@article {pmid41896437,
year = {2026},
author = {Jin, H and Zhou, W and Ying, R},
title = {Impact of ileostomy reversal on gut microbiome and metabolome in rectal cancer: a review of mechanisms and clinical consequences.},
journal = {Langenbeck's archives of surgery},
volume = {411},
number = {1},
pages = {},
pmid = {41896437},
issn = {1435-2451},
support = {2024S00023//the Social Development Science and Technology Project of Wenling City, Zhejiang Province/ ; },
abstract = {Prophylactic ileostomy is a critical measure for preventing anastomotic leakage after low rectal cancer surgery; however, the incidence of diarrhea following stoma reversal remains high, posing a major clinical challenge. Recent studies have revealed that the underlying pathophysiology involves not only anal sphincter dysfunction but also a comprehensive imbalance in the gut microbiota–metabolite–immune axis. This review systematically elucidates the dynamic evolution of the gut microbiome after stoma reversal and its interplay with host metabolism. It further delves into multidimensional pathophysiological mechanisms, including gut dysbiosis, reduced production of short-chain fatty acids, dysregulated bile acid metabolism, and impaired intestinal barrier integrity. In light of recent advances, this article analyzes the clinical characteristics and subtypes of postoperative diarrhea, summarizes precision diagnostic strategies based on multi-omics technologies, and provides an objective assessment of emerging therapies such as probiotics, fecal microbiota transplantation, metabolic interventions, and nutritional support. Finally, the necessity of establishing an integrated multidisciplinary management model is discussed, with the aim of offering new perspectives and a theoretical foundation for improving the quality of life in rectal cancer patients after surgery.},
}

@article {pmid42088511,
year = {2026},
author = {Smout, J and Lesker, TR and Hoenicke, L and Ortiz, D and Zou, M and Kruse, F and Pirr, S and Willers, M and Härtel, C and Falk, C and Torow, N and Viemann, D and Strowig, T and Huehn, J},
title = {Probiotic-conditioned microbiota from preterm infants modulate immune response to pathogen challenge in a microbiota-humanized mouse model.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1761680},
pmid = {42088511},
issn = {1664-3224},
mesh = {Animals ; *Probiotics/administration & dosage/pharmacology ; *Gastrointestinal Microbiome/immunology ; Mice ; *Infant, Premature/immunology ; Humans ; Female ; Infant, Newborn ; Disease Models, Animal ; Immunity, Innate ; Animals, Newborn ; *Escherichia coli Infections/immunology/microbiology ; Enteropathogenic Escherichia coli/immunology ; Feces/microbiology ; },
abstract = {Early-life host-microbe interactions critically shape immune development, lifelong homeostasis, and disease susceptibility. The PRIMAL trial (Priming Immunity at the Beginning of Life) demonstrated that multistrain probiotics shifted the gut microbiota of very preterm infants toward eubiosis without affecting sepsis incidence, yet the immunological consequences remained unresolved. To explore this, we colonized germ-free female mice with fecal samples from probiotic- or placebo-treated preterm infants from the PRIMAL trial. Microbiota composition was vertically transmitted and stable across generations. At steady-state, 3-week-old pups colonized with probiotic-conditioned microbiota exhibited markedly reduced populations of innate immune cells, particularly in the colon, with subtler effects in the small intestine and spleen, while adaptive immune subsets were less affected. Upon enteropathogenic Escherichia coli challenge at day 5, pups harboring probiotic-conditioned microbiota displayed reduced growth and impaired bacterial clearance, correlating with diminished numbers of key innate immune cell populations. These findings demonstrate that probiotic-driven shifts in human-derived microbial communities can attenuate immune cell development in mice and alter early-life infection outcomes. Our study underscores the complex, context-dependent effects of probiotics on the neonatal microbiota-immune axis and provides mechanistic insight into how interventions in preterm infants may influence susceptibility to infection.},
}

Animals
*Probiotics/administration & dosage/pharmacology
*Gastrointestinal Microbiome/immunology
Mice
*Infant, Premature/immunology
Humans
Female
Infant, Newborn
Disease Models, Animal
Immunity, Innate
Animals, Newborn
*Escherichia coli Infections/immunology/microbiology
Enteropathogenic Escherichia coli/immunology
Feces/microbiology

@article {pmid42088615,
year = {2026},
author = {Zhang, Z and Li, C and Tang, Y and Liu, B and Wang, J and Kong, L and Bao, W and Lai, H and Chen, T and Li, J},
title = {Indole-3-Carbaldehyde from Limosilactobacillus reuteri Boosts Chemotherapy Response in Diffuse Large B Cell Lymphoma by Blocking the Mechanistic Target of Rapamycin Pathway.},
journal = {Research (Washington, D.C.)},
volume = {9},
number = {},
pages = {1267},
pmid = {42088615},
issn = {2639-5274},
abstract = {Diffuse large B cell lymphoma (DLBCL) presents a critical clinical challenge due to declining chemosensitivity and difficult-to-manage dose-limiting toxicities. Although gut microbiota modulation shows potential for "toxicity reduction and efficacy enhancement", its mechanism in DLBCL remains unclear. Comparative analysis revealed a marked reduction of beneficial bacteria in patients with DLBCL versus healthy volunteers, with a marked decrease in the abundance of core probiotics, particularly Limosilactobacillus reuteri. Fecal microbiota transplantation from healthy donors into DLBCL mouse models reduced tumor burden, improved chemosensitivity, and alleviated intestinal toxicity. A core probiotic strain, L. reuteri HG001, was isolated and shown to replicate these effects alone, with the tryptophan metabolite indole-3-carbaldehyde (ICAld) identified as the key component responsible for its adjunctive antitumor activity. Mechanistic studies demonstrated that ICAld exerts significant adjunctive antitumor effects both in vitro and in vivo in a dose-dependent manner in mouse models; it acts by activating the aryl hydrocarbon receptor (AHR)/cytochrome P450 family 1 subfamily A member 1 (CYP1A1)/reactive oxygen species (ROS) axis, inhibiting the phosphatidylinositol 3-kinase (PI3K)/AKT/mechanistic target of rapamycin (mTOR) signaling pathway, promoting apoptosis, and synergizing with cyclophosphamide. An aryl hydrocarbon receptor antagonist reversed both the chemosensitizing and intestinal protective effects of L. reuteri HG001 and ICAld. This study elucidates a microbiota-mediated mechanism in DLBCL and supports L. reuteri HG001 as a probiotic adjuvant to enhance therapy while reducing toxicity.},
}

@article {pmid42090907,
year = {2026},
author = {Su, X and Li, A and Liu, J and Guo, Y and Yu, H and Yu, J and Wang, R and Garza, DR and Qu, J and Wen, B and Liu, B},
title = {From microbes to molecules: Gut microbiota as a prerequisite threshold determinant for cancer immunotherapy efficacy.},
journal = {Microbiological research},
volume = {309},
number = {},
pages = {128539},
doi = {10.1016/j.micres.2026.128539},
pmid = {42090907},
issn = {1618-0623},
abstract = {Cancer immunotherapy, represented by immune checkpoint inhibitors, adoptive cell therapy, and cancer vaccines, has revolutionized the clinical management of multiple malignant tumors, yet profound interindividual heterogeneity in treatment response and widespread primary/acquired resistance remain the most critical bottlenecks restricting its long-term clinical benefits. Accumulating preclinical and clinical evidence has unequivocally established the gut microbiota as a pivotal regulator of host anti-tumor immune responses. However, the vast majority of existing studies and reviews frame the gut microbiota as a mere adjuvant enhancer of immunotherapy efficacy, focusing solely on its role in boosting the upper limit of treatment effects, while neglecting its more fundamental role as a prerequisite for establishing a responsive immune baseline. In this review, we propose a unifying, evidence-based original core hypothesis: the gut microbiota is not merely an enhancer of cancer immunotherapy efficacy, but an indispensable prerequisite condition that sets the minimal baseline threshold for therapeutic responsiveness-a central thesis that distinguishes this review from previous descriptive work. Guided by this hypothesis, we systematically dissect the taxonomic and functional characteristics of threshold-determining gut microbiota, and clarify that microbial metabolites (e.g., short-chain fatty acids, bile acids, tryptophan derivatives) act as core molecular mediators translating microbial signals into host immune activation, which is critical for establishing the baseline efficacy threshold required for effective immunotherapy. We further perform a critical synthesis of clinical data from prospective cohorts, randomized controlled trials, and microbiota intervention studies, validating that threshold-based microbial signatures serve as non-invasive predictive biomarkers for immunotherapy outcomes, and propose mechanism-driven translational strategies targeting the gut microbiota (e.g., fecal microbiota transplantation, probiotic supplementation, dietary modulation) to reset the impaired immunotherapy efficacy threshold. This review provides a novel theoretical framework for understanding the microbiota-immunotherapy axis, which not only deepens the mechanistic insight into microbial metabolite-mediated immune regulation, but also facilitates the development of microbiota-guided personalized cancer immunotherapy and the overcoming of primary treatment resistance.},
}

@article {pmid42092466,
year = {2026},
author = {Gavini, CK and Raux, L and Labouèbe, G and Gornick, E and Mc Hugh, S and Elshareif, N and Calcutt, NA and Di Summa, PG and Gorostidi, F and Vonaesch, P and Mansuy-Aubert, V},
title = {A gut-adipose-nerve axis mediates inulin protection against Western diet-induced somatosensory dysfunction.},
journal = {Brain, behavior, and immunity},
volume = {137},
number = {},
pages = {106795},
doi = {10.1016/j.bbi.2026.106795},
pmid = {42092466},
issn = {1090-2139},
abstract = {Westernized diets (WDs)-high in fat and sugar and low in fiber-produce somatosensory deficits, chronic pain, and neuropathy, yet the mechanisms linking diet to peripheral nervous system (PNS) pathology remain incompletely defined. Emerging evidence implicates gut-derived metabolites in sensory homeostasis; for example, fecal microbiota transplantation (FMT) from lean donors to WD fed mice reduces hypersensitivity and attenuates PNS inflammation potentially via modifying short chain fatty acid (SCFA) levels, although FMT outcomes are variable. We therefore tested whether targeted modulation of the gut microbiota with fermentable complex carbohydrates (inulin) producing SCFA could reproducibly improve somatosensory function in WD-fed mice. Using an integrated pipeline-behavioral and physiological assays, peripheral nerve electrophysiology, and molecular and immune profiling-we show that inulin improved thermal and mechanical sensory function indirectly by improving metabolic health and remodeling immune cells in adipose tissue depots. Interestingly, in separate genetic experiments we found that deletion of the SCFA receptor FFAR2 (GPR43) in myeloid cells altered thermal sensitivity and adipose inflammatory gene expression, indicating that immune SCFA sensing can modulate pain-related behavior. These findings identify mechanisms by which dietary fiber indirectly preserves PNS function through effects on adiposity and systemic inflammation and provide a tractable alternative to FMT for mitigating WD-associated sensory neuropathy.},
}

@article {pmid42092473,
year = {2026},
author = {Liu, T and Zhao, Y and Wang, X and Ding, L and Yu, G and Lin, X and Wu, X},
title = {Comparative Pharmacodynamic Material Basis of Oral and Colonic Administration of Baitouweng Decoction in Experimental Ulcerative Colitis.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {121805},
doi = {10.1016/j.jep.2026.121805},
pmid = {42092473},
issn = {1872-7573},
abstract = {Baitouweng Decoction (BTWD) is a traditional Chinese medicine formula widely used in clinical practice for treating ulcerative colitis (UC). However, its precise therapeutic mechanisms remain unclear.

AIM OF THE STUDY: This study investigates the therapeutic effects of BTWD administered via colon and oral routes in a UC model induced by fecal microbiota transplantation (FMT) and dextran sodium sulfate (DSS). It further explores the distinct pharmacological mechanisms associated with each route of administration.

MATERIALS AND METHODS: Male rats with UC induced by human-derived FMT and DSS were treated with BTWD via oral or colonic administration. Therapeutic outcomes were evaluated through clinical indicators and histopathology. Drug metabolites in serum and colon contents were analyzed by Ultra Performance Liquid Chromatography-Q Exactive-Orbitrap Mass Spectrometer (UPLC-QE-Orbitrap MS). Serum and fecal metabolomics identified disease-related biomarkers. Potential active substances were screened by correlating serum and fecal biomarkers with BTWD-derived components. Key active substances and targets were identified through network pharmacology and molecular docking, clarifying the pharmacological basis of each administration route. Surface plasmon resonance (SPR) and Western blot were performed to experimentally validate the binding interactions and target protein expression.

RESULTS: Both administration routes of BTWD significantly alleviated UC symptoms. Compared to the model group, BTWD-treated rats exhibited reduced weight loss, lower disease activity index (DAI) scores, and recovered colon length. Serum levels of pro-inflammatory cytokines IL-6, IL-17, and IL-1β were decreased, while anti-inflammatory IL-10 was increased. Expression of Occludin and MUC2 proteins in colon tissue was significantly upregulated. In total, 82 serum and 70 colon components were identified following oral administration, while colonic administration yielded 73 serum and 78 colon components. Correlation analysis screened 36 active components associated with colonic administration and 25 with oral administration. Network pharmacology and molecular docking suggested that core components from colon administration (Anemoside B4, Betulonic acid) may act via targets such as EGFR, LCK, and MET, while oral components (Berberine, Oxyepiberberine) may target AURKA, MET, and PTGS2. SPR confirmed direct binding of anemoside B4 and berberine to EGFR with KD values of 9.47E-04 M and 2.96E-04 M, respectively. Western blot revealed route-dependent modulation of EGFR, PTGS2, LCK and AURKA expression, corroborating the predicted targeting.

CONCLUSION: BTWD is effective in treating UC through both colonic and oral administration. This study provides a comprehensive "efficacy-component-metabolism-target" analysis that reveals distinct pharmacological mechanisms underlying each administration route. These findings support the traditional use of BTWD and offer a theoretical foundation for developing optimized, route-specific therapies for UC.},
}

@article {pmid42093245,
year = {2026},
author = {Hamdan, A and Ziad, AN},
title = {Reframing obesity through the gut microbiota: functional dysbiosis and metabolic disease.},
journal = {Current opinion in clinical nutrition and metabolic care},
volume = {},
number = {},
pages = {},
pmid = {42093245},
issn = {1473-6519},
abstract = {PURPOSE OF REVIEW: Obesity and its metabolic complications remain major global health challenges. Beyond excess caloric intake, emerging evidence implicates diet-induced gut microbiota dysfunction as a modulator of metabolic homeostasis. This review examines recent advances in understanding how functional alterations of the gut microbiota contribute to obesity pathogenesis.

RECENT FINDINGS: Current data indicate that obesity is characterized less by specific microbial taxa and more by disruption of key microbial functions. Diet-induced dysbiosis alters short-chain fatty acid production, bile acid metabolism, tryptophan-derived signaling, and intestinal barrier integrity. These changes promote metabolic endotoxemia, impair enteroendocrine hormone secretion, and disrupt gut-brain and gut-liver communication, contributing to adipose tissue inflammation, hepatic steatosis, and insulin resistance. Experimental and clinical studies further suggest that microbiota-targeted interventions, including dietary fiber enrichment, prebiotics, synbiotics, and fecal microbiota transplantation, can partially restore microbial metabolic function and improve selected metabolic outcomes.

SUMMARY: Obesity is increasingly conceptualized as a state of diet-driven functional gut microbiota disruption. Targeting microbial metabolic pathways rather than individual taxa may offer a promising adjunctive strategy to complement established therapies for obesity-related metabolic disease.},
}

@article {pmid42093801,
year = {2026},
author = {Busmail, H and Weerakoon, S and Mandefro, BT and Sundara, SV and Lu, X and Avula, S and Mohammed, L},
title = {Fecal Microbiota Transplantation in Inflammatory Bowel Disease: A Systematic Review of Efficacy and Safety.},
journal = {Cureus},
volume = {18},
number = {4},
pages = {e106453},
pmid = {42093801},
issn = {2168-8184},
abstract = {Inflammatory bowel disease (IBD), comprising ulcerative colitis (UC) and Crohn's disease (CD), is a chronic inflammatory condition of the gastrointestinal tract associated with immune dysregulation and alterations in the gut microbiota. Growing evidence suggests that intestinal microbial dysbiosis plays an important role in disease pathogenesis, prompting interest in microbiome-targeted therapies, such as fecal microbiota transplantation (FMT). This systematic review aimed to evaluate the efficacy and safety of FMT in adult patients with IBD. A comprehensive literature search was conducted in PubMed, Embase, Scopus, and the Cochrane Library for studies published between 2020 and 2025 using keywords related to "fecal microbiota transplantation" and "inflammatory bowel disease." Eligible studies included randomized controlled trials (RCTs), cohort studies, systematic reviews, and meta-analyses involving adult patients with UC or CD. Due to clinical and methodological heterogeneity, a structured narrative synthesis was performed in accordance with Synthesis Without Meta-analysis (SWiM) guidelines. Nine studies comprising 1,847 participants met the inclusion criteria, including five RCTs, two systematic reviews, and two meta-analyses. In patients with UC, clinical remission rates ranged from 32% to 40%, with response rates between 44% and 52%. In CD, remission rates ranged from 24% to 31%, although evidence remained limited and heterogeneous. Multi-donor stool preparations and repeated FMT administrations were associated with improved clinical outcomes compared with single-donor protocols or single-dose protocols. Adverse events occurred in approximately 12-15% of patients and were predominantly mild gastrointestinal symptoms, while serious adverse events were rare (<2%). Current evidence suggests that FMT may induce clinical remission in a subset of patients with UC, while evidence in CD remains less consistent. Larger randomized trials with standardized protocols and long-term follow-up are needed to determine optimal donor selection, dosing strategies, and long-term safety.},
}

@article {pmid42094762,
year = {2026},
author = {Pan, Z and Zhang, T and Ren, Z and Zhang, H and Wang, J and Ma, Y and Man, R and Peng, J and Yu, Y},
title = {Microbiota-immune crosstalk in the regulation of intestinal motility in constipation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1828926},
pmid = {42094762},
issn = {1664-302X},
abstract = {Constipation is a common functional gastrointestinal disorder with a complex pathogenesis. Traditional studies have primarily explained its development in terms of reduced intestinal motility or impaired defecatory coordination; however, these mechanisms alone cannot fully account for the multifactorial pathological processes underlying the condition. In recent years, increasing attention has been directed toward the roles of intestinal microbial dysbiosis and alterations in immune homeostasis in the development of constipation. The gut microbiota continuously interacts with the intestinal immune system through its structural components, metabolic products, and secreted molecules. These interactions modulate the mucosal immune microenvironment and participate in the regulation of intestinal motility by influencing the enteric nervous system, interstitial cells of Cajal, and smooth muscle function. Conversely, the immune system can reshape the composition and spatial distribution of the gut microbiota through mechanisms such as the mucosal barrier, immunoglobulin A, and antimicrobial peptides, thereby forming a bidirectional regulatory network. Accumulating evidence suggests that during the onset and progression of constipation, microbial dysbiosis, shifts in immune homeostasis, and abnormalities in intestinal motility may evolve through a progressively amplifying dynamic process, ultimately establishing a self-sustaining chronic cycle. In addition, microbiota-targeted interventions-including probiotics, prebiotics, and fecal microbiota transplantation-have demonstrated potential benefits in improving stool frequency and stool consistency in several clinical studies. However, the immunological mechanisms underlying these effects remain relatively underexplored. This review systematically summarizes the molecular mechanisms by which gut microbiota-immune interactions regulate intestinal motility. By integrating current evidence on disease progression and clinical studies, we propose a conceptual model of the "microbiota-immune-motility regulatory axis," aiming to provide a new perspective for understanding the pathogenesis of constipation and for optimizing microbiota-based therapeutic strategies.},
}

