affect oxidized oil induced intestinal damage in chickens by modulation of gut microbiota and short-chain fatty acid metabolism.},
journal = {Animal nutrition (Zhongguo xu mu shou yi xue hui)},
volume = {24},
number = {},
pages = {522-533},
pmid = {41716824},
issn = {2405-6383},
abstract = {This study investigated in vivo interactions between oil quality and trace mineral sources (organic vs. inorganic) on oxidative stress and intestinal damage in chickens. A total of 360 one-day-old male Lingnan yellow-feathered chickens with similar initial body weight (40 ± 2 g) were randomly assigned to four treatments in a 2 × 2 factorial design, with two oil qualities (fresh or oxidized) and two trace mineral sources (inorganic or organic). The experiment lasted for 21 days, with 6 replicates per treatment and 15 birds per replicate. Results showed that oxidized soybean oil (OSO) impaired jejunal barrier function (damaged morphology, downregulated tight junction genes), associated with reduced antioxidant capacity, elevated proinflammatory cytokines, and altered gut microbiota/short-chain fatty acid (SCFA) metabolism. Significant interactions were observed between oil quality and trace mineral sources (P < 0.05): only in the OSO group, organic trace minerals (OTM) outperformed inorganic ones (ITM) in enhancing total antioxidant capacity (P = 0.005) and glutathione peroxidase activity (P = 0.001), suppressing proinflammatory cytokines (e.g., interleukin-1β, P = 0.019; interleukin-2, P = 0.019; interleukin-6, P = 0.014; tumor necrosis factor-α, P = 0.001), increasing SCFA-producing bacteria (e.g., Lactobacillus and Butyricicoccus) while reducing pathogens (e.g., Helicobacter), and elevating SCFAs (P = 0.030). Furthermore, targeted metabolomic analysis revealed that OTM significantly increased the production of SCFAs, especially butyric acid (P = 0.001), which were positively correlated with the OTM-enriched microbiota. Mantel-test analysis revealed that the altered microbiota and metabolites showed strong correlations with specific parameters of intestinal health. The fecal microbiota transplantation experiment further confirmed that the intestinal protective effect is likely mediated by OTM-altered gut microbiota and their metabolites. In summary, the replacement of ITM by OTM in chicken diets can minimize the negative impact on OSO induced intestinal damage by improving intestinal barrier function and alleviating inflammatory responses mediated by gut microbiota modulation and SCFA metabolism.},
}

@article {pmid41716676,
year = {2026},
author = {Wang, R and Tong, A and Jin, K and Yu, R and Lin, D and Yang, D and Liu, X and Cui, J and Niu, J and Cui, Y and Zhu, H and Zhou, M},
title = {Harnessing the gut-immune-joint axis: Oral microalgae-based thermoresponsive microspheres enhance intra-articular therapy for rheumatoid arthritis.},
journal = {Bioactive materials},
volume = {61},
number = {},
pages = {72-91},
pmid = {41716676},
issn = {2452-199X},
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disease primarily caused by an aberrant immune response that erroneously attacks the synovial joints, leading to inflammation and joint damage. Emerging evidence suggests that impaired intestinal barrier integrity and imbalanced gut microbiota play crucial roles in driving RA development, promoting systemic inflammation, and exacerbating joint pathology. Here we propose a synergistic therapeutic strategy that concurrently addresses both the systemic gut-immune axis and local joint inflammation. This approach integrates intra-articular injection of triamcinolone acetonide (TAA) with oral administration of thermoresponsive microspheres encapsulating Chlorella vulgaris (CV) and ginseng polysaccharides (GPS), designated as CG@GelMA. The microspheres undergo temperature-induced gelation at body temperature, thereby facilitating gastric transit and enabling prolonged drug release in the intestinal tract. Oral administration of CG@GelMA restored intestinal barrier function by enhancing tight junction protein expression and exerting anti-inflammatory effects, while intra-articular TAA synergistically alleviated synovial inflammation, improved locomotor function, and preserved bone and cartilage integrity. Moreover, the combination therapy elicited superior immune modulation, characterized by increased regulatory T cells, reduced Th17 cells, and a systemic cytokine shift toward elevated interleukin-10 and reduced interleukin-17. Notably, this systemic immunomodulation was driven by CG@GelMA-mediated remodeling of the gut ecosystem, which enriched beneficial taxa (e.g., Lactobacillus), reduced potentially pathogenic genera (e.g., Escherichia-Shigella), and, importantly, led to a significant increase in the intestinal levels of immunomodulatory metabolites, including several short-chain fatty acids (SCFAs). Fecal microbiota transplantation (FMT) and depletion studies definitively established the gut microbiota as the central mediator of these therapeutic effects. Together, these findings highlight a synergistic combinatorial strategy that couples microbiota-driven systemic immunomodulation with potent local anti-inflammatory effects, offering a promising avenue for the treatment of RA and other systemic inflammatory disorders.},
}