@article {pmid42094772,
year = {2026},
author = {Luo, H and Shen, Z and Jian, Y and Wang, M and Luo, S and Wang, J and Nan, L and Tang, L and Rehman, MU and Carbonero, F},
title = {Editorial: Unravelling the wildlife gut microbiome: the crucial role of gut microbiomes in wildlife conservation strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1838495},
pmid = {42094772},
issn = {1664-302X},
}

@article {pmid42095982,
year = {2026},
author = {Răzniceanu, V and Țichindeleanu, A and Răducu, EV and Trella, ȘE and Nenu, I},
title = {Gut dysbiosis and nitric oxide dysregulation in cirrhosis progression: mechanistic insights and pathophysiological implications.},
journal = {Journal of physiology and biochemistry},
volume = {82},
number = {1},
pages = {},
pmid = {42095982},
issn = {1877-8755},
mesh = {Humans ; *Dysbiosis/metabolism/microbiology/immunology ; *Nitric Oxide/metabolism ; *Gastrointestinal Microbiome ; *Liver Cirrhosis/metabolism/microbiology/pathology/physiopathology ; Animals ; Disease Progression ; Liver/metabolism/pathology ; Hypertension, Portal/metabolism/microbiology ; Signal Transduction ; Nitric Oxide Synthase Type III/metabolism ; },
abstract = {Cirrhosis represents the end stage of chronic liver injury, characterized by progressive fibrosis and architectural distortion that precipitate portal hypertension and systemic complications. Recent evidence positions gut microbiota dysbiosis and nitric oxide (NO) dysregulation as central, interacting pathophysiological mechanisms in cirrhosis progression. Intestinal barrier dysfunction facilitates bacterial translocation and thereby exposes the liver to lipopolysaccharides and pathogen-associated molecular patterns that trigger hepatic inflammation via Toll-like receptor signalling, a phenomenon aggravated by dysbiosis. This immune activation stimulates inducible NO synthase in Kupffer cells and systemic endothelium, generating excess NO that drives splanchnic vasodilation and worsens portal hypertension. Paradoxically, intrahepatic endothelial NO synthase activity becomes impaired, reducing sinusoidal NO availability and increasing intrahepatic vascular resistance. These interconnected disturbances perpetuate inflammation and fibrogenesis, contributing to cirrhosis decompensation and spontaneous bacterial peritonitis. Despite substantial mechanistic insight into these pathways, therapeutic translation remains limited. Statins show promise by restoring intrahepatic eNOS function and reducing portal pressure, while microbiota-targeted interventions (antibiotics, probiotics, fecal transplantation) address gut-derived inflammation. This review synthesizes our current understanding of the gut-liver-NO axis in cirrhosis, highlighting how dysbiosis and aberrant NO signalling reinforce each other through inflammatory feedback loops, and identifies critical gaps between mechanistic knowledge and clinical application that warrant further investigation.},
}

Humans
*Dysbiosis/metabolism/microbiology/immunology
*Nitric Oxide/metabolism
*Gastrointestinal Microbiome
*Liver Cirrhosis/metabolism/microbiology/pathology/physiopathology
Animals
Disease Progression
Liver/metabolism/pathology
Hypertension, Portal/metabolism/microbiology
Signal Transduction
Nitric Oxide Synthase Type III/metabolism

@article {pmid42096120,
year = {2026},
author = {Wu, R and Yao, G},
title = {Research advancement on the correlation between gut microbiota and chronic kidney disease.},
journal = {Antonie van Leeuwenhoek},
volume = {119},
number = {6},
pages = {},
pmid = {42096120},
issn = {1572-9699},
support = {010086//the Beijing Major Epidemic Prevention and Control Key Specialty Intensive Care Medicine Construction Project under Grant/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Renal Insufficiency, Chronic/microbiology/therapy ; Dysbiosis/microbiology ; Probiotics ; Animals ; },
abstract = {Chronic kidney disease (CKD) represents a significant global health challenge, with its progression and complications associated with dysbiosis of the gut microbiota. Patients with CKD demonstrate stage-dependent alterations in the composition of gut microbiota and a reduction in diversity, which is characterized by a decline in beneficial bacteria (e.g., Bifidobacterium, Lactobacillus) and an increase in pathogenic species. This dysbiosis disrupts the gut-kidney axis, resulting in a depletion of protective metabolites such as short-chain fatty acids (SCFAs) and secondary bile acids, while facilitating the accumulation of toxic metabolites including trimethylamine N-oxide (TMAO), indoxyl sulfate (IS), and p-cresyl sulfate (pCS). These toxins contribute to the progression of CKD and cardiovascular complications through mechanisms that involve oxidative stress, inflammation (e.g., NF-ĸB/NLRP3 activation), fibrosis (e.g., TGF-β/Smad signaling), and endothelial dysfunction. Therapeutic strategies aimed at modulating the gut microbiota encompass dietary interventions (such as increasing fiber and plant-based protein), microecological agents (including probiotics and prebiotics), fecal microbiota transplantation (FMT), and adsorbents (e.g., targeting uremic toxins). Although these approaches show promise in delaying CKD progression and alleviating complications, they necessitate further validation through large-scale clinical trials to confirm their efficacy, safety, and the development of personalized protocols. Investigating the gut-kidney axis may provide novel biomarkers and therapeutic opportunities for enhancing CKD outcomes.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Renal Insufficiency, Chronic/microbiology/therapy
Dysbiosis/microbiology
Probiotics
Animals

@article {pmid42097400,
year = {2026},
author = {Wang, H and Li, T and Yang, J and Zhang, W and Chen, S and Song, M and Wang, S and Liu, C},
title = {Drinking water temperatures modulate gut microbiota-L-cysteine axis to enhance adipose thermogenesis and alleviate obesity-related metabolic disorders in mice.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124438},
doi = {10.1016/j.lfs.2026.124438},
pmid = {42097400},
issn = {1879-0631},
abstract = {AIMS: Although people living in different countries prefer to drink water at various temperatures, the influence of drinking water temperature on metabolic homeostasis remains largely unexplored. This study investigated how different drinking-water temperatures affect metabolic regulation and the underlying gut microbiota-metabolite interactions.

MATERIALS AND METHODS: High-fat diet (HFD)-fed mice were given water at 0 °C, 25 °C, or 40 °C. Metabolic alterations were assessed by histopathology, serum biochemistry, and body-composition analysis, with food intake and core temperature monitored. Gut microbiota causality was examined using antibiotic depletion and reciprocal fecal microbiota transplantation (FMT). 16S rRNA gene sequencing and metabolomics were performed to characterize fecal microbial and metabolite profiles. Adipose stromal vascular fraction (SVF) cells were used in vitro to examine the effects of L-cysteine on lipid metabolism.

KEY FINDINGS: Both 0 °C and 40 °C water ameliorated HFD-induced metabolic dysfunction through increased energy expenditure, reduced liver steatosis, and enhanced adipose-tissue thermogenesis, independent of differences in intake. Cold water selectively enriched Bifidobacterium pseudolongum and Adlercreutzia equolifaciens, whereas warm water increased Bacteroides acidifaciens, Alistipes inops and Alistipes obesi, indicating distinct microbiota configurations. Antibiotic ablation blunted these benefits, while cross-group FMT reproduced the metabolic and thermogenic phenotypes, confirming a microbiota-dependent mechanism. Despite divergent microbiota structures, both temperature regimens consistently elevated L-cysteine, which reduced lipid accumulation and enhanced thermogenic gene expression in SVF cells.

SIGNIFICANCE: These findings highlight drinking-water temperature as a simple, safe, and sustainable lifestyle factor with translational potential to mitigate obesity-related metabolic dysfunction, potentially via a gut microbiota-L-cysteine axis that enhances adipose thermogenesis and systemic metabolic homeostasis.},
}

@article {pmid42097699,
year = {2026},
author = {Xu, T and Lu, R and Oakland, DN and Estaleen, R and Rawlings, A and Montano, H and Diab, S and Michaelis, JS and Pop, M and Bankole, A and Reilly, CM and Luo, XM},
title = {Double humanised lupus mouse model with human immune system and faecal microbiota from patients with SLE.},
journal = {Lupus science & medicine},
volume = {13},
number = {1},
pages = {},
doi = {10.1136/lupus-2026-001982},
pmid = {42097699},
issn = {2053-8790},
mesh = {Animals ; *Lupus Erythematosus, Systemic/immunology/microbiology/therapy ; Humans ; Disease Models, Animal ; Mice ; *Fecal Microbiota Transplantation ; Female ; Feces/microbiology ; Immunoglobulin G/blood ; Gastrointestinal Microbiome ; Immunoglobulin M/blood ; Hematopoietic Stem Cell Transplantation ; T-Lymphocytes/immunology ; Terpenes ; Spleen/immunology ; Male ; },
abstract = {OBJECTIVE: We aimed to create a double humanised lupus mouse model with a human immune system and faecal microbiota from patients with SLE.

METHODS: We established the Double humanised SLE (DhuSLE) mouse by engrafting NSG immunodeficient mice with human CD34[+] haematopoietic stem and progenitor cells (NSG-hu mice) and performing faecal microbiota transplantation from patients with SLE (SLE-FMT).

RESULTS: While FMT in general transiently suppressed the development of human T cells in NSG-hu mice, SLE-FMT but not FMT from non-SLE donors promoted superficial skin lesions. Importantly, the combination of SLE-FMT and pristane in NSG-hu, now called the DhuSLE-P mouse, induced proteinuria although this clinical sign observed in mice did not reflect that of the microbiota donors. DhuSLE-P mice exhibited a higher level of human IgM in the circulation than NSG-hu mice, which was positively correlated with the frequency of plasma cells in the spleen. In the splenic sections of DhuSLE-P mice, nuclear BCL6 was minimally detected but CD138 expression was evident, suggesting that most plasma cells generated were not class switched and produced IgM. Some human IgG was detected in the kidney of DhuSLE-P mice with a trend towards increased total IgG in the serum. Analysis of the faecal microbiota revealed that the gut microbiota compositions were different between DhuSLE-P mice and NSG-hu mice due to SLE-FMT but not the injection of pristane.

CONCLUSION: Together, these results introduced the first humanised lupus mouse model combining the human immune system and gut microbiota from patients with SLE. However, limitations exist and the model may benefit from methods that promote antibody class switching. On further development, the DhuSLE model can be useful for elucidating mechanisms and/or evaluating SLE treatments.},
}

Animals
*Lupus Erythematosus, Systemic/immunology/microbiology/therapy
Humans
Disease Models, Animal
Mice
*Fecal Microbiota Transplantation
Female
Feces/microbiology
Immunoglobulin G/blood
Gastrointestinal Microbiome
Immunoglobulin M/blood
Hematopoietic Stem Cell Transplantation
T-Lymphocytes/immunology
Terpenes
Spleen/immunology
Male

@article {pmid42083540,
year = {2026},
author = {YuXuan, G and Iqbal, MK and Khan, B and Khan, H and Ud Din Shah, SS and Al-Hussain, F and Kiyani, MM and Bashir, S},
title = {The Gut-Brain Connection: Exploring the Connection Between the Gastrointestinal System and Parkinson's Disease.},
journal = {CNS & neurological disorders drug targets},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715273419693251206130059},
pmid = {42083540},
issn = {1996-3181},
abstract = {Parkinson's disease (PD) is a complex neurodegenerative disorder characterized by motor and non-motor symptoms. Recent studies indicate that the gut-brain axis contributes to both the initiation and progression of PD, a disorder that primarily affects the central nervous system. This article reviews current research on the interaction between the central nervous system and the gastrointestinal tract in PD. The vagus nerve, areas of the enteric nervous system (ENS), systemic inflammation, and the microbiome are all involved in this interaction. For example, recent studies have shown PD-related effects such as abnormal distribution of gut bacteria, increased gut barrier permeability, and α-synuclein transport from the gut to the brain. A comprehensive evaluation of motor and non-motor symptoms was conducted. Additionally, we explored drugs that specifically target the gastrointestinal system, the possible gastrointestinal symptoms of PD, and how these symptoms may serve as early indicators of the disease. Our article also discusses dietary modifications, probiotics, and fecal microbiota transplantation as potential treatments for PD. By reviewing clinical and basic scientific research as well as translational applications, this article highlights the relationship between the central nervous system and the digestive system in PD. A better understanding of this complex connection may lead to improved detection and treatment of this debilitating disease and offer new opportunities for prevention and therapy. Finally, this paper suggests directions for further research in this area.},
}

@article {pmid42083785,
year = {2026},
author = {Wu, Y and Liu, J and Ren, Y and Zou, C},
title = {Unravelling the Gut-Skin Axis in Chronic Urticaria: Dysbiosis, Metabolites and Immunological Mechanisms.},
journal = {Experimental dermatology},
volume = {35},
number = {5},
pages = {e70261},
doi = {10.1111/exd.70261},
pmid = {42083785},
issn = {1600-0625},
support = {2025C02080//the Key Research and Development Plan of Zhejiang Province/ ; WKJ-ZJ-2409//the National Health Commission Scientific Research Fund/ ; },
mesh = {Humans ; *Dysbiosis/immunology ; *Gastrointestinal Microbiome ; Animals ; *Chronic Urticaria/immunology/microbiology/metabolism ; *Skin/immunology/metabolism ; Mice ; Fatty Acids, Volatile/metabolism ; Mast Cells/immunology ; },
abstract = {Although the core pathophysiological pathways of chronic urticaria (CU) are increasingly understood, the upstream triggers and factors contributing to disease chronicity remain poorly understood. Emerging evidence suggests that gut microbiota dysbiosis represents a potentially modifiable upstream factor, which has been predominantly investigated in patients with chronic spontaneous urticaria (CSU). Multi-omics and Mendelian randomization studies have provided convergent evidence linking gut dysbiosis to systemic inflammation and mast cell instability. This is characterized primarily by the depletion of short-chain fatty acid (SCFA)-producing taxa (e.g., Faecalibacterium, Roseburia and Bifidobacterium) and the relative enrichment of pro-inflammatory Proteobacteria (particularly Enterobacteriaceae). Mechanistically, these alterations may lower the mast cell activation threshold and promote systemic immune dysregulation through specific metabolic shifts, such as the depletion of SCFAs and unsaturated fatty acids, and the translocation of endotoxins (e.g., lipopolysaccharide) due to compromised intestinal barrier function. In this review, we discuss how the use of Mendelian randomization (MR) and germ-free mouse models can advance the gut-urticaria axis (with a primary focus on CSU) from mere correlation to causation, while highlighting the crucial need to account for clinical confounders. Finally, we evaluate the clinical translational potential and associated challenges of microbiome-targeted interventions (e.g., probiotics, faecal microbiota transplantation) as novel adjuvant therapies.},
}

Humans
*Dysbiosis/immunology
*Gastrointestinal Microbiome
Animals
*Chronic Urticaria/immunology/microbiology/metabolism
*Skin/immunology/metabolism
Mice
Fatty Acids, Volatile/metabolism
Mast Cells/immunology

@article {pmid42086265,
year = {2026},
author = {Bénard, MV and Van Der Spek, MJ and Davids, M and Visser, CE and Zoetendal, EG and Rethans, B and Zwezerijnen-Jiwa, FH and Visschedijk, MC and Ponsioen, CY and Oldenburg, B and Weersma, RK},
title = {Transfer of faeces in ulcerative colitis 2: improving efficacy - study protocol for a multicentre randomised controlled trial (TURN2 study).},
journal = {BMJ open},
volume = {16},
number = {5},
pages = {e107097},
doi = {10.1136/bmjopen-2025-107097},
pmid = {42086265},
issn = {2044-6055},
mesh = {Humans ; *Colitis, Ulcerative/therapy/microbiology ; *Fecal Microbiota Transplantation/methods ; Double-Blind Method ; Gastrointestinal Microbiome ; *Feces/microbiology ; Multicenter Studies as Topic ; Randomized Controlled Trials as Topic ; Treatment Outcome ; Adult ; Male ; Female ; Enema ; },
abstract = {INTRODUCTION: The interaction between the gut microbiota and the host immune system is implicated in the pathogenesis of inflammatory bowel disease, including ulcerative colitis (UC). Targeting the gut microbiota with faecal microbiota transplantation (FMT) from a healthy donor has shown promise in inducing remission in patients with active UC. However, mixed results and protocol heterogeneity have limited its practical application. Our previous Transfer of Faeces in Ulcerative Colitis; Restoring Homeostasis (TURN) trial found a correlation of clinical response with specific strains and butyrate production. Since most gut microbes, including many butyrate producers, are anaerobes, anoxic processing of donor stool may be essential to increase efficacy of FMT in UC. This trial aims to enhance FMT efficacy by applying strict anoxic processing, selecting donors based on microbial composition and using repetitive dual-route administration.

METHODS AND ANALYSIS: This randomised, double-blind, placebo-controlled, multicentre study evaluates the efficacy of strictly anoxic prepared donor FMT compared with anoxic prepared autologous FMT in patients with mild to moderate active UC. An open-label extension option is available for non-responders in the autologous arm. Included patients will receive 4 weekly FMTs, comprising two double-route administrations (nasoduodenal administration combined with enema) and two single enemas. Donors are selected based on their microbiota profile, informed by our previous TURN trial and literature. A total of 76 patients evaluable for the primary endpoint will be included. The primary endpoint is steroid-free clinical and endoscopic remission at week 8, assessed by the adapted Mayo score. An interim analysis will be conducted midway through the study by a Data Safety Monitoring Board to monitor efficacy and safety. Other outcomes of this study include the evaluation of clinical, endoscopic and histological response. In addition to clinical results, this study aims to provide valuable insights into specific microbial strains, metabolites and mechanisms correlated with response, aiding in the development of future microbial therapies.

ETHICS AND DISSEMINATION: Ethics approval was obtained from the medical ethics committee of the Amsterdam University Medical Centre in the Netherlands (reference number 2018_057). All participants will provide written informed consent. The results of the trial will be disseminated through publication in a peer-reviewed journal and presentations at (inter)national conferences.

TRIAL REGISTRATION NUMBER: Prospectively registered in May 2018 in the Dutch Trial Register (NTR/LTR) as NL7770. Assigned NL-OMON52507 following the transition of the Dutch Trial Register to the Overview of Medical Research in the Netherlands. Also registered at ClinicalTrials.gov (NCT05998213).},
}

Humans
*Colitis, Ulcerative/therapy/microbiology
*Fecal Microbiota Transplantation/methods
Double-Blind Method
Gastrointestinal Microbiome
*Feces/microbiology
Multicenter Studies as Topic
Randomized Controlled Trials as Topic
Treatment Outcome
Adult
Male
Female
Enema

@article {pmid42088008,
year = {2026},
author = {Sgarbossa, C and Forth, E and Squires, S and Groth, A and Farid, M and Gallant, K and Desai, D and Redfearn, W and Milev, R},
title = {Neurobiological effects of microbial treatments within psychiatry: a systematic review.},
journal = {Frontiers in psychiatry},
volume = {17},
number = {},
pages = {1745964},
pmid = {42088008},
issn = {1664-0640},
abstract = {OBJECTIVE: Though microbial interventions such as probiotics and fecal microbiota transplantation have had a growing body of evidence suggesting their efficacy in alleviating the symptoms of psychiatric illnesses, their exact mechanisms of action and impacts on the brain are still not fully characterized. The aim of this review is to compile and summarize the current literature regarding neurobiological changes associated with microbial interventions targeting psychiatric symptoms in healthy and psychiatric populations.

METHODS: A systematic search of four databases was conducted using key terms related to neuroimaging, microbial interventions, and psychiatric illnesses and/or symptoms. All results were then evaluated based on specific eligibility criteria.

RESULTS: 10 studies met eligibility criteria and were included in this systematic review. Three of the five healthy control studies and all five of the studies conducted within psychiatric populations, observed significant neurobiological changes associated with probiotic intervention either in areas with psychiatric relevance, in the direction of a healthier profile, or correlated with improved psychiatric and/or affective symptoms. The interventions used in these studies consisted of probiotics with bacterial species primarily from the lactobacillus and bifidobacterium genera, at doses ranging from 1-900 billion CFU, taken for durations ranging from 4 weeks to 6 months.

CONCLUSIONS: The findings from this review suggest that probiotic intervention may be associated with neurobiological changes, and that these changes could play a role in ameliorating psychiatric symptoms. More research is needed to replicate these findings, explore other psychiatric populations and microbial interventions, and fully elucidate the mechanisms driving these promising neurobiological and clinical changes.},
}

@article {pmid41615004,
year = {2026},
author = {Tremblay, C and Edger-Lacoursière, Z and Schneider, G and Jean, S and Calva, V and Nedelec, B},
title = {Rehabilitation Evaluation and Treatment for Skin Graft Complications of the Genitalia.},
journal = {Journal of burn care & research : official publication of the American Burn Association},
volume = {47},
number = {3},
pages = {868-878},
doi = {10.1093/jbcr/irag016},
pmid = {41615004},
issn = {1559-0488},
mesh = {Humans ; Male ; *Skin Transplantation/adverse effects ; Adult ; *Fournier Gangrene/surgery/rehabilitation ; Aged ; *Fasciitis, Necrotizing/surgery/rehabilitation ; Perineum ; },
abstract = {Skin graft complications may include pain, contractures, hypertrophic scars (HSc), hypersensitivity, and recurrent wounds. Complications involving grafts to the genitalia, perineum, and/or buttocks can be particularly challenging, directly affecting walking, sitting, voiding, bowel elimination, sexual function, and intimacy, ultimately diminishing quality of life. Perineal and pelvic floor rehabilitation (PPFR) is commonly used to treat various pelvic floor disorders; however, its application following burn injury or necrotizing fasciitis has not been previously described. This manuscript presents the evaluation and treatment outcomes of patients with necrotizing fasciitis or Fournier's gangrene. Initial evaluation was conducted approximately 4 months postadmission by a certified pelvic floor physiotherapist and occupational therapist. Treatment included pelvic floor rehabilitation, patient education, sensory re-education, bladder and bowel training, use of adapted pressure garments, gel application, cutaneous and myofascial stretching, and manual therapy. This report details the outcomes of 2 male patients (37 and 69 years old) who underwent skin grafting and reconstructive surgery following necrotizing fasciitis and Fournier's gangrene. Both presented with complex wounds that closed approximately 4 months postadmission, accompanied by contractures, HSc, altered sensory perception, incontinence, and sexual intimacy dysfunction. Following PPFR treatment, improvements were observed in pruritus, urinary and fecal retention capacity, sexuality-related fear avoidance, penile deviation, lower extremity range of motion, satisfaction with sexual function, and sensory perception. This is the first description of a standardized PPFR protocol in this context, demonstrating that specialized interdisciplinary rehabilitation can enhance sexual function, body-image satisfaction, and overall quality of life in patients with genital, perineal, and/or buttock grafts.},
}

Humans
Male
*Skin Transplantation/adverse effects
Adult
*Fournier Gangrene/surgery/rehabilitation
Aged
*Fasciitis, Necrotizing/surgery/rehabilitation
Perineum

@article {pmid42079588,
year = {2026},
author = {Qie, RJ and Qin, JB and Wu, HY and Ji, ZH},
title = {Key messengers in the gut-nose axis: mechanisms of gut microbial metabolites in the immunomodulation of allergic rhinitis.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1796775},
pmid = {42079588},
issn = {1664-3224},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Rhinitis, Allergic/immunology/metabolism/microbiology/therapy ; *Immunomodulation ; Animals ; *Nasal Mucosa/immunology/metabolism/microbiology ; },
abstract = {Allergic rhinitis (AR) is a common clinical chronic inflammatory respiratory disease, in which immune imbalance serves as a core component of its complex pathogenesis. In recent years, the gut-nose axis has emerged as a novel pathway mediating immune crosstalk between the intestinal tract and the nasal cavity, garnering significant academic attention. Gut microbial metabolites (such as short-chain fatty acids, tryptophan metabolites, bile acids, and polyamines) are profoundly involved in the pathophysiology of AR by reshaping the nasal mucosal immune microenvironment via systemic circulation and neural pathways and regulating the Th2/Treg balance, innate lymphoid cells (ILC2s), and mast cell functions. This article systematically reviews the immunomodulatory mechanisms of core gut microbial metabolites, explores their impact on nasal mucosal epithelial barrier function and immune cell activity, and summarizes metabolite-based clinical intervention strategies, including postbiotic therapy (bioactive compounds derived from microbial cells or metabolites), precision nutritional interventions, and fecal microbiota transplantation. Additionally, the paper analyzes current challenges such as heterogeneity and dose-response effects, aiming to provide a theoretical foundation for understanding the immunomodulatory mechanisms of the gut-nose axis and a reference for developing novel precision strategies for the prevention and treatment of AR.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Rhinitis, Allergic/immunology/metabolism/microbiology/therapy
*Immunomodulation
Animals
*Nasal Mucosa/immunology/metabolism/microbiology

@article {pmid42079748,
year = {2026},
author = {Zheng, L and Jia, T and Li, Y and Zhang, Z and Su, H and Zhang, R},
title = {The interplay between gastrointestinal dysfunction and gut microbiota dynamics in sepsis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1761536},
pmid = {42079748},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Sepsis/microbiology/physiopathology/complications/immunology ; *Dysbiosis/microbiology ; Animals ; *Gastrointestinal Diseases/microbiology ; *Gastrointestinal Tract/microbiology/physiopathology ; Intestinal Mucosa/microbiology ; Multiple Organ Failure ; },
abstract = {Sepsis frequently involves early gastrointestinal dysfunction, in which intestinal barrier breakdown and microbiota dysbiosis amplify systemic inflammation and contribute to multi-organ failure. Emerging evidence indicates that the gut is not merely a bystander in sepsis but an active driver of pathogenic cascades through epithelial injury, mucosal immune dysregulation, ischemia-reperfusion stress, and impaired motility, collectively promoting microbial translocation and immune deviation. In parallel, sepsis is associated with profound remodeling of the gut microbiome, characterized by reduced commensal diversity, expansion of pathobionts, and functional shifts in key microbial metabolites, including short-chain fatty acids, bile acids, and tryptophan-derived products, which further compromise mucosal integrity and host immune tone. This narrative review synthesizes experimental, translational, and clinical findings to elucidate the bidirectional interaction gut barrier-microbiota interplay in sepsis and to summarize mechanistic links across epithelial, immune, and metabolic signaling pathways, including gut-liver and gut-brain axes relevant to sepsis-associated organ dysfunction. dysfunctional microbial community leads to systemic immune deviation, multi-organ dysfunction and sepsis-associated encephalopathy, a common and severe neurological complication of sepsis. We also discuss emerging therapeutic strategies targeting the gut-microbiota axis-such as early enteral nutrition, prebiotics/postbiotics, defined microbial consortia, fecal microbiota transplantation, and metabolite-based supplementation-and evaluate their potential and limitations in septic populations. Finally, we highlight key challenges, including unresolved causality, inter-individual variability, context-dependent responses, and safety concerns, underscoring the need for longitudinal multi-omic profiling, host-microbiome phenotyping, and mechanism-informed interventional trials to enable precision microbiome-based approaches for sepsis.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Sepsis/microbiology/physiopathology/complications/immunology
*Dysbiosis/microbiology
Animals
*Gastrointestinal Diseases/microbiology
*Gastrointestinal Tract/microbiology/physiopathology
Intestinal Mucosa/microbiology
Multiple Organ Failure

@article {pmid42081036,
year = {2026},
author = {Yang, F and Liu, S and Liu, G and Luo, L and Lu, X and Lin, W and Chen, J and Lin, R},
title = {Fecal microbiota transplantation from different pig breeds alters fat deposition and gut microbiota in mice.},
journal = {Applied microbiology and biotechnology},
volume = {},
number = {},
pages = {},
doi = {10.1007/s00253-026-13823-z},
pmid = {42081036},
issn = {1432-0614},
support = {2023J01446//Natural Science Foundation of Fujian Province/ ; 2019-144//Fujian Modern Agricultural Pig Industry Technology System Project/ ; },
abstract = {Gut microbiota plays a vital role in nutrient digestion, energy metabolism, and immune regulation in pigs. However, the core bacterial species influencing fat deposition remain poorly defined due to the complexity and diversity of the intestinal microbial ecosystem. In this study, healthy Putian Black (PT) pigs and Duroc × Landrace × Yorkshire (DLY) pigs of similar ages were used as fecal microbiota transplantation (FMT) donors, with male ICR mice as recipients. A control group (CM) received saline, while the experimental groups were gavaged fecal suspensions from PT pigs (PM) or DLY pigs (DM). Results showed that intramuscular fat content, triglyceride levels, and adipogenic gene expression (PPARG, FABP4, LPL, ATGL) were extremely significant higher in the PM group than in the DM group (P<0.01). 16 S rRNA sequencing revealed that both PM and DM groups had lower Firmicutes abundance but higher Bacteroidetes abundance compared to the CM group (P<0.05). Notably, the PM group exhibited higher Firmicutes and lower Bacteroidetes abundance than the DM group (P<0.05). Correlation analysis identified S_uncultured_bacterium_g_Prevotella as negatively correlated with FASN and DGAT2 expression (P<0.01), while Lactobacillus species showed positive correlations with PPARG, FASN, and ATGL expression (P<0.05). These findings demonstrate that FMT alters gut microbiota composition and host gene expression, thereby influencing fat deposition, with Prevotella and Lactobacillus emerging as potential key genera. KEY POINTS: ∙ FMT resulted in extremely significant higher intramuscular fat content in the PM group compared to the DM group. ∙ Lactobacillus may be a key genus regulating fat deposition in PT pigs. ∙ Prevotella may be a key genus regulating fat deposition in DLY pigs.},
}

@article {pmid42083059,
year = {2026},
author = {Diop, K and Benlaïfaoui, M and Hunter, S and Méndez-Salazar, EO and Hakozaki, T and Richard, C and Prifti, DK and Kourtian, S and Proulx-Rocray, F and Naimi, S and Ponce, M and Messaoudene, M and Cauchois, F and Belkaid, W and Bataille, V and Lee, K and Mihalcioiu, C and Watson, IR and Elkrief, A and Routy, B},
title = {Metagenomics and culturomics reveal the dual role of the gut microbiome in the development of immune-related toxicities and the efficacy of immune checkpoint inhibitors in cancer.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02419-4},
pmid = {42083059},
issn = {2049-2618},
support = {284894//Fonds de recherche du Québec/ ; },
abstract = {BACKGROUND: Despite their major impact on cancer treatment, immune checkpoint inhibitors (ICI) are frequently associated with immune-related adverse events (irAE). Growing evidence suggests that the occurrence of irAE may be correlated with enhanced ICI efficacy, although the underlying mechanisms remain unknown. Most studies investigating the role of the gut microbiome in oncology have relied on sequencing approaches, particularly shotgun metagenomics. Although microbiome profiling revealed strong associations between specific bacterial taxa and clinical outcomes, it has limitations, including an inability to detect low-abundance bacteria and to recover live cultivable bacteria. To overcome these limitations, we combined shotgun metagenomics and culturomics on fecal samples collected from patients with melanoma and non-small cell lung cancer (NSCLC), at baseline and at the onset of immune related (ir)-colitis.

RESULTS: We first validated across three independent cohorts of 589 patients with melanoma or NSCLC treated with ICI that grade ≥ 2 irAE were associated with significantly longer overall survival (OS) and progression-free survival (PFS). Complementary analysis using shotgun metagenomics and culturomics revealed that patients who developed grade ≥ 2 irAE had a lower alpha diversity compared to those who did not develop grade ≥ 2 irAE. Metagenomics results showed enrichment of Ruminococcus gnavus and Streptococcus vestibularis at baseline in grade ≥ 2 irAE patients, while Clostridium paraputrificum and Streptococcus spp. were isolated by culturomics from baseline stool samples from ir-colitis patients. Longitudinal analysis of paired stool samples revealed a shift in microbiome composition with enrichment of Paraclostridium bifermentans and Clostridium paraputrificum, lower lipopolysaccharide and higher flagellin concentrations at baseline compared with the time of ir-colitis. Fecal microbiome transplantation from a patient with ir-colitis into mice induced surrogate markers of colonic inflammation and enhanced the anti-tumor activity of combined anti-PD-1/CTLA-4. P. bifermentans isolated from this patient sample demonstrated direct epithelial barrier disruption in Caco-2 monolayers, characterized by decreased ZO-1 and Occludin immunofluorescence signal and increased TNF-α and IL-1β expression. Moreover, in the dextran sodium sulfate (DSS) colitis model, P. bifermentans worsened weight loss. In a separate tumor model, it amplified the anti-tumor effect of dual ICI. This beneficial effect was also maintained after treatment with P. bifermentans < 3 kDa filtered supernatant.

CONCLUSION: Altogether, our results suggest that P. bifermentans promotes subclinical colitis while increasing the efficacy of dual ICI. This provides a potential microbiome-derived link between irAE and improved anti-tumor responses. Video Abstract.},
}

@article {pmid42083117,
year = {2026},
author = {Helliwell, JA and Sciberras, P and Dosis, A and Burke, J and Chilton, CH and Wood, HM and Jayne, DG},
title = {Modulation of the gut microbiota as a novel strategy to prevent anastomotic leak after colorectal surgery: Systematic scoping review.},
journal = {Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland},
volume = {28},
number = {5},
pages = {e70472},
doi = {10.1111/codi.70472},
pmid = {42083117},
issn = {1463-1318},
mesh = {Humans ; *Anastomotic Leak/prevention & control/microbiology ; *Gastrointestinal Microbiome/physiology/drug effects ; Probiotics/therapeutic use ; *Colorectal Surgery/adverse effects ; Fecal Microbiota Transplantation ; Animals ; Female ; Male ; },
abstract = {BACKGROUND: Anastomotic leak (AL) remains a major source of morbidity following colorectal surgery. Increasing evidence implicates the gut microbiome in the pathogenesis of AL, with certain microbial species disrupting tissue repair through collagen degradation. Perioperative modulation of the microbiome may offer a novel strategy to improve anastomotic healing. This scoping review aimed to map available evidence on microbiome-targeted interventions, synthesise mechanistic insights, and identify translation gaps in relation to anastomotic outcomes.

METHODS: A systematic scoping review was performed. MEDLINE, Embase and Cochrane Central Registry of Controlled Trials databases were searched from database inception to 5th August 2025. Studies were eligible if they investigated perioperative interventions that modulated the gut microbiome and evaluated anastomotic healing or leak rates. Both clinical and preclinical studies were included. A narrative synthesis was performed by charting key findings.

RESULTS: Of 4209 records screened, 27 studies met the inclusion criteria: 9 clinical and 18 preclinical. Interventions included bowel preparation, probiotics, synbiotics, arginine/omega-3 supplementation, dietary modification, faecal microbiota transplantation (FMT), phosphate, tranexamic acid, morphine and infliximab. Among clinical studies, only oral antibiotics combined with mechanical bowel preparation were associated with a significant reduction in leak rates. Preclinical studies showed interventions such as high-fibre diets, FMT, rectal tranexamic acid and phosphate supplementation improved anastomotic healing via enhanced microbial diversity, suppression of pathogenic organisms, or inhibition of collagenolytic activity.

CONCLUSION: This review highlights a range of microbiome-targeted interventions with potential to reduce AL. While clinical evidence remains limited, several preclinical strategies demonstrate promise and warrant evaluation in early-phase human trials.},
}

Humans
*Anastomotic Leak/prevention & control/microbiology
*Gastrointestinal Microbiome/physiology/drug effects
Probiotics/therapeutic use
*Colorectal Surgery/adverse effects
Fecal Microbiota Transplantation
Animals
Female
Male

@article {pmid42083350,
year = {2026},
author = {Bashir, S and Shah, IM and Javeed, S and Rafiquee, A and Mir, B and Hassan Mir, R and Geer, MI and Ganie, MA},
title = {Beyond Conventional Therapy: A Comprehensive Review of Herbal, Traditional, and Emerging Interventions for Polycystic Ovary Syndrome.},
journal = {Current molecular medicine},
volume = {},
number = {},
pages = {},
doi = {10.2174/0115665240406897251206074722},
pmid = {42083350},
issn = {1875-5666},
abstract = {Polycystic ovary syndrome (PCOS) is the most common and multifactorial endocrine disorder that leads to significant changes in the reproductive, metabolic, and psychological domains of women's health in their reproductive years. In addition, the conventional therapies (lifestyle modification, metformin, oral contraceptives, and ovulation-inducing agents) that are the mainstay of management of the syndrome may still not be able to fully address the diverse pathophysiology of PCOS as well as the long-term risks associated with it. This narrative review highlights clinical and mechanistic data from studies on various complementary and alternative medicine (CAM) modalities as first-line treatments for PCOS, in addition to conventional therapy. Correspondingly, herbal and botanical agents (berberine, cinnamon, licorice, Vitex agnus-castus, curcumin, and epigallocatechin gallate) modulate insulin signalling, androgen synthesis, inflammatory pathways, and oxidative stress, with initial clinical trials reporting improvements in metabolism and hormones to a similar extent as standard therapies in selected populations. Traditional Chinese Medicine (TCM), both multi-herb prescriptions and acupuncture, provides tailored formulas that might not only regulate ovulation and endocrine parameters but also lower metabolic indices, despite the high variability across studies. Stress reduction, physical fitness, and the quality of life are among the achievements of mind-body interventions (yoga, tai chi, qigong, and mindfulness-based stress reduction). Improvements in hyperinsulinemia, hypolipidemia, ovulation, and hyperandrogenemia, along with the related insulinresistant and vitamin D-deficient phenotypes, have been steadily reported with the use of the nutraceutical combinations of inositols, vitamin D, omega-3 fatty acids, Nacetylcysteine, coenzyme Q10, and resveratrol. New non-conventional methods, such as fecal and vaginal microbiota transplantation, platelet-rich plasma, and kisspeptin analogues, have been identified as potential therapeutic routes but are still in their infancy in terms of development. Although CAM therapies have multiple advantages in controlling many PCOS domains, the official integration into clinical practice would require standardization, rigorous randomized controlled trials, and continuous safety monitoring. If correctly and cautiously applied, CAM may be useful as an adjunct alongside established therapy, rendering PCOS management more holistic and personalized.},
}

@article {pmid42068877,
year = {2026},
author = {Liao, W and Gao, J and Zhang, J and Wu, Y and Jiang, Y and Liu, H and Chen, S and Xiu, L and Zhong, G},
title = {Haizao Yuhu Decoction alleviates goiter via the gut-thyroid axis: Microbiota-derived SCFAs promote hormone synthesis and restore apoptosis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {156},
number = {},
pages = {158256},
doi = {10.1016/j.phymed.2026.158256},
pmid = {42068877},
issn = {1618-095X},
abstract = {BACKGROUND AND PURPOSE: Haizao Yuhu Decoction (HYD) is a classic Traditional Chinese Medicine for goiter, but its mechanism related to the "gut-thyroid axis" remains unknown. This study investigates whether HYD treats goiter via this axis and elucidates the underlying mechanisms.