@article {pmid41716460,
year = {2026},
author = {Guo, Y and Wang, X and Wu, Y and Li, Y and Wei, X},
title = {The role of the microbial-immune-bone axis in bone tumor development: mechanistic integration, systems modeling, and intervention prospects.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1762046},
pmid = {41716460},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; *Bone Neoplasms/immunology/pathology/microbiology ; Tumor Microenvironment/immunology ; *Bone and Bones/immunology/pathology ; Bone Remodeling ; },
abstract = {The emergence and development of bone tumors stem from a combination of intrinsic genetic alterations in tumor cells, remodeling of the bone marrow microenvironment, and shifts in the host's systemic immune-metabolic state. In recent years, gut microorganisms have been shown not only to influence bone mass regulation and conditions involving disrupted bone homeostasis, such as osteoporosis, but also to substantially affect the formation of primary bone tumors and metastatic lesions by modulating immune cell differentiation, inflammatory activity, and the coupling of bone remodeling. Focusing on the "Microbiota-Immune-Bone axis" (MIB), a growing body of fundamental and translational research indicates that alterations in gut microbial composition and function can reshape metabolite profiles-including short-chain fatty acids, bile acids, indole derivatives-and pathogen-associated molecular patterns (PAMPs). These signals act on the intestinal barrier and bone marrow immunity through G-protein-coupled receptors, nuclear receptors, and pattern-recognition receptors, thereby shifting the balance between bone resorption and formation and modifying the immune characteristics of the bone microenvironment, ultimately facilitating bone tumor cell colonization, proliferation, and immune escape. This review takes the MIB axis as its central framework to integrate the major pathways through which gut microbes and their metabolites regulate intestinal and myeloid immunity, bone remodeling, and bone tumor biology, to construct a systems-level model of tumor initiation and progression, to identify druggable signaling nodes, and to assess the potential and challenges of microbiota-modulating approaches-including antibiotics, probiotics, dietary strategies, and fecal microbiota transplantation-in preventing and treating bone tumors, thereby offering a theoretical foundation for developing integrated interventions targeting the gut microbiota and the MIB axis.},
}

Humans
*Gastrointestinal Microbiome/immunology
Animals
*Bone Neoplasms/immunology/pathology/microbiology
Tumor Microenvironment/immunology
*Bone and Bones/immunology/pathology
Bone Remodeling

@article {pmid41716434,
year = {2026},
author = {Mohiuddin, M},
title = {Chronic Antibiotic Use, Gut Microbiota Dysbiosis, and Increased Risk of Colorectal Cancer: An Emerging Threat.},
journal = {Health science reports},
volume = {9},
number = {2},
pages = {e71866},
pmid = {41716434},
issn = {2398-8835},
abstract = {BACKGROUND AND AIMS: The gut microbiota plays a vital role in host health by regulating metabolic processes, immune function, and epithelial barrier functions. Chronic use of antibiotics can alter this environment and introduce gut dysbiosis, which is defined as an alteration of microbial communities characterized by a loss of beneficial microbes and overgrowth of pathogenic microbes. Gut dysbiosis is increasingly associated with the development and progression of colorectal cancer (CRC). We explored the relationship between long-term antibiotic exposure, gut microbiota dysbiosis, and CRC risk, as well as strategies for preventing and restoring gut microbiomes.

METHODS: Relevant information was extracted from published articles available in PubMed, Scopus, and Google Scholar. The keywords "Gut," "Dysbiosis," "Antibiotic," "Colorectal," and "Microbiota" were used to search for relevant information.

RESULTS: Studies have demonstrated that chronic antibiotic exposure significantly reduces microbial diversity, particularly by decreasing beneficial species (e.g., Lactobacillus, Bifidobacterium, and Faecalibacterium), while favoring pathogenic species (e.g., Klebsiella pneumoniae and Enterococcus faecium). Antibiotic-induced dysbiosis reduces the production of microbial metabolites, including short-chain fatty acids, which are essential for supporting epithelial integrity and immune homeostasis. Prior antibiotic use is associated with a 13% increased risk of CRC, with antibiotic-induced microbiota alterations lasting for months to years. Several factors, including diet, pollution, and over-the-counter access to antibiotics in low-and middle-income countries, may contribute to an increased risk of dysbiosis and CRC. Additionally, interventions such as dietary fiber, probiotic supplementation, fecal microbiota transplantation, next-generation probiotics, and phage therapy may be potential strategies to restore the microbiome and achieve gut health.

CONCLUSION: Substantial use of antibiotics may alter the gut microbiota and increase the risk of CRC. To mitigate this risk, it is essential to practice prudent antibiotic use and adopt dietary, probiotic, and microbiome-restoring practices to support the health of the gut microbiome.},
}

@article {pmid41716280,
year = {2026},
author = {Jiang, HB and Zhang, JQ and Liang, H and Sun, LY and Deng, CQ and Yang, SF},
title = {Exploring osteosarcopenia from the gut microbiota perspective: mechanistic insights and therapeutic potentials based on the gut-muscle-bone Axis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1729870},
pmid = {41716280},
issn = {1664-302X},
abstract = {The aging society presents a growing challenge in the form of osteosarcopenia (OS). This syndrome is marked by the concomitant deterioration of bone (osteoporosis) and muscle (sarcopenia), and significantly elevates the risks of fractures, disability, and mortality. Despite its clinical relevance, the shared pathophysiology and effective interventions for OS remain elusive. Emerging evidence highlights the gut microbiota (GM) as a critical modulator of musculoskeletal health. This review integrates current evidence to delineate "gut-muscle-bone Axis" framework, summarizing current evidence on how GM dysbiosis may be involved in OS through multifaceted mechanisms, including intestinal barrier disruption, chronic inflammation, endocrine dysregulation, impaired nutrient absorption, and disrupted muscle-bone crosstalk. GM-derived metabolites, such as short-chain fatty acids (SCFAs), interact with immune, metabolic, and hormonal pathways to influence osteoblast/osteoclast activity and muscle protein synthesis. Furthermore, systemic inflammation triggered by GM imbalance exacerbates bone resorption and muscle atrophy. The axis also highlights bidirectional feedback between muscle and bone, mediated by myokines (e.g., irisin) and osteokines (e.g., osteocalcin), which synergistically regulate musculoskeletal homeostasis. Therapeutic strategies targeting GM modulation-such as dietary optimization (plant-based proteins, high-fiber diets), probiotics/prebiotics, exercise, and fecal microbiota transplantation (FMT)-suggest a potential capacity to modulate gut-muscle-bone interactions, which may be relevant to osteosarcopenia-related pathophysiological processes. This review proposes an integrative conceptual framework for understanding the pathogenesis of OS, synthesizing evidence primarily derived from osteoporosis and sarcopenia research, as well as animal and mechanistic studies. While direct clinical evidence in OS remains limited, emerging findings suggest that microbiota-centered strategies may hold potential for future preventive and therapeutic exploration.},
}

@article {pmid41716272,
year = {2026},
author = {Li, M and Xiao, S and Wang, Y and Li, T and Hu, Q and Dong, L and Guo, Y and Shi, Z and Yang, Q and Cai, W and Li, Q and Peng, B and Li, P and Weng, X and Wang, Y and Li, Y and Dong, Y and Zhu, X and Gong, Z and Chen, Y},
title = {Wuji Pill and Akkermansia muciniphila alleviates intestinal dysfunction and depression-like behavior in irritable bowel syndrome through the microbiota-gut-brain axis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1739408},
pmid = {41716272},
issn = {1664-302X},
abstract = {INTRODUCTION: Irritable bowel syndrome (IBS) is a typical disorder of gut-brain interaction (DGBI). The microbiota-gut-brain (MGB) axis is pivotal in preventing and treating IBS. Wuji Pill is a traditional Chinese medicine commonly used to treat IBS. This study aimed to investigate the mechanism by which Wuji Pill improves IBS via the MGB axis.

METHODS: The visceral sensitivity and colonic motor function were evaluated using the abdominal wall withdrawal reflex test and the colonic motility curve. Depression-like behavior were evaluated using sucrose preference test, open field test, novelty-suppressed feeding test, and forced swimming tests. The intestinal mucus secretion and the activation status of microglia was detected using AB-PAS staining and immunofluorescence staining, respectively. The species composition and abundance of gut microbiota were detected through 16S rRNA sequencing and RT-qPCR. Targeted metabonomics and RT-qPCR were used for metabolites and metabolic enzymes analysis.

RESULTS: In this study, Wuji Pill improved the symptoms of IBS rats and increased the relative abundance of Akkermansia muciniphila in feces. Additionally, antibiotics affected the repair of intestinal mucus secretion and significantly reduced the level of short-chain fatty acids. Subsequently, fecal microbiota transplantation and A. muciniphila transplantation can improve the symptoms of IBS rat by increasing intestinal mucus secretion, elevating the levels of acetic acid and butyric acid in feces. Additionally, the microglia in the cortex were suppressed, and the tryptophan-kynurenine pathway in the hippocampus was inhibited, leading to the conversion of tryptophan into 5-HT.