METHODS: A rat goiter model was induced with propylthiouracil (PTU), followed by two weeks of HYD treatment. Gut microbiota was analyzed by metagenomic sequencing; fecal and serum short-chain fatty acids (SCFAs) were quantified by targeted LC-MS/MS analysis. Thyroid function was assessed via iodine content and hormone levels. Key proteins in hormone synthesis and apoptosis were evaluated by Western blot and immunohistochemistry. Fecal microbiota transplantation (FMT) supported microbiota causality.

RESULTS: HYD alleviated goiter and hypothyroidism. It restored gut microbiota diversity and enriched SCFA-producing bacteria (e.g., Bifidobacterium pseudolongum), coincident with increased SCFAs including butyrate. These SCFA changes correlated with reduced HDAC1/2/3/8 in thyroid tissue, consistent with enhanced histone acetylation, and were accompanied by upregulation of NIS, TG, TPO, and DUOX2. Concurrently, elevated SCFAs were associated with AKT/Mdm2 pathway inhibition, p53 stabilization, downstream activation of P21 and Caspase-3, and suppression of Bcl-2, supporting a model of promoted thyroid cell apoptosis. FMT supported that HYD-modulated microbiota alone reproduced these effects.

CONCLUSION: HYD alleviates PTU-induced goiter in rats in a manner associated with gut microbiota remodeling and increased SCFA production, which correlate with enhanced thyroid hormone synthesis and restored apoptosis-a relationship supported by FMT experiments. However, direct interactions between HYD and PTU cannot be fully excluded. These findings are consistent with a model in which HYD acts through the gut-thyroid axis, providing mechanistic insights into its therapeutic effects.},
}

@article {pmid42069299,
year = {2026},
author = {Meng, F and Xue, M and Li, H and Tao, G and Chen, W and Li, Y and Pei, H and Liu, Z and Yin, D and Qin, S and Xue, J and Liu, B},
title = {Consumption of hydrogen-rich water ameliorates atherosclerosis by modulating gut microbiota and enhancing short-chain fatty acid levels.},
journal = {Life sciences},
volume = {397},
number = {},
pages = {124418},
doi = {10.1016/j.lfs.2026.124418},
pmid = {42069299},
issn = {1879-0631},
abstract = {AIMS: Molecular hydrogen (H2) is a safe gaseous signaling molecule with anti-inflammatory properties. This study aimed to explore the anti-atherosclerotic effects of hydrogen-rich water (H2W) and clarify the underlying mechanism involving the gut microbiota and its metabolites.

MATERIALS AND METHODS: ApoE[-/-] mice were administered H2W to evaluate atherosclerotic plaque development and stability. Gut microbiota composition and short-chain fatty acid levels were analyzed. Antibiotic-induced microbiota depletion and fecal microbiota transplantation (FMT) were used to verify the mediating role of the gut microbiota. In vitro assays were performed to examine the effects of propionate on macrophage inflammation and polarization.

KEY FINDINGS: H2W consumption significantly attenuated plaque formation and enhanced plaque stability in ApoE[-/-] mice, accompanied by altered gut microbiota structure and short-chain fatty acid profiles. Antibiotic treatment abolished the protective effects of H2W, while FMT from H2W-treated mice transferred the anti-atherosclerotic phenotype. H2W notably increased propionate levels in cecal contents and serum. Propionate directly suppressed inflammatory responses and M1 macrophage polarization in vitro.

SIGNIFICANCE: This study demonstrates that H2W alleviates atherosclerosis by modulating the gut microbiota-propionate-macrophage axis. Our findings highlight H2W as a promising and safe intervention for atherosclerosis and provide new mechanistic insights into the crosstalk between gut microbial metabolites and vascular inflammation.},
}

@article {pmid42069657,
year = {2026},
author = {de Oliveira Andrade, F and Staley, C and Jin, L and Ozgul-Onal, M and McDermott, M and Kenanoglu, S and de Oliveira, KA and Verma, V and Hilakivi-Clarke, L},
title = {Gut microbiome modulates breast cancer risk in socially isolated mice.},
journal = {Breast cancer research : BCR},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13058-026-02292-x},
pmid = {42069657},
issn = {1465-542X},
abstract = {BACKGROUND: Breast cancer risk and mortality are associated with disrupted gut microbiome functions which in turn can affect tumor immune responses. One source of disruption could be stress. Social isolation (SI) stress consistently increases breast cancer risk and mortality in preclinical models and women, but whether SI promotes mammary tumor growth by affecting gut microbiome has not been studied.

METHODS: We investigated if increased E0771 mammary tumorigenesis in SI female C57BL/6 mice was associated with changes in their gut microbiome by treating mice with an antibiotic mix that suppresses bacterial abundance and by performing fecal microbiota transplantation (FMT) from SI or group-housed (GH) donors to GH host. The effect of SI on anti-tumor CD8 + T and immunosuppressive Foxp3 + Treg cells was also studied.

RESULTS: Fecal bacteria that were present at different abundances between GH and SI mice were short chain fatty acid (SCFA) producers, and the most consistent change across three replicate studies was decreased fecal abundance of Akkermansia genus in SI mice. In addition, fecal propionic acid levels were reduced in SI mice, compared with GH mice, in agreement with Akkermansia being propionic acid producer. SI reduced the activation of CD8 + T cells systemically and in the tumor microenvironment, while the levels and activation of immunosuppressive Foxp3 Tregs were increased. Antibiotic treatment reversed increased mammary tumorigenesis and immunosuppression in SI mice but did not affect GH mice. Further, FMT from SI donors increased tumor growth in GH host, compared with FMT from GH donor.

CONCLUSION: Gut dysbiosis caused by SI may be driving their increased mammary tumorigenesis, potentially through gut dysbiosis induced immunosuppression.},
}

@article {pmid42072400,
year = {2026},
author = {Lin, Y and Lu, P and Ding, Q and Liu, M},
title = {Current Perspectives on the Inflammatory Bowel Disease Pathogenesis of Microbiota and the Gut-Brain Axis, and Emerging Therapeutics.},
journal = {Biomedicines},
volume = {14},
number = {4},
pages = {},
doi = {10.3390/biomedicines14040859},
pmid = {42072400},
issn = {2227-9059},
abstract = {The pathogenesis of inflammatory bowel disease (IBD) is driven by an interplay among intestinal dysbiosis and aberrant mucosal immune responses. This review centers on the microbiota as a pivotal pathogenic hub, systematically dissecting how three hallmark features of dysbiosis-reduced microbial alpha diversity, depletion of immunomodulatory commensals, and expansion of pro-inflammatory pathobionts-collectively compromise epithelial barrier function, promote bacterial translocation, and sustain chronic mucosal inflammation. We further integrate emerging evidence implicating bidirectional gut-brain axis communication in amplifying both peripheral inflammation and central nervous system (CNS)-mediated behavioral comorbidities. Building on this mechanistic framework, we critically evaluate next-generation microbiota-targeted interventions: standardized fecal microbiota transplantation (FMT), rationally designed live biotherapeutic products (LBPs), precision phage cocktails targeting defined pathobionts, and microbiome-informed dietary strategies. Collectively, these approaches represent a paradigm shift-from broad-spectrum immunosuppression toward mechanism-guided, ecosystem-level modulation-thereby advancing the goal of precision medicine in IBD.},
}

@article {pmid42072403,
year = {2026},
author = {Shajahan, SR and Hamid, N and Okunsai, B and Shari, N and Ramli, MDC},
title = {Microbiota-Gut-Brain Axis in Alzheimer's Disease: Linking Oxidative Stress, Mitochondrial Dysfunction and Amyloid Pathology-A Systematic Review.},
journal = {Biomedicines},
volume = {14},
number = {4},
pages = {},
doi = {10.3390/biomedicines14040860},
pmid = {42072403},
issn = {2227-9059},
abstract = {Background: Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder characterized by amyloid-β aggregation, tau hyperphosphorylation, oxidative stress, and mitochondrial dysfunction. Emerging evidence indicates that the gut microbiota plays a critical role in modulating neuroinflammatory, and metabolic pathways involved in AD pathogenesis through the microbiota-gut-brain axis. Objective: This systematic review aims to comprehensively evaluate the role of the microbiota-gut-brain axis in Alzheimer's disease, with a particular focus on its mechanistic links to oxidative stress, mitochondrial dysfunction, and amyloid pathology, as well as its therapeutic potential. Methodology: A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases, focusing on studies evaluating gut microbiota composition, metabolomic changes, oxidative stress markers, mitochondrial activity, and therapeutic interventions in AD models and patients. Results: Altered gut microbial composition in AD is associated with increased pro-inflammatory taxa (Escherichia-Shigella, Bacteroides) and depletion of short-chain fatty acid (SCFA) producing bacteria (Faecalibacterium, Roseburia). Dysbiosis contributes to systemic inflammation, disrupted intestinal permeability, and microglial activation, leading to oxidative damage and mitochondrial impairment in neurons. Preclinical and clinical studies indicate that probiotics, prebiotics, and fecal microbiota transplantation can restore redox balance, reduce neuroinflammation, and improve cognitive outcomes. Multi-omics and AI-based models are emerging as tools for identifying microbiome-derived biomarkers for early AD detection. Conclusion: The gut microbiota-mitochondria-oxidative stress axis represents a promising therapeutic target in Alzheimer's disease. Future research should focus on longitudinal human studies, standardized microbial profiling, and personalized microbiome-based interventions to translate these mechanistic insights into clinical benefit.},
}

@article {pmid42073392,
year = {2026},
author = {Yang, M and Chen, Q and Meng, Z and Gu, X and Bai, C},
title = {The Microbiota-Gut-Brain Axis in Insomnia: Mechanisms and Intervention Strategies.},
journal = {Life (Basel, Switzerland)},
volume = {16},
number = {4},
pages = {},
doi = {10.3390/life16040583},
pmid = {42073392},
issn = {2075-1729},
support = {82574999//National Natural Science Foundation of China/ ; zyyzdxk-2023264//National Administration of Traditional Chinese Medicine/ ; 2024-JYB-JBZD-038//The Fundamental Research Funds for the Central Universities/ ; },
abstract = {Insomnia is one of the most common sleep disorders. Traditionally, its pathophysiology has been interpreted mainly from the perspective of the central nervous system (CNS). However, accumulating evidence suggests that the microbiota-gut-brain axis (MGBA), a bidirectional communication network linking the gut and the CNS, may play an important role in the development, maintenance, and treatment of insomnia. This review summarizes the major signaling pathways of the MGBA and discusses its potential mechanisms in insomnia. Current evidence indicates that gut microbiota and their metabolites may influence sleep-wake homeostasis through neural, immune, endocrine, and circadian pathways. At the same time, insomnia-related stress responses, immune imbalance, and lifestyle disturbances may in turn affect the gut microbiota, thereby forming a bidirectional regulatory network. Animal and clinical studies further support a close association between gut microbial dysbiosis and insomnia. In addition, this review systematically summarizes factors that may affect the MGBA, including diet, lifestyle, psychosocial stress, medications, and medical exposures. On this basis, MGBA-targeted interventions, such as dietary modification, prebiotics and probiotics, lifestyle interventions, fecal microbiota transplantation, and natural medicines, may provide promising new strategies for the prevention and treatment of insomnia. Nevertheless, the current evidence still relies largely on animal studies and cross-sectional research, and further longitudinal studies and high-quality interventional trials are needed to clarify causality, long-term efficacy, and standardized therapeutic approaches.},
}

@article {pmid42073476,
year = {2026},
author = {Ichim, C and Boicean, A and Mihaila, R and Todor, SB and Anderco, P and Birlutiu, V},
title = {Effect of Fecal Microbiota Transplantation on Arterial Stiffness in Alcohol-Related Liver Cirrhosis: A Prospective Pilot Study.},
journal = {Life (Basel, Switzerland)},
volume = {16},
number = {4},
pages = {},
doi = {10.3390/life16040668},
pmid = {42073476},
issn = {2075-1729},
abstract = {BACKGROUND: Alcohol-related liver disease is frequently associated with systemic vascular dysfunction and increased arterial stiffness. This may contribute to adverse clinical outcomes. Modulation of the gut microbiota through fecal microbiota transplantation (FMT) has emerged as a potential therapeutic strategy in liver cirrhosis, but its influence on vascular stiffness in humans remains insufficiently characterized.

METHODS: This prospective study evaluated arterial stiffness in patients with alcohol-related liver cirrhosis undergoing FMT. A control group received standard care. Vascular stiffness was assessed non-invasively using an oscillometric arteriograph based on pulse wave analysis. Measurements were performed at baseline and at one and three months after FMT under standardized conditions. The main indices assessed included aortic pulse wave velocity, augmentation index, ejection duration and return time. Direct microbiome sequencing and metabolomic profiling were not performed.

RESULTS: At baseline, the study and control groups had comparable vascular stiffness profiles. Only minor differences in selected hemodynamic parameters were observed. At one month after intervention, no statistically significant differences in arterial stiffness indices were observed between groups. Longitudinal analysis within the FMT group also showed no significant changes in direct markers of arterial stiffness across the three-month follow-up period. A non-significant tendency toward reduced ejection duration was noted.

CONCLUSIONS: In patients with advanced alcohol-related liver cirrhosis, FMT did not produce measurable short-term improvements in arterial stiffness. These findings suggest that short-term vascular effects of microbiota modulation may be difficult to detect in patients with advanced alcohol-related liver cirrhosis. Larger studies including earlier-stage patients, longer follow-up and direct microbiome and metabolomic assessment are needed to clarify potential vascular effects of FMT.},
}

@article {pmid42073922,
year = {2026},
author = {Zheng, M and Wei, X and Chen, R and Wang, C and Xin, L},
title = {The Gut Microbiota and Autism Spectrum Disorder: Current Research and Therapeutic Insights.},
journal = {Behavioral sciences (Basel, Switzerland)},
volume = {16},
number = {4},
pages = {},
doi = {10.3390/bs16040559},
pmid = {42073922},
issn = {2076-328X},
abstract = {Autism Spectrum Disorder (ASD) is a collective term for neurodevelopmental disorders with core features of social communication impairment, restricted and repetitive behaviors, and narrow interests. These include classic autism, Asperger's syndrome, and pervasive developmental disorder not otherwise specified. ASD is currently managed with behavioral interventions, rehabilitation training, and family support, but there is no curative medication. Recent studies suggest that some patients with ASD may experience gastrointestinal symptoms. Perhaps this is associated with the disturbances of gut microbiota. Increasing evidence has demonstrated that the composition of gut microbiota in ASD individuals is different from that in normal population and may be associated with neurodevelopmental processes via the gut-brain axis. This article reviews the evidence for the association between gut microbiota and ASD, describes the characteristics of microbial changes, and analyzes the mechanism by which changes in the composition of the microbiota affect the occurrence and development of ASD. Finally, we review recent advances in microbiota-targeted therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation, which provide new approaches to alleviate and improve autism-related symptoms and point out the future research direction.},
}

@article {pmid42074015,
year = {2026},
author = {Papacocea, RI and Iliuță, FP and Papacocea, IR},
title = {Gut Microbiome Dysregulation Across Schizophrenia Spectrum Disorders: Bacteria-, Fungi- and Virome-Level Alterations with Molecular and Immunological Implications.},
journal = {International journal of molecular sciences},
volume = {27},
number = {8},
pages = {},
doi = {10.3390/ijms27083372},
pmid = {42074015},
issn = {1422-0067},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Schizophrenia/microbiology/immunology ; *Virome ; *Bacteria ; Dysbiosis/microbiology ; *Fungi ; Animals ; },
abstract = {Schizophrenia spectrum disorders (SSD) are severe psychiatric conditions characterized by disturbances in cognition, emotion, and behavior, with increasing evidence suggesting an involvement of the gut microbiome in their pathophysiology. This PRISMA-informed structured review synthesizes 114 studies using a taxa-centered framework that maps microbial changes across SSD stages and phenotypes and serves as a structural basis for identifying cross-study patterns. Across heterogeneous cohorts, convergent alterations include depletion of short-chain fatty acid (SCFA)-producing taxa (including Faecalibacterium, Roseburia, and Coprococcus) and enrichment of potentially pro-inflammatory and fermentative taxa (such as Proteobacteria, Enterobacteriaceae, Streptococcus, Collinsella, and Desulfovibrio). These taxonomic patterns suggest potential functional alterations, including reduced SCFA availability. Reduced abundance of butyrate-producing taxa has been associated with impaired intestinal barrier function and increased microbial translocation (e.g., lipopolysaccharide), which may contribute to the activation of immune pathways, including Toll-like receptor 4 signaling and elevated inflammatory markers such as IL-6 and TNF-α. Additional alterations reported across studies include changes in lactate metabolism, bile acid profiles, aromatic amino acid metabolism, and the tryptophan-kynurenine pathway. These pathways may interact with neurobiological processes relevant to SSD, including glutamate-GABA balance, NMDA receptor function, microglial activation, and synaptic regulation, although much of the current evidence remains associative. Multi-kingdom studies and fecal microbiota transplantation models provide further support for the functional relevance of these observations, though causal relationships remain to be fully established. Overall, SSD-associated dysbiosis appears to reflect ecosystem-level metabolic alterations rather than isolated taxonomic abnormalities, supporting a Microbiota-Gut-Immune-Glia conceptual framework and highlighting the gut ecosystem as a potential therapeutic target.},
}

Humans
*Gastrointestinal Microbiome
*Schizophrenia/microbiology/immunology
*Virome
*Bacteria
Dysbiosis/microbiology
*Fungi
Animals