DISCUSSION: This study highlights the Wuji Pill may alleviate IBS symptoms by modulating A. muciniphila and regulating the tryptophan metabolism pathway through MGB axis.},
}

@article {pmid41715264,
year = {2026},
author = {Kumar, R and Elangovan, S and Asrani, S},
title = {Emerging Therapeutic Regimens as Alternatives to Glucocorticoids for Severe Alcohol-Associated Hepatitis: A Comprehensive Review.},
journal = {Clinical and molecular hepatology},
volume = {},
number = {},
pages = {},
doi = {10.3350/cmh.2025.1163},
pmid = {41715264},
issn = {2287-285X},
abstract = {Severe alcohol-associated hepatitis (SAH) is the most aggressive form of alcohol-associated liver disease and is associated with very high short-term mortality. It is characterized by the acute onset of jaundice in the context of ongoing alcohol use, most commonly defined by a Maddrey Discriminant Function ≥32 or a Model for End-Stage Liver Disease score ≥ 20. Despite its increasing global burden and substantial healthcare costs, therapeutic options remain limited, and outcomes are poor. The severity of liver failure, systemic inflammation, infectious complications, and extrahepatic organ dysfunction determines the prognosis in SAH. The pathophysiology of SAH is multifactorial, involving direct hepatotoxicity from alcohol metabolites, oxidative stress, dysregulated immune activation, gut dysbiosis with increased intestinal permeability, impaired hepatic regeneration, and genetic susceptibility. These interrelated mechanisms culminate in an exaggerated inflammatory response driven by macrophage activation and cytokine release, resulting in hepatocellular injury and multi-organ failure. Glucocorticoids remain the guideline-recommended standard of care for selected patients; however, their benefit is limited to modest short-term survival gains, with high rates of non-response and infection. Numerous investigational therapies targeting inflammation, oxidative stress, liver regeneration, bile acid signaling, epigenetic regulation, and the gut-liver axis have been evaluated, with largely disappointing results. Emerging approaches, including interleukin-22 agonists and epigenetic modulators such as larsucosterol, show promise but require validation in well-designed trials. This review synthesizes current evidence on the definition, prognostic assessment, and pathophysiology of SAH, critically appraises existing and emerging therapies, and highlights the need for combination strategies, improved patient stratification, and personalized treatment approaches.},
}

@article {pmid41714082,
year = {2026},
author = {Mahajan, S and Nk, A and Banerjee, SK},
title = {Recent advances of microbial medicine to prevent and treat cardiovascular disease.},
journal = {Progress in molecular biology and translational science},
volume = {220},
number = {},
pages = {305-337},
doi = {10.1016/bs.pmbts.2026.01.028},
pmid = {41714082},
issn = {1878-0814},
mesh = {Humans ; *Cardiovascular Diseases/therapy/prevention & control/microbiology ; Animals ; Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; },
abstract = {Cardiovascular diseases (CVDs) remain the leading cause of global mortality, with standard pharmacological interventions often failing to fully address their complex pathophysiology. Recent advances in microbial medicine highlight the human gut microbiome as a critical regulator of cardiovascular health. Gut microbial metabolites such as short-chain fatty acids (SCFAs), trimethylamine-N-oxide (TMAO), and indole derivatives play pivotal roles in modulating inflammation, lipid metabolism, immune function, and vascular homeostasis. Dysbiosis, or microbial imbalance, has been strongly associated with atherosclerosis, hypertension, and heart failure. Consequently, therapies targeting the gut microbiota including probiotics, prebiotics, synbiotics, and postbiotics have emerged as promising adjuncts in CVD prevention and treatment. Moreover, fecal microbiota transplantation (FMT) and synthetic biology approaches using engineered microbes offer novel strategies to restore microbial balance and deliver therapeutic molecules. Dietary interventions, particularly Mediterranean and fiber-rich diets, further support cardiovascular health through microbiota modulation. While preclinical and clinical studies underscore the potential of microbiome-based interventions, challenges related to strain specificity, delivery systems, and regulatory frameworks remain. Nonetheless, integrating microbial medicine into cardiovascular care represents a transformative shift toward precision, holistic, and personalized treatment paradigms. This chapter explores these cutting-edge therapeutic interventions and their implications for reshaping the future landscape of cardiovascular disease management.},
}

Humans
*Cardiovascular Diseases/therapy/prevention & control/microbiology
Animals
Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Probiotics/therapeutic use

@article {pmid41714079,
year = {2026},
author = {Bhowmick, J and Bagchi, A},
title = {Fecal microbiota transplantation in liver diseases: Therapeutic potential and associated risks.},
journal = {Progress in molecular biology and translational science},
volume = {220},
number = {},
pages = {229-246},
doi = {10.1016/bs.pmbts.2026.01.001},
pmid = {41714079},
issn = {1878-0814},
mesh = {Humans ; *Fecal Microbiota Transplantation/adverse effects ; *Liver Diseases/therapy/microbiology ; Risk Factors ; Animals ; },
abstract = {Fecal microbiota transplantation (FMT) is a biologically coherent strategy to modulate the gut-liver axis by restoring ecosystem structure and function. This chapter synthesizes current evidence and practice of FMT in various liver disease conditions. In cirrhosis with recurrent hepatic encephalopathy (HE), randomized trials demonstrate adjunctive benefits of FMT, reducing recurrence and hospitalizations as well as improving cognition, with route flexibility (lower-GI infusions or oral capsules) and emerging microbiome predictors of response. In severe alcohol-associated hepatitis and ACLF, early single-center trials suggest fewer infections and short-term survival gains, warranting confirmation in multicenter, blinded studies for further outcomes. For MASLD/MASH, FMT consistently shifts intestinal permeability, bile-acid signatures, and hepatic transcriptomics, although it has not reliably improved MRI-PDFF or insulin resistance in unselected cohorts; future success likely requires phenotype enrichment and function-matched donors or defined consortia. Data in chronic hepatitis B remain exploratory, positioning FMT, if at all, as an adjunct to antivirals. Methods are standardized around rigorous donor screening, controlled manufacturing, indication-specific endpoints, and strain-resolved engraftment analytics linking mechanism to outcome. Refractory Clostridium difficile is the only FDA-approved indication of FMT. Use of FMT in hepatology use should remain protocolled and regulated. Priorities include precision donor matching, next-generation consortia, platform trials, and long-term safety registries.},
}

Humans
*Fecal Microbiota Transplantation/adverse effects
*Liver Diseases/therapy/microbiology
Risk Factors
Animals

@article {pmid41714075,
year = {2026},
author = {Konar, D},
title = {Clinical applications of live biotherapeutics: Current trends and future prospects.},
journal = {Progress in molecular biology and translational science},
volume = {220},
number = {},
pages = {103-138},
doi = {10.1016/bs.pmbts.2026.01.003},
pmid = {41714075},
issn = {1878-0814},
mesh = {Humans ; Animals ; *Biological Therapy/trends/methods ; *Biological Products/therapeutic use ; },
abstract = {Live biotherapeutic (LBP) is defined by the FDA as a biological product that: (1) contains live organisms, such as bacteria; (2) applies to the prevention, treatment, or cure of a disease or condition of human beings; and (3) is not a vaccine. Progress in microbiome science and the limitations of antibiotics have necessitated the use of LBPs to complement or replace conventional therapies across multiple medical disciplines. The most important advancement is in the infectious disease domain, where fecal microbiota transplantation validated ecological restoration for recurrent Clostridioides difficile infection and paved the way for the first approved LBPs (REBYOTA® and VOWST™/SER-109). Constructing rational microbial consortia and strain-level strategies aim to induce commensal resilience and prevent the establishment of multidrug-resistant organisms. In oncology, gut microbial composition modulates response to immune checkpoint inhibitors. So, defined microbial consortia and engineered E. coli Nissle are being developed to enhance antitumor immunity and localize payloads. Early studies in animals and humans also support the application of this approach in metabolic disease, allergy, and oral health. Translation from benchside to bedside, however, is fraught with hurdles-variable patient response, manufacturing consistency, safety standards, cost, and ethics-exacerbated by heterogeneous global regulations, underscoring the need for harmonization. Precision microbial consortia, programmable "living medicines," and biohybrid formulations could extend LBPs into broader indications and global health, shifting practice toward an ecological model of therapeutics.},
}

Humans
Animals
*Biological Therapy/trends/methods
*Biological Products/therapeutic use