@article {pmid42074174,
year = {2026},
author = {Ratajczyk, K and Kaczorowska, E and Wyka, K and Tarasiuk-Zawadzka, A and Fichna, J and Gajos, A},
title = {Gut-Brain Signaling in Parkinson's Disease: A Narrative Review.},
journal = {International journal of molecular sciences},
volume = {27},
number = {8},
pages = {},
doi = {10.3390/ijms27083531},
pmid = {42074174},
issn = {1422-0067},
support = {Medical University of Lodz (#503/6-127-01/503-61-001 to AG and #503/1-156-04/503-11-001 to JF).//Medical University of Lodz/ ; },
mesh = {Humans ; *Parkinson Disease/metabolism/microbiology/therapy/pathology ; *Gastrointestinal Microbiome/physiology ; *Brain/metabolism ; Animals ; Signal Transduction ; *Brain-Gut Axis ; Neurotransmitter Agents/metabolism ; },
abstract = {The formulation of the gut-brain-microbiota axis (GBA) theory has led to new research directions that have expanded our understanding of the pathogenesis, phenotypic variability, and clinical course of Parkinson's disease (PD). Models of PD pathogenesis, based on the Braak hypothesis, suggest a subtype of the disease in which pathological changes begin in the gut many years before the onset of brain pathology and the manifestation of motor symptoms. Gut microbiota may influence nervous system function along the GBA by influencing intestinal permeability, chronic inflammation, and α-synuclein aggregation. Accumulating evidence suggests that the gut microbiota may also regulate the synthesis and metabolism of neurotransmitters, including dopamine (DA), serotonin (5-HT), acetylcholine (ACh) and γ-aminobutyric acid (GABA), both in the gut and brain, and indirectly stimulate central nervous system activity via the vagus nerve, which receives signals from the enteric nervous system. Research on the effects of microbiota on GBA has paved the way for the identification of novel treatment strategies, including probiotics, prebiotics, synbiotics, postbiotics, antibiotics, and fecal microbiota transplantation (FMT), aimed at not only symptomatic but also disease-modifying treatment of PD. In this article, we propose a novel approach to GBA as a link between gut microbiota and gut and brain neurotransmitter metabolism in PD. We review the latest research on the gut epithelial barrier. We analyze and summarize the potential of therapeutic interventions targeting gut microbiota and their impact on neurotransmitter regulation in PD.},
}

Humans
*Parkinson Disease/metabolism/microbiology/therapy/pathology
*Gastrointestinal Microbiome/physiology
*Brain/metabolism
Animals
Signal Transduction
*Brain-Gut Axis
Neurotransmitter Agents/metabolism

@article {pmid42075006,
year = {2026},
author = {Zhang, X and Chen, F and Luo, Y and Li, D and Ji, J and Ma, L and Ma, C and Hu, X},
title = {Young Human-Derived Microbiota Ameliorates Cognitive Decline and Reproductive Senescence in Aged Mice.},
journal = {Nutrients},
volume = {18},
number = {8},
pages = {},
doi = {10.3390/nu18081193},
pmid = {42075006},
issn = {2072-6643},
support = {2023YFF1104005//National key research and development program/ ; },
mesh = {Animals ; Mice ; Humans ; Male ; Bifidobacterium/growth & development ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/physiology ; *Cognitive Dysfunction/microbiology/therapy ; *Cellular Senescence/physiology ; Mice, Inbred C57BL ; Reproduction/physiology ; Dysbiosis/microbiology/therapy ; *Aging/physiology/psychology ; },
abstract = {Background/Objectives: Age-related gut microbiota dysbiosis leads to systemic oxidative stress, chronic inflammation, and multi-organ functional decline. However, there is limited evidence supporting microbiota-based therapies for aging. This study aimed to examine the effect of gut microbiota from young donors, particularly those with increasing Bifidobacteria levels through dietary intervention, on age-related declines in fertility, cognition, and reproduction. Methods: We conducted experiments using gut microbiota from young human donors, with or without pre-conditioning with barley leaves (BL), to transplant into aged male mice. Hippocampal metabolome and behavioral assessments were used to identify differences in recognitive regulation during aging. Moreover, testis tissue, semen quality, and offspring studies were determined to investigate the beneficial effects on fertility and underlying mechanism. Conclusions: This preliminary dietary treatment promotes the growth of Bifidobacterium in aged recipient mice. Aged male mice received young fecal microbiota transplants (yFMTs), BL-conditioned yFMTs (BLyFMTs), and a combined treatment of BLyFMT plus recipient BL supplementation. The combined approach significantly increased intestinal Bifidobacterium levels and effectively restored hippocampal metabolomic profiles and cognitive behavior. Additionally, yFMT-based treatments mitigated structural damage to the seminiferous tubules and prevented the germ cell depletion. Consistently, those interventions improved sperm quality and mechanistically enhanced hypothalamic-pituitary-gonadal (HPG) axis activity in aged recipients. These findings highlight Bifidobacterium as a key factor in microbiome-driven rejuvenation, enhancing the effectiveness of yFMTs in addressing aging-related declines.},
}

Animals
Mice
Humans
Male
Bifidobacterium/growth & development
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/physiology
*Cognitive Dysfunction/microbiology/therapy
*Cellular Senescence/physiology
Mice, Inbred C57BL
Reproduction/physiology
Dysbiosis/microbiology/therapy
*Aging/physiology/psychology

@article {pmid42075029,
year = {2026},
author = {Asayesh, M and Nazarzadeh, A and Jamshidi, S and Keramat, S and Ryszkiel, I and Stanek, A},
title = {Modulation of Gut Microbiota Through Dietary Fibers to Enhance Regulatory T Cell-Based Immunotherapy in GVHD Following Hematopoietic Stem Cell Transplantation.},
journal = {Nutrients},
volume = {18},
number = {8},
pages = {},
doi = {10.3390/nu18081216},
pmid = {42075029},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; *Graft vs Host Disease/therapy/immunology/microbiology/prevention & control ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Dietary Fiber/administration & dosage ; *T-Lymphocytes, Regulatory/immunology ; *Immunotherapy/methods ; Prebiotics ; Dysbiosis ; Fecal Microbiota Transplantation ; Probiotics ; },
abstract = {Graft-versus-host disease (GVHD) is one of the principal complications seen in the recipients of allogenic hematopoietic stem cell transplantation (allo-HSCT), and persists as a leading cause of post-transplant morbidity and mortality. Increasing evidence highlights the crucial influence of the gut microbiome (GM) on transplant outcomes. Microbial dysbiosis, characterized by reduced bacterial diversity and pathogenic overgrowth, is strongly associated with higher rates of complications and mortality. Patients with lower microbial diversity exhibit poorer overall survival (OS) and an increased incidence of acute GVHD (aGVHD). Conversely, restoration of beneficial commensal communities has been shown to enhance immune homeostasis, mitigate GVHD severity, and decrease infection risk. Emerging therapeutic strategies now focus on modulating the intestinal microbiome through dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation (FMT). It has been demonstrated that bacterial metabolites, such as short-chain fatty acids (SCFAs) from the diet, especially a diet rich in fibers, reduce the occurrence/severity of GVHD by inducing regulatory T cells (Tregs), which release anti-inflammatory cytokines and regulate the host immune system. Hence, the implementation of dietary fibers (DFs) could increase beneficial commensals, Treg induction, and improve outcomes such as GVHD and OS in recipients of allo-HCT. Hereupon, this review addresses how a fiber-rich diet modulates GM composition, reinforces epithelial barrier integrity, and improves the efficacy of Treg-based immunotherapy by stabilizing their regulatory phenotype and increasing their functional persistence, ultimately leading to a reduction in GI complications associated with GVHD. Unlike prior reviews that primarily cover the microbiome-GVHD axis or Treg therapies in isolation, this review emphasizes fermentable dietary fibers as a mechanistically grounded, clinically actionable strategy to support Treg stability and persistence via microbiota-derived metabolites. We integrate mechanistic evidence with emerging clinical feasibility data and ongoing trials of prebiotic supplementation in allogeneic HSCT.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
*Graft vs Host Disease/therapy/immunology/microbiology/prevention & control
*Hematopoietic Stem Cell Transplantation/adverse effects
*Dietary Fiber/administration & dosage
*T-Lymphocytes, Regulatory/immunology
*Immunotherapy/methods
Prebiotics
Dysbiosis
Fecal Microbiota Transplantation
Probiotics

@article {pmid42075307,
year = {2026},
author = {Burdette, RA and Whitt, CC and Cios Phillips, KJ and Worthington, MT and Behm, BW and Warren, CA},
title = {Treating Initial and Recurrent C. difficile: A Retrospective Analysis of 100 Referred Patients.},
journal = {Microorganisms},
volume = {14},
number = {4},
pages = {},
doi = {10.3390/microorganisms14040911},
pmid = {42075307},
issn = {2076-2607},
abstract = {Treatment guidelines for Clostridioides difficile infection (CDI) have been published by infectious disease and gastroenterology professional societies; however, adherence in clinical practice remains poorly characterized, particularly for recurrent disease. We conducted a retrospective chart review of 100 patients with CDI (350 episodes: 115 initial, 235 recurrent) referred to a tertiary complicated CDI clinic between 2018 and 2023. Guideline adherence was assessed by comparing treatment with IDSA/SHEA and ACG recommendations, and referring diagnoses were compared with final specialist diagnoses. Guideline adherence was significantly higher in initial compared to recurrent episodes (70.4% vs. 41.3%, p < 0.0001). Among guideline non-adherent recurrent episodes, 51.3% used standard antibiotic regimens inappropriate for the recurrence tier. Specialist review reclassified 12.0% of episodes, with colonization increasing from 2.6% to 8.9%. Misdiagnosed colonization cases had a 6.2-fold higher treatment failure rate than confirmed CDI (39.3% vs. 6.3%, p < 0.0001). Guideline non-adherence showed a non-significant trend toward treatment failure (10.0% vs. 6.7%, p = 0.31). Guideline adherence for recurrent CDI is inadequate in pre-referral settings, and diagnostic misclassification is common. Early specialist involvement may improve both diagnostic accuracy and treatment appropriateness for patients with recurrent CDI.},
}

@article {pmid42075777,
year = {2026},
author = {Lagos, I and Pérez de Arce, E and Faggiani, I and D'Amico, F and Zilli, A and Furfaro, F and Massironi, S and Cicerone, C and Solitano, V and Parigi, TL and Peyrin-Biroulet, L and Danese, S and Allocca, M},
title = {The Role of Microbiota and Fecal Transplantation in Inflammatory Bowel Disease.},
journal = {Pathogens (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
doi = {10.3390/pathogens15040451},
pmid = {42075777},
issn = {2076-0817},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Gastrointestinal Microbiome ; *Inflammatory Bowel Diseases/therapy/microbiology ; Crohn Disease/therapy/microbiology ; Colitis, Ulcerative/therapy/microbiology ; Feces/microbiology ; Treatment Outcome ; },
abstract = {Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD), are consistently associated with alterations in gut microbial communities, although the extent and characteristics of these alterations vary across studies, supporting a potential role of the microbiota in disease pathogenesis and therapeutic modulation. We conducted a systematic review to synthesize current evidence on microbiota alterations in IBD and the clinical application of fecal microbiota transplantation (FMT). A total of 118 studies were included (76 focused on microbiota profiling and 42 evaluated FMT as therapy). Across heterogeneous study designs and microbial characterization methods, reduced microbial diversity was the most consistently reported alteration, generally more pronounced in CD than in UC. Depletion of Faecalibacterium prausnitzii-a key butyrate producer with anti-inflammatory properties-was commonly reported, often accompanied by functional impairment in short-chain fatty acid production. Microbial patterns were frequently associated with mucosal inflammation and varied across disease phenotypes; these patterns have been increasingly explored as predictors of treatment response and relapse, although mechanistic interpretation remains limited and causal relationships are difficult to establish. Evidence from randomized controlled trials suggests potential efficacy of FMT in UC, particularly with intensive or repeated protocols, whereas data in CD remain limited and heterogeneous, with signals of benefit often appearing transient. FMT was generally well tolerated, but long-term safety data remain scarce. Emerging multi-omic approaches are reshaping the field by integrating taxonomic and functional insights, with potential implications for risk stratification, diagnosis, prognosis, and therapeutic optimization. Further standardized, longitudinal, and mechanistically oriented studies are required to translate microbiome research into clinically actionable strategies in IBD.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Gastrointestinal Microbiome
*Inflammatory Bowel Diseases/therapy/microbiology
Crohn Disease/therapy/microbiology
Colitis, Ulcerative/therapy/microbiology
Feces/microbiology
Treatment Outcome

@article {pmid42077461,
year = {2026},
author = {Wu, J and Qiu, Y and Deng, J and Li, Y and Jia, B and Cao, Z and Tao, J and Guo, J},
title = {Faecal microbiota transplantation and glucolipid metabolic disorders: the interventional role of gut microbiota.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1806638},
pmid = {42077461},
issn = {1664-2392},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/physiology ; Animals ; *Metabolic Diseases/therapy/microbiology/metabolism ; },
abstract = {Glucolipid metabolic disorders (GLMD) have emerged as a significant global public health issue, posing a significant threat to human health. With changes in modern social structures and an ageing population, the incidence of GLMD is on the rise and is increasingly affecting younger populations. Faecal microbiota transplantation (FMT) directly modifies the gut microbiota to reestablish its equilibrium and metabolites, consequently reinstating gut barrier integrity, mitigating chronic low-grade inflammation, and affecting the onset and progression of GLMD through the regulation of the gut-liver axis. This paper reviews the application of FMT in the treatment of GLMD, emphasizing research outcomes and efficacy assessments in clinical trials and animal studies. As a simple and secure intervention, FMT is anticipated to provide new therapeutic alternatives for GLMD patients in the future with the deepening of relevant research, the screening of specific probiotics and the revelation of functional mechanisms. This paper aims to clarify the potential mechanism of FMT in addressing GLMD, summarise recent research developments in this field, and anticipate the opportunities and challenges of FMT in clinical application.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/physiology
Animals
*Metabolic Diseases/therapy/microbiology/metabolism

@article {pmid42063504,
year = {2026},
author = {Yu, B and Zhao, WW and Tao, L and Li, K},
title = {The microbiota-gut-brain axis perspective: mechanisms and intervention strategies for the comorbidity of chronic constipation and depression.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1800520},
pmid = {42063504},
issn = {1664-302X},
abstract = {BACKGROUND: Chronic constipation and depression are highly prevalent worldwide. These two conditions frequently co-occur in clinical practice. Accumulating evidence indicates that gut microbiota dysbiosis mediates this comorbidity through the microbiota-gut-brain axis (MGBA).

METHODS: This narrative review systematically summarizes current research on MGBA bidirectional communication mechanisms, gut microbiota alterations in comorbid patients, and microbiota-targeted intervention strategies.

RESULTS: The MGBA facilitates bidirectional communication through four major pathways: neural pathways via the vagus nerve, immune pathways via cytokines, endocrine pathways via the HPA axis, and metabolic pathways via short-chain fatty acids and neurotransmitter precursors. Gut dysbiosis is associated with comorbidity and may contribute to its pathogenesis through multiple mechanisms. First, neurotransmitter metabolism becomes dysregulated, particularly in the serotonin and GABA systems. Second, chronic low-grade inflammation develops with elevated pro-inflammatory cytokines. Third, intestinal barrier dysfunction occurs, leading to increased permeability and bacterial translocation. Fourth, HPA axis hyperactivity emerges. Fifth, production of microbial metabolites is altered, including short-chain fatty acids and tryptophan metabolites. Comorbid patients exhibit characteristic microbiota signatures. These include reduced abundance of butyrate-producing bacteria such as Faecalibacterium, Roseburia, and Coprococcus. Microbial diversity decreases significantly. Pro-inflammatory taxa become enriched. Several evidence-based interventions show promise. These include psychobiotics, fecal microbiota transplantation, and dietary modifications such as Mediterranean diet and high-fiber intake. Exercise and integrative approaches including traditional Chinese medicine also demonstrate beneficial effects.

CONCLUSION: The gut microbiota represents a critical hub connecting gastrointestinal and mental health. Microbiota-targeted therapies offer promising strategies for managing chronic constipation-depression comorbidity. Future research should establish causal relationships and develop reliable microbial biomarkers. Precision medicine approaches based on individual microbiome profiles are needed to optimize therapeutic outcomes.},
}

@article {pmid42067917,
year = {2026},
author = {Fang, Q and Huang, S and Zhang, C and Li, M and Ye, Z and Guo, H and Xiao, M and Wang, S and Yu, L and Zhang, H and Zhao, J and Tian, F and Chen, W and Zhai, Q},
title = {Capsaicin ameliorates glycemic levels via gut microbiota-derived 5-aminolevulinic acid in mice.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02415-8},
pmid = {42067917},
issn = {2049-2618},
support = {BX20250339//Postdoctoral Fellowship Program and China Postdoctoral Science Foundation/ ; U23A20259//National Natural Science Foundation of China/ ; JUSRP622013//Fundamental Research Funds for the Central Universities/ ; },
abstract = {BACKGROUND: Capsaicin, a natural alkaloid in chili peppers, regulates glycemic levels; however, its mechanisms and therapeutic potential remain unclear. This study aimed to elucidate the role of gut microbiota and their metabolites in mediating capsaicin's glycemic regulatory effects. We conducted experiments in specific pathogen-free (SPF) and germ-free (GF) mice, transient receptor potential vanilloid 1 (TRPV1) receptor ablation studies, and fecal microbiota transplantation (FMT) to demonstrate the involvement of gut microbiota in capsaicin-mediated glycemic control. Metagenomics and metabolomics analyses were employed to identify key microbial strains and metabolic pathways. Keystone strains and metabolites were supplemented in GF mice without capsaicin intervention to validate their effects on glycemic regulation. In vitro co-culture experiments were performed to investigate the mutualistic relationships among keystone strains under capsaicin treatment.

RESULTS: Gut microbiota constitute an important component of capsaicin-mediated glycemic regulation, acting in concert with but not solely dependent on TRPV1 signaling. Gut microbiota altered by capsaicin promote the production of 5-aminolevulinic acid (5-ALA), which contributes to heme synthesis and enhances glycemic control. Supplementation with Akkermansia muciniphila, Ligilactobacillus murinus, or 5-ALA in GF mice recapitulates the glycemic benefits of capsaicin. Furthermore, capsaicin enriches Akkermansia muciniphila, which in turn supports the growth of Ligilactobacillus murinus.