@article {pmid41713826,
year = {2026},
author = {Yerushalmy-Feler, A and Spencer, EA and Dubinsky, MC and Suskind, DL and Mitrova, K and Hradsky, O and Conrad, MA and Kelsen, JR and Sladek, M and Yeh, PJ and Tzivinikos, C and Henderson, P and Wlazlo, M and Hackl, L and Shouval, DS and Mouratidou, N and Bramuzzo, M and Urlep, D and Olbjørn, C and Mancuso, G and Schneider, AM and Pujol-Muncunill, G and Yogev, D and Kang, B and Gasparetto, M and Rungø, C and Romano, C and Martinelli, M and Kolho, KL and Hojsak, I and Norsa, L and Rinawi, F and Sansotta, N and Rimon, RM and Granot, M and Scarallo, L and Trindade, E and Rodríguez-Belvís, MV and Turner, D and Cohen, S},
title = {Upadacitinib Maintenance Therapy in Pediatric Ulcerative Colitis: 52-week Multicenter Study from the Porto Group of ESPGHAN.},
journal = {Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cgh.2026.02.012},
pmid = {41713826},
issn = {1542-7714},
abstract = {BACKGROUND AND AIMS: Data on upadacitinib therapy in children with ulcerative colitis (UC) or unclassified inflammatory bowel disease (IBD-U) are scarce. We aimed to evaluate the effectiveness and safety of upadacitinib as a maintenance therapy in pediatric UC.

METHODS: Children treated with upadacitinib for maintenance of remission of active UC or IBD-U from 35 centers affiliated with the Porto group of ESPGHAN were enrolled in this retrospective study. Data on demographic, clinical, laboratory, endoscopic, imaging and adverse events (AEs) data were recorded over 52 weeks of follow-up.

RESULTS: A total of 105 children were included (95 UC and 10 IBD-U, mean age 14.6±3.3 years). Prior to upadacitinib, 103/105 (98%) children were treated with biologic therapies and 79 (75%) with ≥2 biologics. Clinical remission and corticosteroid-free clinical remission (CFR) were observed after 8 weeks in 61 (58%) and 53 (51%) children, respectively. By week 52, 75 (71%) children achieved clinical remission and 73 (70%) CFR. Sustained CFR was recorded in 63 (60%) children. CFR with normal C-reactive protein was observed in 56% of children, and CFR with fecal calprotectin levels <150 mcg/g was observed in 38%, by week 52. Fifty-two (50%) children experienced AEs, two of which were serious (an appendiceal neuroendocrine tumor and cytomegalovirus colitis). The most frequent AEs were hyperlipidemia (n=20), infections (n=18), and acne (n=14).

CONCLUSION: Upadacitinib is an effective induction and maintenance therapy for refractory pediatric UC and IBD-U. Effectiveness should be weighed against the potential risks of AEs.},
}

@article {pmid41713817,
year = {2026},
author = {Zhao, Q and Cao, Y and Zhang, Z and Yang, Y and Wang, L and Xu, M and Mao, Y and Zhang, X and Zeng, M and Yang, P and Chen, Q and Yan, H and Yang, G},
title = {Xiao-Chaihu-Tang preserves intestinal barrier and ameliorates irinotecan-evoked delayed diarrhea by anchoring endogenous tryptophol to modulate inflammation and oxidation dependent on AhR-UGT1A1-microbiota axis.},
journal = {Journal of ethnopharmacology},
volume = {363},
number = {},
pages = {121380},
doi = {10.1016/j.jep.2026.121380},
pmid = {41713817},
issn = {1872-7573},
abstract = {Xiao-Chaihu-Tang (XCHT), a well-known traditional formula, is commonly used to treat various types of diarrhea. It also exhibits promising efficacy against chemotherapy irinotecan (CPT-11)-induced delayed diarrhea (DD). However, its underlying mechanisms, specifically concerning endogenous metabolites, key pathways, and functional gut bacteria at the species level, remain unclear, severely restricting its clinical application.

AIM OF THE STUDY: This study aimed to elucidate the biomarkers, pathways, and functional bacteria involved in XCHT's alleviating CPT-11-evoked DD using multi-omics approaches, antagonists, and fecal microbiota transplantation (FMT).

MATERIALS AND METHODS: First, the ingredients of XCHT and absorbed compounds in rat plasma were identified using liquid chromatography-mass spectrometry (LC-MS). Next, the therapeutic effects of XCHT were assessed by monitoring perianal status, body weight, disease activity index, food and water intake, and histopathological changes in the colon (hematoxylin and eosin, alcian blue-periodic acid-schiff staining). The underlying mechanisms were studied using metabolomics and network pharmacology, which highlighted the role of endogenous biomarkers and associated pathways. Tryptophol was identified as a key correlate, and its efficacy was further validated in rat and Caco-2 models using antagonists of potential targets (AhR and UGT1A1). The levels of inflammatory cytokines, and oxidative stress markers, intestinal barrier proteins, and mucins were detected by enzyme-linked immunosorbent assay (ELISA), Western blotting, and immunofluorescence. Furthermore, functional gut bacteria were identified using metagenomic sequencing and validated using FMT, while gut leakage was detected using fluorescence in situ hybridization (FISH). Finally, the interactions between tryptophol with targets of AhR and UGT1A1 were examined using molecular docking, molecular dynamics, and surface plasmon resonance.