CONCLUSION: Capsaicin-induced changes in the gut microbiota promote 5-ALA synthesis, leading to improved glycemic control. These findings suggest that dietary or probiotic interventions targeting gut microbiota, particularly Akkermansia muciniphila and 5-ALA, may offer promising strategies for managing glycemic disorders, including type 2 diabetes (T2D). Video Abstract.},
}

@article {pmid42068031,
year = {2026},
author = {Chen, S and Feng, H and Wang, Y and Huang, J and Xu, S and Gong, Y and Liu, X and Ouyang, Y and Ye, Q and Zheng, D and Sun, K and Wang, A and Chen, Y},
title = {Intestinal epithelial Syndecan-1 maintains mucosal homeostasis in inflammatory bowel disease by enhancing Faecalibacterium prausnitzii biofilm formation.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2665870},
doi = {10.1080/19490976.2026.2665870},
pmid = {42068031},
issn = {1949-0984},
mesh = {Animals ; *Syndecan-1/genetics/metabolism ; *Inflammatory Bowel Diseases/microbiology/metabolism/genetics ; Mice ; *Intestinal Mucosa/microbiology/metabolism ; Gastrointestinal Microbiome ; *Biofilms/growth & development ; Mice, Knockout ; Humans ; *Faecalibacterium prausnitzii/physiology/genetics/growth & development ; Mice, Inbred C57BL ; Homeostasis ; Disease Models, Animal ; Dextran Sulfate ; Colitis/microbiology/chemically induced ; Male ; Fecal Microbiota Transplantation ; },
abstract = {Despite the rising global incidence of inflammatory bowel disease (IBD), curative therapies remain unavailable. While our previous work implicated the intestinal proteoglycan Syndecan-1 (SDC1) in IBD-associated barrier dysfunction and inflammation, the underlying mechanism was unclear. This study aimed to elucidate how SDC1 maintains intestinal barrier integrity through interactions with the gut microbiome. In DSS-induced colitis, global knockout of Sdc1 (Sdc1[-/-]) exhibited exacerbated inflammatory infiltration and greater impairment of barrier structure and function than wild-type (WT). Formation of intestinal organoids was independent of genotype, indicating that Sdc1[-/-] does not impair barrier function via disrupting epithelial development. The heightened colitis susceptibility in Sdc1[-/-] mice was abolished in the antibiotic-treated pseudo-germ-free models, and transmissible to WT mice via fecal microbiota transplantation. Similar results were reproduced in a germ-free mouse model. Metagenomic sequencing identified Faecalibacterium prausnitzii as the most significantly depleted species upon Sdc1 knockout. In vitro, SDC1-attached glycosaminoglycans (heparan sulfate (HS) and chondroitin sulfate (CS)) but not the SDC1 core protein promoted F. prausnitzii growth. Prokaryotic transcriptome profiling indicated that HS/CS induces cobalamin biosynthesis in F. prausnitzii. The critical role of cobalamin as a mediator was confirmed, as its synthetic inhibition significantly diminished the growth-promoting effect of HS/CS. Mechanism studies showed that HS/CS enhanced biofilm formation in F. prausnitzii, thereby facilitating cobalamin biosynthesis. Oral administration of HS ameliorated DSS-induced colitis and promoted mucosal colonization of F. prausnitzii, independent of the host genotype. Finally, human IBD biopsies revealed a positive correlation between epithelial SDC1 and mucosal F. prausnitzii, as well as an inverse correlation with bacterial translocation and the number of LPS‑positive cells. Our study elucidates a novel mechanism in which the glycosaminoglycan chains of SDC1 promote F. prausnitzii colonization and growth through enhanced biofilm formation and cobalamin synthesis, thereby highlighting the therapeutic potential of HS for IBD and offering a new basis for host-directed microbiota regulation.},
}

Animals
*Syndecan-1/genetics/metabolism
*Inflammatory Bowel Diseases/microbiology/metabolism/genetics
Mice
*Intestinal Mucosa/microbiology/metabolism
Gastrointestinal Microbiome
*Biofilms/growth & development
Mice, Knockout
Humans
*Faecalibacterium prausnitzii/physiology/genetics/growth & development
Mice, Inbred C57BL
Homeostasis
Disease Models, Animal
Dextran Sulfate
Colitis/microbiology/chemically induced
Male
Fecal Microbiota Transplantation

@article {pmid42068814,
year = {2026},
author = {Kanannejad, Z and Taylor, WR and Ghatee, MA and Mohkam, M},
title = {Microbial regulation of immune tolerance during embryonic implantation and pregnancy.},
journal = {Journal of reproductive immunology},
volume = {175},
number = {},
pages = {104898},
doi = {10.1016/j.jri.2026.104898},
pmid = {42068814},
issn = {1872-7603},
abstract = {Maternal immune tolerance is essential for successful embryo implantation and maintenance of pregnancy. The maternal microbiome, particularly in the gut, vagina, and possibly the placenta, has emerged as an important regulator of immune adaptation during gestation. Through continuous interaction with the maternal immune system, the microbiota influence key immune cell populations such as regulatory T cells, uterine natural killer cells, and dendritic cells. These cells promote a tolerogenic environment necessary for embryo acceptance and proper placental development. Microbial-derived metabolites, including short-chain fatty acids and tryptophan derivatives, play important roles in modulating cytokine production and immune cell differentiation. Disruption of microbial balance, or dysbiosis, has been associated with a range of pregnancy complications, including implantation failure, preeclampsia, gestational diabetes, and preterm birth. Additionally, the maternal microbiome may influence fetal immune development, with implications for the offspring's long-term health. Emerging translational research suggests that interventions targeting the maternal microbiota, such as probiotics, prebiotics, and fecal microbiota transplantation, may beneficially modulate immune responses during pregnancy. While these approaches are promising, variability in individual microbiome composition and immune responses underscores the need for personalized strategies. In summary, the maternal microbiome is a dynamic and influential factor in shaping immune tolerance during pregnancy. A deeper understanding of microbiota-immune interactions may pave the way for novel, microbiome-based therapies to enhance reproductive outcomes and promote maternal-fetal health.},
}

@article {pmid42062271,
year = {2026},
author = {Jang, S and Kim, YJ and Park, J and Kim, D and Kim, TH and Lee, S and Kim, DJ and Ryu, CM and Seo, HW},
title = {A Muribaculaceae-enriched microbiota exacerbates TLR4-dependent Acinetobacter baumannii-induced hyperinflammatory sepsis.},
journal = {Nature communications},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41467-026-72435-3},
pmid = {42062271},
issn = {2041-1723},
abstract = {Host survival during sepsis depends not only on pathogen burden but also on inflammatory thresholds calibrated by the gut microbiota. Here, we show that different survival outcomes were observed in genetically equivalent female C57BL/6 mouse populations depending on their specific gut microbiota configuration. A Muribaculaceae-enriched gut microbiota, characterized by the dominance of Sangeribacter muris KT1-3, predisposed mice to fatal sepsis caused by Acinetobacter baumannii via TLR4-dependent hyperinflammation. This lethal phenotype, reproduced by colonization with S. muris strain KT1-3, was transferable by fecal microbiota transplantation and co-housing. Notably, fixed-dose LPS challenge and ex vivo stimulation assays demonstrated that this configuration induces a heightened TLR4-dependent inflammatory responsiveness independent of bacterial replication. Single-cell transcriptomics revealed that these microbiota-derived factors establish a transcriptionally pre-activated macrophage state, resulting in production of excessive pro-inflammatory cytokines upon challenge. Mechanistically, S. muris strain KT1-3 releases heat-stable and low-molecular-weight (<3 kDa) metabolites that are sufficient to potentiate systemic cytokine surges under a fixed-dose endotoxin challenge in vivo, effectively lowering the host's activation threshold for TLR4-driven signaling. Tlr4-deficient mice harboring the KT1-3-enriched susceptible microbiota survived despite persistent bacterial dissemination, demonstrating that the microbiota-TLR4 axis dictates hyperinflammatory A. baumannii-induced sepsis outcomes by modulating inflammatory magnitude rather than pathogen clearance. Our results provide a conceptual framework for how specific gut microbiota configurations modulate host susceptibility and drive infection resilience.},
}

@article {pmid42061692,
year = {2026},
author = {Duan, L and Liang, J and Zhang, W and Liu, Z and Kang, H and Huang, D and Wang, Z and Jiang, G and Gao, A},
title = {EtCBN-associated olfactory dysfunction involves Irf7 signaling and a microbiota-metabolite axis.},
journal = {Chemico-biological interactions},
volume = {434},
number = {},
pages = {112109},
doi = {10.1016/j.cbi.2026.112109},
pmid = {42061692},
issn = {1872-7786},
abstract = {Liquid crystal monomers (LCMs) are emerging environmental contaminants with neurotoxic potential; however, their impact on olfactory function, a key early indicator of neurodegenerative diseases, is unknown. Here, we observed that exposure to LCM mixtures at an environmentally relevant dose (180 μg/kg) was associated with olfactory deficits in mice. Further investigation focused on a prevalent LCM monomer (EtCBN) found in indoor dust, a compound known to disrupt endothelial cell proliferation, as a key component of this effect. Mice exposed to environmentally relevant (20 μg/kg) or elevated (200 μg/kg) EtCBN for 12 weeks exhibited significant olfactory impairment, supported by behavioral deficits, magnetic resonance imaging (MRI)-based olfactory bulb atrophy, histopathological changes, and neuroinflammation. Molecular docking predicted that EtCBN may interact with Irf7 with a binding energy of -4.86 kcal/mol, suggesting a potential interaction that could serve as a candidate molecular initiating event (MIE). This interaction was associated with elevated IL-1β and TNF-α levels and may be linked to the onset of neuroinflammation. In addition, a reduced abundance of Dubosiella was found to correlate with phenylalanine accumulation, potentially further contributing to Irf7 activation through a microbiota-metabolite-inflammation axis. Fecal microbiota transplantation (FMT) and probiotic supplementation provided evidence suggesting a role for the intestinal microbiota. Exogenous nicotinamide adenine dinucleotide (NAD[+]) was observed to be associated with mitigation of these effects. Together, these findings are consistent with a proposed adverse outcome pathway (AOP) framework that suggests a link between the EtCBN-Irf7 interaction and LCM-associated neurotoxicity, offering potential mechanistic insights and therapeutic targets for olfactory dysfunction.},
}

@article {pmid42062245,
year = {2026},
author = {Korten, NM and Blischke, L and Thelen, AC and Schulze Eckel, A and van Egmond, M and Verspohl, V and Neumann, M and Kneisel, L and Tran, M and Beyer, C and Herpertz-Dahlmann, B and Keller, L and Bang, C and Andreani, NA and Seitz, J and Trinh, S and Voelz, C},
title = {From gut to brain: effects of fecal microbiota transplants from humans to rats on hippocampal gene regulation - a study on anorexia nervosa.},
journal = {Translational psychiatry},
volume = {16},
number = {1},
pages = {},
pmid = {42062245},
issn = {2158-3188},
mesh = {*Fecal Microbiota Transplantation ; *Hippocampus/metabolism ; *Anorexia Nervosa/therapy/microbiology/genetics/metabolism ; Animals ; Female ; Humans ; *Gastrointestinal Microbiome ; Rats, Wistar ; Rats ; Brain-Derived Neurotrophic Factor/metabolism ; Adult ; Adolescent ; Anti-Bacterial Agents/pharmacology ; Young Adult ; Disease Models, Animal ; Gene Expression Regulation ; },
abstract = {Fecal microbiota transplantation (FMT) has emerged as a novel approach for understanding anorexia nervosa (AN), a complex eating disorder characterized by severe underweight, fear of weight gain and distorted body image. Patients with AN show alterations in the gut microbiome, brain structure, and inflammatory processes, indicating the importance of the microbiome‒gut‒brain axis in AN pathology. This study aimed to investigate whether FMT from patients with AN into antibiotic-treated rats could transfer a phenotype associated with the disease inducing AN-like symptoms and hippocampal alterations. Female Wistar rats received antibiotics followed by FMT from healthy controls, patients with AN, or water. Gut microbiota effects were assessed through 16S rRNA gene sequencing, alongside post-mortem analyses of glial cells, neurogenesis markers, and inflammatory markers. The results revealed dysregulated microbial diversity after antibiotic treatment, which was partially restored after FMT. Successful transfer of human bacterial species was observed, but AN-like symptoms and changes in glial/neuronal counts were not detected. Notably, a decrease in hippocampal Bdnf expression was detected in the antibiotic control group, which was reversed by healthy control stool transplantation but not in the AN-transplanted group. Similar patterns were observed for neuroinflammation and Mki67, a marker of cell neogenesis. These findings suggest potential links between microbial changes, neuroinflammation and neuroplasticity in the hippocampus with the potential to correct deficits with FMT. Future studies should extend these findings by exploring the combination of FMT and starvation phases to better understand the roles of specific microbial populations in neuroinflammatory processes and, ultimately, clinical outcomes in AN.},
}

*Fecal Microbiota Transplantation
*Hippocampus/metabolism
*Anorexia Nervosa/therapy/microbiology/genetics/metabolism
Animals
Female
Humans
*Gastrointestinal Microbiome
Rats, Wistar
Rats
Brain-Derived Neurotrophic Factor/metabolism
Adult
Adolescent
Anti-Bacterial Agents/pharmacology
Young Adult
Disease Models, Animal
Gene Expression Regulation

@article {pmid42053886,
year = {2026},
author = {Wu, XM and Hou, LY and Liu, C and Hu, Y and He, Q},
title = {Targeting the Gut Microbiota-Bile Acid-FXR Axis: The Therapeutic Mechanism of Yudantong Decoction in Cholestatic Liver Disease.},
journal = {Current medical science},
volume = {},
number = {},
pages = {},
pmid = {42053886},
issn = {2523-899X},
support = {Grant No. L222131//Beijing Municipal Natural Science Foundation/ ; 82104926//National Natural Science Foundation of China (NSFC)/ ; },
abstract = {OBJECTIVE: To elucidate the therapeutic mechanism of Yudantong decoction (YDTD) in cholestatic liver disease (CLD), focusing on the gut microbiota-bile acid-intestinal farnesoid X receptor (FXR) axis.

METHODS: A CLD mouse model induced by α-naphthylisothiocyanate was treated with YDTD. Hepatic injury, gut microbiota composition (16S rRNA sequencing), bile acid profiles (high-performance liquid chromatography-tandem mass spectrometry, HPLC-MS/MS), intestinal FXR/NLRP3 signaling, and barrier function were assessed. Fecal microbiota transplantation, bile salt hydrolase (BSH) inhibition, and FXR antagonism were employed for mechanistic validation.

RESULTS: CLD mice exhibited hepatocellular steatosis, lobular necrosis, and elevated serum markers. These pathological changes were associated with gut dysbiosis, impaired bile acid metabolism via bile salt hydrolase (BSH) suppression, FXR signaling inhibition, and NLRP3 inflammasome activation. YDTD restored BSH activity and bile acid homeostasis, upregulated FXR expression, suppressed NLRP3 inflammasome activation, and improved intestinal barrier integrity. Fecal microbiota transplantation experiments confirmed that YDTD-modified microbiota mediated these therapeutic benefits, whereas pharmacological inhibition of BSH or FXR attenuated YDTD's therapeutic effects.

CONCLUSION: YDTD alleviates CLD, at least in part, by targeting the gut microbiota-bile acid-FXR signaling pathway, highlighting the gut microbiota as a promising therapeutic target for CLD.},
}

@article {pmid42054188,
year = {2026},
author = {Yuan, C and Wang, M and Yuan, Y and Jin, X and Wang, K},
title = {High-Salt Diet Promotes Kidney Stone Formation Through Gut Microbiota-Dependent Inflammatory Pathways.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {9},
pages = {e71854},
doi = {10.1096/fj.202503466R},
pmid = {42054188},
issn = {1530-6860},
support = {82270799//MOST | National Natural Science Foundation of China (NSFC)/ ; 82570894//MOST | National Natural Science Foundation of China (NSFC)/ ; 2024ZYD0053//Science and Technology Department of Sichuan Province (SPDST)/ ; 2024NSFSC1499//SPDST | Natural Science Foundation of Sichuan Province ()/ ; 2025HXBH053//Postdoctoral Research and Development Fund of West China Hospital, Sichuan University/ ; 2023SCUH0054//Fund of Sichuan University/ ; 2023HXFH014//Clinical Research Incubation Project of West China Hospital of Sichuan University/ ; CZ2026001//National Outstanding Physician Fund/ ; },
mesh = {*Gastrointestinal Microbiome/physiology/drug effects ; Animals ; *Kidney Calculi/metabolism/etiology/microbiology/pathology/chemically induced ; Humans ; Mice ; Mice, Inbred C57BL ; Male ; *Inflammation/metabolism/pathology ; *Sodium Chloride, Dietary/adverse effects ; Female ; Methylamines/metabolism ; NF-kappa B/metabolism ; Middle Aged ; Calcium Oxalate/metabolism ; Signal Transduction ; },
abstract = {High salt intake is a recognized risk factor for calcium oxalate (CaOx) kidney stones, but the underlying biological mechanisms beyond urinary calcium excretion remain unclear. We investigated whether a high-salt diet promotes CaOx stone formation through gut microbiota-dependent inflammatory pathways involving trimethylamine (TMA), trimethylamine N-oxide (TMAO), and NF-κB signaling. In a clinical cohort of 153 subjects, high salt intake was independently associated with CaOx stones after multivariable adjustment (adjusted OR 2.52, 95% CI 1.10-5.94, p = 0.031). The gut microbiota of high-salt diet stone formers was enriched for inflammation-associated bacteria and NF-κB, tight junction, and sodium-calcium reabsorption pathways. In C57BL/6J mice, a one-month high-salt diet disrupted intestinal barrier integrity, induced renal inflammation with elevated TNF-α, IL-6, and IL-1β, and increased CaOx crystal deposition. 16S rRNA sequencing showed depletion of beneficial genera (Akkermansia, Bifidobacterium) and enrichment of TMA-producing bacteria. Cecal TMA and plasma TMAO were elevated in high-salt mice, while urinary TMA and TMAO were reduced, indicating impaired renal metabolite clearance. Fecal microbiota transplantation from high-salt diet donors reproduced the elevated TMAO, renal inflammation, and crystal deposition in recipient mice, confirming a causal role for the gut microbiota. In vitro, TMA disrupted tight junction proteins in Caco-2 intestinal epithelial cells, and TMAO activated NF-κB and increased CaOx crystal adhesion in HK-2 renal tubular cells; both effects were reversed by the NF-κB inhibitor QNZ. These findings identify the gut microbiota-TMA/TMAO-NF-κB axis as a mechanism linking high salt intake to CaOx kidney stone formation.},
}

*Gastrointestinal Microbiome/physiology/drug effects
Animals
*Kidney Calculi/metabolism/etiology/microbiology/pathology/chemically induced
Humans
Mice
Mice, Inbred C57BL
Male
*Inflammation/metabolism/pathology
*Sodium Chloride, Dietary/adverse effects
Female
Methylamines/metabolism
NF-kappa B/metabolism
Middle Aged
Calcium Oxalate/metabolism
Signal Transduction

@article {pmid42056116,
year = {2026},
author = {Ao, RF and Huang, YS and Hu, YT and Yong, HR and Wang, SC and Li, HZ and Gao, JW and Tu, C and Zhuang, JS and Zhong, ZM},
title = {Intermittent fasting alleviates hyperalgesia in ovariectomized mice via gut microbiota remodeling.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-00990-0},
pmid = {42056116},
issn = {2055-5008},
support = {82404244//the National Natural Science Foundation of China/ ; 82304154//the National Natural Science Foundation of China/ ; 2024A1515010611//the Basic and Applied Basic Research Foundation of Guangdong Province/ ; },
abstract = {Pain is a common symptom of menopause, yet effective therapeutic options are limited. Intermittent fasting (IF) has emerged as a promising dietary intervention; however, its effects on menopausal pain are still unclear. In this study, we established a hyperalgesia model in mice through ovariectomy (OVX) and subjected them to an alternate-day fasting regimen. IF significantly elevated the pain thresholds for mechanical, hot and cold stimuli in OVX mice and reduced the expression of pain-related molecules, including transient receptor potential vanilloid 1 (TRPV1) and calcitonin gene-related peptide (CGRP) in dorsal root ganglion (DRG). Moreover, IF remodeled the gut microbiota and metabolite profile, marked by a substantial increase in the abundance of Akkermansia muciniphila and its key metabolite, indole-3-propionic acid (IPA). Depletion of the gut microbiota via antibiotic treatment abolished the analgesic effects of IF on OVX-induced hyperalgesia. Conversely, fecal microbiota transplantation from IF-treated donors restored microbial composition and alleviated hyperalgesia in OVX recipients. Administration of A. muciniphila increased IPA levels and alleviated hyperalgesia in OVX mice. Importantly, exogenous IPA supplementation not only alleviated hyperalgesia but also reduced the excitability of DRG neurons. Together, these findings demonstrate that IF mitigates estrogen deficiency-related hyperalgesia through remodeling gut microbiota and metabolite profile, and identify IPA as a potential therapeutic target, offering new perspectives for the clinical management of menopausal pain.},
}

@article {pmid42057349,
year = {2026},
author = {Cheng, C and Wang, J and Xie, J and Yin, H and Xu, Z and Xie, Y and He, T and Jiang, Z and Wang, Y and Wu, W and Lou, W and Wang, J and Liu, L and Pu, N},
title = {Gut microbiota and pancreatic cancer: tumorigenesis, progression, and clinical applications.},
journal = {Cancer biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.20892/j.issn.2095-3941.2025.0650},
pmid = {42057349},
issn = {2095-3941},
support = {82572967//National Natural Science Foundation of China/ ; 82503105//National Natural Science Foundation of China/ ; 82473459//National Natural Science Foundation of China/ ; 82273382//National Natural Science Foundation of China/ ; 20254Y0181//Shanghai Municipal Health Commission Scientific Research Project/ ; 20244Y0023//Shanghai Municipal Health Commission Scientific Research Project/ ; 201940019//Shanghai Municipal Health Commission Scientific Research Project/ ; 23XD1400600//Program of Shanghai Academic/Technology Research Leader/ ; 24SF1900300//Shanghai Science and Technology Commission Innovative Pharmaceutical Products Application Demonstration Project/ ; SACA-CY24B09//Shanghai Anticancer Association EYAS PROJECT/ ; Y-2022METAZQN-0003//Beijing Xisike Clinical Oncology Research Foundation/ ; Y-Gilead2024-PT-0002//Beijing Xisike Clinical Oncology Research Foundation/ ; Y-HR2022MS-0251//Beijing Xisike Clinical Oncology Research Foundation/ ; ZSLCYJ202329//Shanghai "Rising Stars of Medical Talents" Youth Development Program, the Clinical Research of Zhongshan Hospital/ ; 202305AF150148//Liu Liang Expert Workstation of Yunnan Province/ ; },
abstract = {Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive malignancies of the digestive system, with a 5-year survival rate of only 13%, which is largely due to late-stage diagnosis and limited therapeutic options. Emerging evidence indicates that the gut microbiota has a critical role in PDAC tumorigenesis, progression, and therapeutic response. This review comprehensively summarizes current insights into gut microbiota-PDAC interactions, highlighting microbial alterations across taxonomic, functional, and clinical dimensions. Gut dysbiosis, which is marked by depletion of beneficial species and enrichment of pathogenic taxa, contributes to carcinogenesis through chronic inflammation, immune dysregulation, and metabolic reprogramming. In particular, the loss of butyrate-producing bacteria reduces anti-inflammatory activity and weakens CD8[+] T cell function, thereby promoting tumor development. In addition to initiation, the gut microbiota also shapes PDAC progression through direct translocation to pancreatic tissue and systemic regulation of the tumor microenvironment (TME), influencing immune cell dynamics and fostering therapeutic resistance. Clinically, distinct microbial signatures are emerging as potential diagnostic and prognostic biomarkers. Moreover, microbiota-targeted interventions, including probiotics, synbiotics, fecal microbiota transplantation (FMT), metabolite supplementation, and dietary modulation, show promise as adjunctive therapeutic strategies. However, significant challenges remain in defining causal mechanisms and translating these findings into practice. Future research should integrate multi-omics profiling with well-designed clinical trials to delineate the gut microbiota-PDAC interaction network, guide precision microbiota-based interventions, and ultimately enable earlier detection and personalized treatment of this lethal disease.},
}

@article {pmid42058119,
year = {2026},
author = {Qu, HL and Li, JN and Gao, Y and Zhang, XB and Yang, SD},
title = {From association to intervention: Semantic trajectories and knowledge frontiers in epilepsy-gut microbiota research revealed by bibliometrics and NLP.},
journal = {IBRO neuroscience reports},
volume = {20},
number = {},
pages = {609-624},
pmid = {42058119},
issn = {2667-2421},
abstract = {BACKGROUND: Research on the epilepsy-gut microbiota axis is accelerating, yet its conceptual evolution and translational signals remain difficult to track across disciplines. Here, we propose a semantic-bibliometric fusion framework that combines network-based science mapping with phrase- and topic-level natural language processing (NLP) to resolve both structural and linguistic dynamics in the field.

METHODS: Publications indexed in the Web of Science Core Collection from January 1997 to November 17, 2025 were retrieved and analyzed using CiteSpace, VOSviewer, Pajek, and Scimago Graphica, complemented by an NLP pipeline for topic modeling and temporal phrase tracking. In total, 516 records were included.

RESULTS: Annual output rose sharply after 2021 and peaked in 2024, with China and the United States leading contributions. Beyond conventional hotspots, semantic analyzes revealed a field-wide shift from early infection/safety-oriented discourse to mechanism- and intervention-driven themes dominated by the microbiota-gut-brain axis.

CONCLUSION: The most prominent and expanding intervention clusters involved the ketogenic diet, short-chain fatty acids, probiotics, and fecal microbiota transplantation, while "Mendelian randomization" emerged as a nascent frontier signaling movement from correlation to causal inference. By integrating knowledge-network topology with discourse dynamics, this study delivers an up-to-date, multi-resolution map of epilepsy-microbiome research and highlights actionable directions for future work, including causal validation, multi-omics stratification, and trial-ready microbiome-informed interventions.},
}

@article {pmid42058800,
year = {2026},
author = {Hegde, AV and Gupta, S and Mohan, LN and Rozario, A},
title = {Unforeseen consequence of colovesical fistula in diverticulitis presenting as septic cellulitis: A case report.},
journal = {World journal of methodology},
volume = {16},
number = {2},
pages = {111784},
pmid = {42058800},
issn = {2222-0682},
abstract = {BACKGROUND: Colovesical fistula (CVF) is an uncommon but serious complication most often linked to diverticular disease of the colon. Its diagnosis can be at times challenging as the symptoms are nonspecific, and timely intervention is crucial to avoid morbidity.

CASE SUMMARY: A 65-year-old Indian male was admitted with right lower limb cellulitis and was in septic shock. Despite initial management, he remained oliguric with persistent loose stools. On post-fasciotomy day 4, fecaluria was noted, prompting suspicion of a bowel-urinary tract fistula. Microscopic urine examination confirmed fecal matter. A computed tomography urogram with cystogram revealed a CVF at the sigmoid colon, likely secondary to diverticulitis. Baseline carcinoembryonic antigen levels were normal. An exploratory laparotomy was performed, which revealed dense adhesions between the sigmoid colon and bladder were noted, and the findings were consistent with diverticulitis though no discrete diverticulum was separately visualized. The fistulous tract was excised (frozen section was negative for malignancy), a two-layer bladder repair was performed, and the affected sigmoid colon segment was resected using a Hartmann's procedure. Multiple bladder washes were also done. Postoperatively, the patient recovered well, with resolution of oliguria and diarrhea. He was discharged on postoperative day 8. Histopathology confirmed diverticulitis without malignancy. A successful stoma reversal occurred 2 months later, and he remained symptom-free at the 6-month follow-up.

CONCLUSION: CVF should be considered in cases of persistent urinary symptoms or fecaluria, particularly in patients with risk factors such as older age and diverticular disease, even in regions with low incidence of colonic diverticula. Early diagnosis using imaging modalities and prompt surgical management are key to favorable outcomes.},
}

@article {pmid42060056,
year = {2026},
author = {Böhm, D and Guchelaar, HJ and Smidt, ML and Deenen, MJ},
title = {Microbiome-Modulating Strategies in Anticancer Therapy: A Review of Current Evidence and Recommendations for Further Treatment Improvement.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42060056},
issn = {1867-1314},
}

@article {pmid42061262,
year = {2026},
author = {Zhao, H and Akram, MZ and Comer, L and Corion, M and Fako, E and Everaert, N},
title = {Early gut microbiota transplantation in broiler chicks exerts effects on intestinal health depending on the donor's microbial composition.},
journal = {Poultry science},
volume = {105},
number = {7},
pages = {106999},
doi = {10.1016/j.psj.2026.106999},
pmid = {42061262},
issn = {1525-3171},
abstract = {Fecal microbiota transplantation (FMT) is a promising strategy for modulating the gut microbiota to enhance broilers' health. This study investigated the effects of FMT of broilers (FMT1), laying hens (FMT2), and broiler breeders (FMT3) as donor on the intestinal health of chicks as recipients. A total of 144 newly hatched Ross 308 male broilers were randomly assigned to four groups and reared until D 14. For the first three days after hatching, the control group received 1 mL of saline daily via oral gavage, while the FMT groups received their respective inocula. Body weight, intestinal length, and ileal histomorphology were assessed on D 5, D 7, and D 14. In addition, on D 7 and D 14, ileal tissues and serum were collected. The expression of critical genes related to barrier function, nutrient transport, mitochondrial function, antioxidant defense, signal transduction, innate immunity, cytokine response, and programmed cell death were measured using high-throughput qPCR. Furthermore, serum metabolites related to tryptophan metabolism were also determined. Group differences were analyzed using one-way ANOVA with Tukey's post-hoc test. Partial Least Squares Regression (PLSR) model was used to evaluate the interaction between observed changes and dominant microbiota. No significant effects on body weight or intestinal length were observed. On D 7, FMT1 induced innate immune stress, characterized by upregulated Toll-like receptor signaling, apoptosis, and mitochondrial biogenesis. In contrast, FMT2 and FMT3 improved intestinal histomorphology. Notably, FMT2 enhanced antioxidant defenses and changed tryptophan metabolism, while reducing reliance on glucose transporters. Meanwhile, FMT3 suppressed pyroptosis and enhanced barrier integrity. PLSR analysis identified 9 features that contribute over 30% of observed variations, with Olsenella, Blautia, and unclassified Lachnospiraceae being the most pronounced. By D 14, most effects had diminished, although antioxidant effects in FMT1 and immune markers in FMT2 and FMT3 persisted. Overall, FMT exerted donor-dependent patterns of influence on intestinal health, and our study proved programming of gut physiology through fecal microbiota transplantation.},
}

@article {pmid42061404,
year = {2026},
author = {Su, Q and Chen, S and Lau, LH and Lui, RN and Wang, Y and Xu, Z and Cheung, CP and Ching, JYL and Shen, X and Peng, Y and Tun, HM and Ianiro, G and Rubin, D and Chang, EB and Chan, FKL and Ng, SC},
title = {Artificial intelligence-driven donor-recipient gut microbiome matching for optimized fecal microbiota transplantation.},
journal = {Cell reports},
volume = {},
number = {},
pages = {117301},
doi = {10.1016/j.celrep.2026.117301},
pmid = {42061404},
issn = {2211-1247},
abstract = {Fecal microbiota transplantation (FMT) has emerged as a promising therapy for gastrointestinal diseases, yet its clinical efficacy remains individually variable. Here, we analyze multi-kingdom and functional profiles in pre- and post-FMT metagenomes from 515 FMTs across 30 cohorts and 12 diseases, in which 94 metagenomes from 44 FMTs are newly collected. We reveal a robust association between clinical efficacy and post-FMT microbiome convergence of recipients toward donors, across diseases. To predict post-FMT microbial convergence, we develop MOZAIC (Microbiome Matching Optimization via Artificial Intelligence), a framework that integrates multi-dimensional donor-recipient microbiota features. MOZAIC achieves an average area under the curve (AUC) of 0.88 and accuracy/recall >0.80 in forecasting microbiome convergence, with 78.7% accuracy in predicting clinical outcomes, and retrospectively simulates a 1.44-fold improvement (from 49.4% to 71.0%) in clinical response rates over baseline. This study establishes microbiome convergence as a key mediator of FMT and provides a scalable tool for precision matching in microbiota-based therapies.},
}

@article {pmid42047661,
year = {2026},
author = {Parker, G},
title = {Faecal Transplantation for Bipolar Disorder.},
journal = {Canadian journal of psychiatry. Revue canadienne de psychiatrie},
volume = {},
number = {},
pages = {7067437261445768},
doi = {10.1177/07067437261445768},
pmid = {42047661},
issn = {1497-0015},
}

@article {pmid42048405,
year = {2026},
author = {Wang, H and Wu, Z and Zhang, Y and Tang, L and Shi, G and Ma, L and Huang, Z and Zhou, J},
title = {Fecal microbiota transplantation mitigates respiratory infection in rats exposed to hypobaric hypoxia by modulating the NLRP3 inflammasome and mucosal immunity.},
journal = {PloS one},
volume = {21},
number = {4},
pages = {e0347857},
doi = {10.1371/journal.pone.0347857},
pmid = {42048405},
issn = {1932-6203},
mesh = {Animals ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/immunology ; *Fecal Microbiota Transplantation ; *Inflammasomes/metabolism/immunology ; Rats ; *Hypoxia/complications/immunology/microbiology ; Male ; Gastrointestinal Microbiome ; *Immunity, Mucosal ; Rats, Sprague-Dawley ; *Respiratory Tract Infections/therapy/microbiology/immunology ; Dysbiosis/therapy ; Fatty Acids, Volatile/blood ; Streptococcus pneumoniae ; RNA, Ribosomal, 16S/genetics ; Cytokines/metabolism ; },
abstract = {OBJECTIVE: To investigate the role of the gut-lung axis in respiratory infection under hypobaric hypoxia and the therapeutic potential of fecal microbiota transplantation (FMT).

METHODS: Rats were exposed to hypobaric hypoxia (simulated 5000 m) for 14 days. Gut microbiota and serum short-chain fatty acids (SCFAs) were analyzed via 16S rRNA sequencing and GC-MS. Rats were then infected with Streptococcus pneumoniae and treated with FMT. Lung inflammation, NLRP3 inflammasome activity, cytokines, bacterial load, and secretory IgA (sIgA) were assessed.

RESULTS: Hypobaric hypoxia triggered gut dysbiosis, marked by reduced abundance of Firmicutes D and Lactobacillus, elevated Bacteroidota, and decreased SCFA levels..FMT restored microbiota composition, increased acetic and butyric acid levels, and attenuated lung inflammation. FMT also enhanced NLRP3 inflammasome activation (NLRP3, ASC, Caspase-1), elevated IL-1β, IL-6, and TNF-α in BALF, reduced bacterial colonies, and increased airway sIgA in infected rats.

CONCLUSIONS: FMT alleviates hypobaric hypoxia-aggravated respiratory infection by restoring gut microbiota, modulating SCFAs, and enhancing NLRP3-mediated mucosal immunity, highlighting the gut-lung axis as a therapeutic target.},
}

Animals
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/immunology
*Fecal Microbiota Transplantation
*Inflammasomes/metabolism/immunology
Rats
*Hypoxia/complications/immunology/microbiology
Male
Gastrointestinal Microbiome
*Immunity, Mucosal
Rats, Sprague-Dawley
*Respiratory Tract Infections/therapy/microbiology/immunology
Dysbiosis/therapy
Fatty Acids, Volatile/blood
Streptococcus pneumoniae
RNA, Ribosomal, 16S/genetics
Cytokines/metabolism

@article {pmid42049093,
year = {2026},
author = {Hu, JJ and Feng, SY and Wu, L and He, SY and Chen, XF and Li, GH and Min, Y and Xu, HL and Sun, QS and Xie, S and Jian-Liu, and Chen, F and Liu, KX and Deng, F},
title = {Chac1 deficiency confers sepsis resistance by enriching gut microbiota-derived indole-3-carboxylic acid to drive macrophage metabolic shifts.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2026.04.065},
pmid = {42049093},
issn = {2090-1224},
abstract = {INTRODUCTION: Sepsis is a life-threatening dysregulated host response to infection, lacks effective therapies. ChaC glutathione-specific γ-glutamylcyclotransferase 1 (CHAC1) is elevated in sepsis and correlates with severity, but its functional role in the pathogenesis of sepsis-induced organ damage is unclear.

OBJECTIVES: We aimed to define the contribution of CHAC1 to sepsis-induced organ injury and elucidate the underlying mechanisms involving gut microbiota-derived metabolites and host immunity.

METHODS: Chac1[-/-] mice were subjected to LPS-induced endotoxemia to evaluate organ injury. The gut microbiota's role was defined by 16S rRNA gene sequencing, microbiota depletion and fecal microbiota transplantation (FMT). The effect of microbiota-derived metabolite indole-3-carboxylic acid (ICA) was assessed in vivo. Underlying mechanisms were investigated via macrophage depletion, AHR pharmacological/genetic inhibition, and in vitro studies with RAW264.7 cells and bone marrow-derived macrophages.

RESULTS: Serum CHAC1 was elevated in septic patients and mice, correlating with disease severity. Chac1 deficiency protected against sepsis-induced multi-organ injury, an effect that was gut microbiota-dependent. Chac1[-]/[-] mice exhibited a remodeled gut microbiota, with enrichment of Akkermansia muciniphila and increased levels of the tryptophan metabolite ICA. Exogenous ICA or A. muciniphila supplementation recapitulated the protective phenotype. ICA treatment improved survival, attenuated inflammation, and reduced organ injury by activating the aryl hydrocarbon receptor (AHR) in macrophages. This was evidenced by AHR nuclear translocation, and siRNA-mediated AHR knockdown abolished ICA's effects. ICA reprogrammed macrophage metabolism, inhibiting glycolysis (reduced lactate) and enhancing oxidative phosphorylation (increased ATP, oxygen consumption rate), leading to suppressed pro-inflammatory responses.

CONCLUSION: Chac1 deficiency confers sepsis resistance by enriching protective gut microbiota and elevating ICA, which acts as a major downstream effector. ICA activates the AHR in macrophages, driving a metabolic shift from glycolysis to oxidative phosphorylation that dampens inflammation and organ injury. This CHAC1-microbiota-ICA-AHR-macrophage axis identifies ICA as a promising therapeutic candidate and CHAC1 as a potential prognostic biomarker for sepsis.},
}

@article {pmid42051335,
year = {2026},
author = {Li, B and Ren, Z and Li, H and Li, M and Zhong, H and Nie, Q and Chen, J and Wu, R and Zheng, JS and Deng, K and Cai, Y},
title = {Microbiota-metabolites interaction associated with glycemic improvement following a dietary herbal intervention in type 2 diabetes.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1793130},
pmid = {42051335},
issn = {2296-861X},
abstract = {BACKGROUND: Type 2 diabetes (T2D) is a global metabolic disorder characterized by chronic hyperglycemia and disruption of the gut microbiome. Nutritional and microbiota-targeted interventions have emerged as promising strategies for glycemic management, yet longitudinal clinical evidence integrating microbial and metabolic mechanisms remains limited. This study investigated microbiota-metabolites alterations during a standardized dietary herbal intervention (QingYun7, QY7) and explored their relationship with glycemic regulation across both animal study and clinical settings.