RESULTS: LC-MS analysis identified 43 phytochemicals in XCHT and 17 compounds absorbed in plasma. XCHT, similar to tryptophol, attenuated DD by improving perianal status, disease activity index, and colon pathology, while increasing body weight, food intake, and water intake. Metabolomics analysis revealed 33 potential endogenous biomarkers, including PGB3, LysoPA, and so on. Integrated with network pharmacology, the results indicated that the therapeutic effect of XCHT involved the regulation of tryptophan metabolism, arachidonic acid metabolism, inflammation, and oxidative stress. Tryptophol, which exhibited a strong correlation with efficacy indices, reduced inflammation and oxidation in vivo/vitro, and enhanced intestinal barrier protein and mucin expression in an AhR-UGT1A1-dependent manner. Furthermore, metagenomic sequencing and FISH demonstrated that both XCHT and tryptophol normalized the abundance of 10 gut bacterial species (for example, Lactobacillaceae bacterium, Massiliimalia timonensis, and Limosilactobacillus reuteri) and inhibited bacterial invasion. Molecular interaction studies confirmed the strong binding between tryptophol with AhR and UGT1A1.

CONCLUSION: This study demonstrates that XCHT preserves intestinal barrier integrity in rats and alleviates CPT-11-induced DD. This protective effect is mediated by modulating inflammation and oxidative stress via the tryptophol- AhR-UGT1A1-microbiota axis, providing a novel paradigm for mechanistic studies on toxicity reduction in clinical chemotherapy drugs.},
}

@article {pmid41713731,
year = {2026},
author = {Xu, J and Hu, R and Zheng, J and Ju, Q and Liu, Y and Chen, S and Liu, Z and Lei, Y and Yang, J and Zhang, D and Shen, W},
title = {Modulation of the intestinal microbiome and reversal of the immunosuppressive microenvironment by nanoparticles for chemoimmunotherapy in prostate cancer.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.02.027},
pmid = {41713731},
issn = {2090-1224},
abstract = {INTRODUCTION: Prostate cancer (PCa), a "cold" tumor with an immunosuppressive microenvironment, exhibits poor sensitivity to immunotherapies, limiting treatment efficacy. Chemotherapeutics often cause intestinal injury and disrupt gut microbiota, further impairing chemoimmunotherapy outcomes. Modulating gut microbiota to reverse immunosuppression represents a potential strategy to enhance PCa treatment.

OBJECTIVES: To develop a novel therapeutic strategy using nanomedicine to regulate intestinal flora, thereby reversing the immunosuppressive microenvironment and improving chemoimmunotherapy efficacy in PCa.

METHODS: Cabazitaxel (CBZ)-loaded, folic acid (FA)-modified pH/ROS dual-responsive nanoparticles (CBZ/FA-CA-OCD NPs) were fabricated. In vitro and in vivo experiments evaluated NPs accumulation, cellular internalization (via FA-mediated endocytosis), drug release, intestinal mucosal injury, and tumor growth inhibition. Gut microbiota modulation (e.g., Lachnospiraceae, Firmicutes, Muribaculaceae, Bacteroidota) and CD4[+]/CD8[+] T-cell infiltration were assessed. Fecal microbiota transplantation (FMT) validated microbiota-mediated immune effects.

RESULTS: The CBZ/FA-CA-OCD NPs accumulated in PCa tissues were internalized by PC-3/LNCaP cells and released CBZ in acid/ROS microenvironments to inhibit tumor growth. Compared to free CBZ, NPs attenuated intestinal injury, modulated microbiota (increased Lachnospiraceae/Firmicutes, decreased Muribaculaceae/Bacteroidota), and enhanced anti-PD-1 efficacy by increasing CD4[+]/CD8[+] T-cell infiltration. FMT confirmed that microbiota from NP-treated mice promoted T-cell infiltration in tumors.

CONCLUSION: CBZ/FA-CA-OCD NPs improve PCa chemoimmunotherapy by regulating gut microbiota, reversing immunosuppression, and enhancing T-cell infiltration. This nanomedicine-based strategy provides a promising approach to boost PCa treatment outcomes.},
}

@article {pmid41713730,
year = {2026},
author = {Li, Y and Zhang, Y and Liu, T and Tuo, Y and Zhang, Y and You, H and Peng, S and Wu, T and Cai, T and Lin, Z and Feng, Z and Liu, Z and Wu, J and Liu, X and Ding, L},
title = {Alleviation of high-fat diet-induced lipid metabolism disorders: role of quinoa peptides in reducing high-activity BSH-producing gut microbiota abundance and modulating BA-FXR/TGR5 signaling.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.02.040},
pmid = {41713730},
issn = {2090-1224},
abstract = {INTRODUCTION: Lipid metabolism disorders contribute significantly to various metabolic diseases and are closely related to gut microbiota dysbiosis. Quinoa intake has been increasingly linked to improved metabolic regulation and body weight control. In our earlier work, oral administration of quinoa-derived peptides (QPep) modulated gut microbiota composition and mitigated hepatic lipid dysregulation in high-fat diet (HFD)-induced obese mice. Nevertheless, the specific mechanisms responsible for these effects remain incompletely understood.

OBJECTIVES: This study aimed to elucidate the mechanisms by which QPep alleviates lipid metabolic disorders in HFD-induced obese mice.

METHODS: Mice were fed a HFD with or without oral QPep intervention. Both antibiotic treatment and fecal microbiota transplantation were employed to assess the microbiota-dependent effects of QPep. Comprehensive multi-omics and molecular analyses were conducted to characterize metabolic phenotypes alongside gut microbial composition, bile acids (BAs) metabolism, and host signaling pathways in the liver, ileum, and adipose tissues.

RESULTS: QPep administration alleviated HFD-induced metabolic disorders, leading to reductions in body weight and adiposity, improvements in serum lipid profiles and hepatic steatosis, and restoration of glucose homeostasis. Microbiota depletion and transplantation experiments suggested a microbiota-dependent contribution to the observed effects. Mechanistically, QPep selectively reduced high-activity bile salt hydrolase (BSH)-producing bacteria abundance, reduced intestinal BSH activity, and preserved conjugated BAs, thereby suppressing ileal FXR-FGF15 signaling, enhancing hepatic BAs synthesis, and activating TGR5 in adipose and ileum tissues to restore systemic lipid metabolism.

CONCLUSION: These findings demonstrate that QPep modulate gut microbiota-BAs signaling to restore lipid homeostasis, highlighting their potential as a dietary intervention for the prevention and management of obesity-related metabolic disorders.},
}

@article {pmid41713032,
year = {2026},
author = {Park, J and Choi, Y and Lee, W and Kang, A and Seo, E and Kim, MG and Jang, KB and Song, M and Oh, S and Kim, Y},
title = {Heat-killed Bacteroides fragilis SLAM_BAF01 alleviates weaning-induced stress responses and cognitive impairments by modulating the gut-brain-microbiome axis.},
journal = {Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie},
volume = {196},
number = {},
pages = {119121},
doi = {10.1016/j.biopha.2026.119121},
pmid = {41713032},
issn = {1950-6007},
abstract = {Weaning transition in porcine industry is marked by nutritional, microbial, and psychological stresses that can impair growth and development. Accumulating evidence indicates that weaning-related stress not only disrupts gut microbial homeostasis but impairs gut-brain axis signaling through activation of stress-related neuroendocrine pathways. However, current interventions have largely focused on improving growth performance or enteric symptoms, while integrated strategies targeting the gut-brain-microbiome axis remain limited. Next-generation probiotics (NGPs) such as Bacteroides fragilis have been reported to exert beneficial effects on both intestinal health and brain function, positioning them as promising candidates for alleviating weaning stress. However, their practical application remains challenging due to the strict anaerobic nature. In this study, we investigated that a porcine-derived heat-killed B. fragilis SLAM_BAF01 exerts beneficial effects under weaning stress through gut-brain-microbiome modulation, thereby enabling a more stable and scalable application. First, to investigate the relationship within the gut-brain-microbiome axis under weaning stress conditions, we employed a fecal microbiota transplantation (FMT)-based mouse model and a physiologically relevant weaning pig model. Multi-omics analyses were conducted to characterize microbial and host responses. B. fragilis SLAM_BAF01 exhibited acid and bile tolerance, preserved structural integrity, and lacked enterotoxicity. In the mouse FMT model, heat-killed SLAM_BAF01 positively modulated gut microbial composition, reinforced intestinal barrier function, and attenuated stress-related responses. Especially, brain γ-aminobutyric acid (GABA) levels increased by 150 %, while serum corticosterone levels were reduced by 17 % compared with the control. In the weaning pig model, heat-killed SLAM_BAF01 improved growth performance by 7 % and significantly reduced inflammation and stress markers. These findings demonstrate that heat-killed postbiotic B. fragilis SLAM_BAF01 as a promising candidate capable of mitigating weaning-associated stress through enhancing gut-brain-microbiome axis function in porcine industry.},
}