METHODS: The metabolic and microbial effects of QY7 were first evaluated in diabetic rats through measurements of blood glucose, and gut microbiota composition. Subsequently, a prospective cohort of 385 patients with T2D received QY7, with longitudinal monitoring of fasting, random, and 2-h postprandial glucose, gut microbiota, and serum metabolites across multiple time points. Fecal microbiota transplantation (FMT) from patients before and after intervention into antibiotic-treated mice was performed to evaluate the causal contribution of the gut microbiome to glycemic improvement. Mediation analyses were conducted to delineate potential pathways linking gut microbes, serum metabolites, and glucose outcomes.

RESULTS: In diabetic rats, QY7 administration significantly reduced blood glucose, and restored gut microbial composition. In the clinical cohort, the intervention was associated with rapid and sustained reductions in fasting, random, and postprandial glucose levels, accompanied by consistent remodeling of the gut microbiome and serum metabolite profile. FMT experiments demonstrated that microbiota derived from post-intervention patients conferred improved glycemic responses in recipient mice, supporting a causal role of gut microbiota in metabolic regulation. Serum metabolomic profiling revealed significant alterations, including enrichment of branched-chain amino acid related pathways. Mediation analyses identified key metabolites, phenyllactic acid, 3-methyl-2-oxobutanoic acid, and anandamide, as mediators linking specific bacterial taxa (Alistipes shahii and Limosilactobacillus mucosae) to fasting and postprandial glucose levels.

CONCLUSION: This study provides translational evidence that a dietary herbal intervention associated with glycemic improvement in T2D through microbiota-mediated metabolic reprogramming. Gut microbiome alterations induced by the intervention exerted causal effects on blood glucose regulation, with serum metabolites acting as potential key intermediaries. These findings highlight the mechanistic insight in nutrition-based microbiome modulation strategy in T2D.},
}

@article {pmid42051455,
year = {2026},
author = {Du, X and Su, H and Huang, Y and Liu, J and Li, Q and Yang, X and Tao, X and Li, R},
title = {Gut microbiome dysbiosis in PCOS: from pathogenesis to microbiome-targeted therapies.},
journal = {Frontiers in endocrinology},
volume = {17},
number = {},
pages = {1747766},
pmid = {42051455},
issn = {1664-2392},
mesh = {Humans ; *Polycystic Ovary Syndrome/microbiology/therapy/etiology/pathology ; *Dysbiosis/microbiology/therapy/complications ; *Gastrointestinal Microbiome/physiology ; Female ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; },
abstract = {(PCOS), one of the most common endocrine and metabolic disorders in women of reproductive age, has a complex pathogenesis that continues to be unraveled by ongoing research. The condition is defined by three key features: hyperandrogenemia, ovulatory dysfunction, and insulin resistance. Recent studies have highlighted the gut microbiome and its metabolites as crucial regulators in PCOS development. Evidence suggests that gut dysbiosis and intestinal barrier dysfunction play a pivotal role in the onset and progression of PCOS. This review comprehensively examines the central role of gut microbiota in PCOS pathogenesis, including shifts in microbial communities such as bacteria, fungi, and viruses, and their impact on critical metabolites like short-chain fatty acids, bile acids, and tryptophan metabolites, which modulate host metabolism and reproductive function. Furthermore, based on mechanistic insights, the review explores targeted gut microbiota interventions, systematically evaluating clinical evidence for dietary modifications, probiotic/prebiotic supplementation and fecal microbiota transplantation. These approaches provide novel perspectives for precision medicine in PCOS treatment. The findings not only deepen our understanding of PCOS pathogenesis but also establish a strong theoretical foundation for innovative microbiome-based therapeutics.},
}

Humans
*Polycystic Ovary Syndrome/microbiology/therapy/etiology/pathology
*Dysbiosis/microbiology/therapy/complications
*Gastrointestinal Microbiome/physiology
Female
Fecal Microbiota Transplantation
Probiotics/therapeutic use

@article {pmid42051692,
year = {2026},
author = {Wang, LM and Chen, C and Danzheng, JC and Zhao, J},
title = {Gut microbiome in sepsis: from dysbiotic biomarker to precision and palliative decision-making.},
journal = {Frontiers in medicine},
volume = {13},
number = {},
pages = {1811304},
pmid = {42051692},
issn = {2296-858X},
abstract = {Sepsis is a major cause of mortality in critically ill patients, necessitating improved early detection, risk stratification, and individualized clinical decision-making. The gut microbiome actively regulates host immunity, metabolism, and barrier function, engaging in bidirectional interactions with sepsis progression. Evidence suggests that gut dysbiosis not only accompanies sepsis but may also accelerate it. Characteristic shifts, including reduced microbial diversity, expansion of opportunistic pathogens, and decreased short-chain fatty acid production, could offer early prognostic signals prior to clinical decline. Advances in multi-omics and computational analytics are enabling the translation of microbial signatures into actionable clinical insights, supporting phenotype-specific stratification in sepsis. Emerging microbiome-targeted interventions such as next-generation probiotics, synbiotics, metabolite supplementation, and fecal microbiota transplantation show potential for modulating host responses in a stage-specific manner. Within a precision medicine framework, microbiome-derived biomarkers may refine both critical care management and palliative decision-making. In advanced or refractory sepsis, these insights could help tailor treatment intensity, prioritize symptom control, and avoid non-beneficial therapeutic escalation. Realizing this potential will require prospective validation and standardized approaches to integrate microbiome data into personalized, goal-concordant sepsis care.},
}

@article {pmid42053098,
year = {2026},
author = {Saad, M and Redman, A and Ata, NA and Anton, C and Fei, L and Vitale, DS and Zhang, Y and Abu-El-Haija, M and Trout, AT},
title = {Predictive Power of Imaging: Assessing Parenchymal Fibrosis in Pediatric Chronic Pancreatitis.},
journal = {Pancreas},
volume = {},
number = {},
pages = {},
doi = {10.1097/MPA.0000000000002658},
pmid = {42053098},
issn = {1536-4828},
abstract = {OBJECTIVES: The primary aim is to identify pancreatic parenchymal imaging markers of fibrosis in children with chronic pancreatitis (CP). Secondary aims include describing the pattern of histopathologic fibrosis in different pancreatic regions and examining the impact of fibrosis on exocrine pancreatic insufficiency (EPI) and baseline glycemic status.

METHODS: Single center cross-sectional study that included children aged 0-21 years who underwent total pancreatectomy islet auto-transplantation (TPIAT) prior to December 2022. Those with prior pancreatic surgeries, missing imaging, or missing histology were excluded.

RESULTS: Ninety-five patients (56% female, median age 13.3 y) were included. Multiple parenchymal imaging variables were significantly associated with histologic pancreatic fibrosis. A 5 mL decrease in segmented pancreas volume (odds ratio (OR)=1.2, 95% confidence interval (CI): 1.1-1.4, P<0.05) and 0.1 unit decrease in T1 signal intensity ratio (SIR) pancreas/spleen (P/s) (OR=1.7, 95% CI: 1.2-2.2, P<0.05) had increased fibrosis odds. A multivariable model with pancreas volume and T1 SIRp/s predicted severe fibrosis with an area under the receiver operating characteristic curve (AUROC) of 0.8 (95% CI:0.7-0.9). Histologic fibrosis scores showed substantial agreement between pancreatic sampling locations (kappa=0.7, 95% CI: 0.6-0.9). EPI by fecal elastase (FE-1) was associated with increased odds of severe fibrosis (OR=11.7, 95% CI: 2.5-54.1, P<0.05) and higher Ammann scores were seen in participants with prediabetes and diabetes (9.0, interquartile range (IQR): 8.0-12.0, P=0.08).

CONCLUSIONS: The pancreatic parenchyma provides insights into pediatric CP through fibrosis assessment, which correlates with pancreatic function. A predictive model using pancreas volume and T1 SIR shows promise for forecasting pancreatic parenchymal fibrosis in children with CP.},
}

@article {pmid42042323,
year = {2026},
author = {Granata, G and Petrosillo, N},
title = {Newer Therapeutics to Selectively Kill Clostridioides difficile and Restore the Microbiome.},
journal = {Infectious disease reports},
volume = {18},
number = {2},
pages = {},
pmid = {42042323},
issn = {2036-7430},
abstract = {BACKGROUND: The antibiotic ibezapolstat and the live biotherapeutic product live-JSLM are promising future approaches for treating Clostridioides difficile infection. Ibezapostat is a highly specific antibiotic for Clostridioides difficile, with minimal impact on the intestinal flora. Live-JSLM is designed to restore healthy intestinal microbiota, thus preventing recurrence of Clostridioides difficile infection. In this narrative review, we reviewed available data on ibezapostat and live-JSLM, considering that they are prototypes of two distinct, unique mechanisms of action against Clostridioides difficile.

METHODS: Data sources: PubMed and SCOPUS databases were searched from 1 January 2012 to 15 November 2025. Original articles reporting data on ibezapolstat and live-JSLM were included.

RESULTS: 31 studies were included. When compared to conventional anti-Clostridioides difficile antibiotics, ibezapolstat had a similar level of effectiveness and minimal impact on the gut microbiota. The available data confirm live-JSLM safety and efficacy in restoring the gut microbiota following the conclusion of the standard anti-Clostridioides difficile antibiotic regimen.

CONCLUSIONS: The results on ibezapolstat efficacy are promising, but require confirmation in larger patient populations through double-blind, randomised phase III trials. In the near future, an integrated approach may enhance the management of Clostridioides difficile infection: starting with highly specific antibiotics, i.e., ibezapolstat, followed by microbiome-based therapies such as live-JSLM.},
}

@article {pmid42043039,
year = {2026},
author = {Lauriola, M and Valkenburg, S and Dejongh, S and Zadora, W and Krukowski, H and Evenepoel, P and Raes, J and Farré, R and Glorieux, G and Meijers, B},
title = {Kidney Function Modulates Gut Microbial Metabolism.},
journal = {Toxins},
volume = {18},
number = {4},
pages = {},
pmid = {42043039},
issn = {2072-6651},
support = {860329//European Union's Horizon 2020 research and innovation program/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Renal Insufficiency, Chronic/metabolism/microbiology/physiopathology ; *Colon/microbiology/metabolism ; Male ; Tryptophan/metabolism ; Feces/microbiology/chemistry ; *Kidney/physiopathology ; Fatty Acids, Volatile/metabolism ; Indoles/metabolism ; Kynurenine/metabolism ; Rats ; Amino Acids/metabolism ; Fermentation ; Rats, Wistar ; Cresols/metabolism ; *Bacteria/metabolism ; },
abstract = {Growing evidence suggests that chronic kidney disease (CKD) profoundly disrupts gut microbiome and its activity. This study explores how CKD affects colon microbial metabolism, focusing on (1) the representativeness of fecal metabolomics, (2) saccharolytic and proteolytic fermentation metabolites, and (3) the gut microbiome's role in the partitioning of tryptophan in its metabolic pathways. Tryptophan's main metabolic pathways include the indolic and the kynurenine pathways, which lead, respectively, to the formation of indoxyl sulfate and kynurenine, both contributing to uremic toxicity. Using a rat model of CKD, we evaluated whether fecal concentrations of microbial compounds, on which most studies are based, reflect the colonic concentrations in contact with the gut mucosa. Thus, we quantified the concentration and content of amino acids, indole, p-cresol, and also short-chain fatty acids, in different colon sections. We demonstrated that CKD promotes increased proteolytic fermentation and an augmented tryptophan partitioning into both the indolic and kynurenine pathways. Depletion of the indolic pathway obtained upon antibiotic treatment leads to a further enhancement of the kynurenine pathway.},
}

Animals
*Gastrointestinal Microbiome
*Renal Insufficiency, Chronic/metabolism/microbiology/physiopathology
*Colon/microbiology/metabolism
Male
Tryptophan/metabolism
Feces/microbiology/chemistry
*Kidney/physiopathology
Fatty Acids, Volatile/metabolism
Indoles/metabolism
Kynurenine/metabolism
Rats
Amino Acids/metabolism
Fermentation
Rats, Wistar
Cresols/metabolism
*Bacteria/metabolism

@article {pmid42045958,
year = {2026},
author = {Huang, J and Chen, Z and Wang, M and Yang, C and Wang, A and Chen, Y},
title = {Efficacy and safety of fecal microbiota transplantation in reducing recurrence of colorectal adenomas after endoscopic resection: study protocol for a multicenter, open-label, randomized, no-treatment-controlled trial.},
journal = {Trials},
volume = {},
number = {},
pages = {},
doi = {10.1186/s13063-026-09740-1},
pmid = {42045958},
issn = {1745-6215},
support = {C2401027//Shenzhen Medical Research Fund/ ; },
abstract = {BACKGROUND: Endoscopic resection is the standard treatment for colorectal adenoma (CRA), a key precursor to colorectal cancer (CRC). However, a high rate of recurrence post-procedure poses a significant challenge for long-term CRC prevention. Growing evidence suggests gut microbial dysbiosis contributes to adenoma development and recurrence. This trial will test the hypothesis that restoring a healthy gut microbiome with fecal microbiota transplantation (FMT) can reduce the recurrence of CRA after endoscopic resection.

METHODS: This protocol describes a multicenter, open-label, randomized, no-treatment-controlled trial that will enroll 466 participants with CRA following endoscopic resection. Participants will be randomly assigned in a 1:1 ratio to receive either FMT or no treatment (control). The FMT intervention consists of an initial colonoscopic infusion and oral capsules, followed by oral maintenance capsules at months 3, 6, and 9. The primary outcome is the rate of CRA recurrence at the 12-month follow-up colonoscopy. Key secondary outcomes include the incidence of all polypoid lesions, changes in the gut and mucosal microbiota composition, the incidence of CRC, and a comprehensive assessment of adverse events to evaluate safety.

DISCUSSION: This trial is designed to provide high-quality evidence on the efficacy and safety of FMT for preventing CRA recurrence. The findings may support a novel, microbiome-based strategy for the secondary prevention of CRC and provide mechanistic insights into the role of the gut microbiota in colorectal carcinogenesis.

TRIAL REGISTRATION: ClinicalTrials.gov NCT06205862. Registered on 16 January, 2024. https://clinicaltrials.gov/study/NCT06205862.},
}

@article {pmid42046871,
year = {2026},
author = {Yang, Y and Tan, X and Zhang, Z and Liang, L and Wu, Z and He, J and Wang, Y and Dong, M and Zheng, J and Zhang, H and Feng, S and Cheng, W and Cui, B and Wei, H and Li, Q},
title = {Metagenomic sequencing reveals high reproducibility of human donor microbiota transplanted into germ-free mice via lower gut route.},
journal = {Journal of Zhejiang University. Science. B},
volume = {27},
number = {4},
pages = {375-389},
doi = {10.1631/jzus.B2400495},
pmid = {42046871},
issn = {1862-1783},
support = {2021YFA0805904//the National Key Research and Development Program of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/genetics ; Humans ; Mice ; Germ-Free Life ; *Fecal Microbiota Transplantation/methods ; Feces/microbiology ; *Metagenomics ; Reproducibility of Results ; High-Throughput Nucleotide Sequencing ; Male ; *Metagenome ; Mice, Inbred C57BL ; Female ; },
abstract = {Human flora-associated (HFA) mice are often used to simulate the structure of human intestinal microbiota and to study the causal relationships between diseases and gut microbiota. However, several factors affect the colonization efficiency of human microbiota in germ-free (GF) mice, and the differential effects of gavage and lower gut transplantation on colonization are still unclear. In this study, we explored the reproducibility of the recipient-to-donor gut microbiota community structure and function under different transplantation routes and the differences in microbial colonization between recipients via gavage transplantation (GT_mice group) and lower gut transplantation (LGT_mice group). High-throughput sequencing of the metagenome was performed on the feces of each subject, and the composition of microbiome of each group was analyzed. As expected, the introduction of human fecal microbiota into GF mice via lower gut transplantation had a high transfer efficiency, which was evident from the similar species community structure to that of the donor (Adonis R[2]=0.713 960 for LGT_mice group‒donor group; Adonis R[2]=0.774 095 for GT_mice group‒donor group) and a higher bacterial colonization rate. The findings provide unique insights into improving the accuracy of constructing humanized microbiota transplantation models, aiding our understanding of the relationships between the human gut microbiota and disease.},
}

Animals
*Gastrointestinal Microbiome/genetics
Humans
Mice
Germ-Free Life
*Fecal Microbiota Transplantation/methods
Feces/microbiology
*Metagenomics
Reproducibility of Results
High-Throughput Nucleotide Sequencing
Male
*Metagenome
Mice, Inbred C57BL
Female

@article {pmid42046887,
year = {2026},
author = {Li, M and Yue, A and Gu, L and Li, F and Ye, N and Xu, S and Gong, Z and Li, D and Xu, P},
title = {Microbiota-metabolite axis in endometriosis: Pathogenic mechanisms and clinical implications.},
journal = {Journal of biomedical research},
volume = {},
number = {},
pages = {1-17},
doi = {10.7555/JBR.39.20250566},
pmid = {42046887},
issn = {1674-8301},
abstract = {Growing evidence highlights the role of microbiota, including those of the gut, reproductive tract, and endometrial tissue, as critical functional drivers in the pathogenesis of endometriosis (EM). Studies have revealed a characteristic microbial imbalance in patients with EM, marked by a reduced abundance of beneficial bacteria and enrichment of opportunistic pathogens. These microbial communities exert their influence primarily through metabolic activity, as demonstrated by metabolomic studies showing their capacity to modulate host immune and endocrine responses. This imbalance leads to multiple key metabolic disturbances, including decreased levels of short-chain fatty acids, particularly butyrate; a shift in tryptophan metabolism toward the kynurenine pathway; elevated β-glucuronidase activity; increased lipopolysaccharide production; and altered secondary bile acid profiles. Functionally, these metabolic alterations converge to promote EM by disrupting immune homeostasis, enhancing estrogen signaling, and driving systemic inflammation, collectively creating a permissive microenvironment for ectopic lesion growth and invasion. Targeted interventions, such as probiotics, high-fiber dietary strategies, fecal microbiota transplantation, and selective modulation of microbial or host metabolic enzymes, are emerging as promising non-hormonal therapeutic approaches. Nonetheless, further studies incorporating longitudinal cohort designs and integrative multi-omics approaches are essential to establish causality and facilitate the development of precise diagnostic and personalized treatment strategies.},
}

@article {pmid41662314,
year = {2026},
author = {van der Sligte, NE and Biedermann, L and Rogler, G and Scharl, M},
title = {Outcomes of Fecal Microbiota Transfer in Patients with Recurrent Clostridioides Difficile Infection: Real-World Data from a Single Center in Switzerland.},
journal = {Digestive diseases (Basel, Switzerland)},
volume = {44},
number = {2},
pages = {225-234},
pmid = {41662314},
issn = {1421-9875},
mesh = {Humans ; *Fecal Microbiota Transplantation/adverse effects/methods ; Female ; Male ; *Clostridium Infections/therapy/microbiology ; Aged ; Middle Aged ; Switzerland ; Recurrence ; Aged, 80 and over ; *Clostridioides difficile ; Adult ; Treatment Outcome ; Retrospective Studies ; Young Adult ; Feces/microbiology ; },
abstract = {UNLABELLED:

Introduction: Clostridioides difficile is the most frequently reported healthcare-associated infection with around 125'000 occurrences and 3'700 deaths annually in Europe. Recurrence rates are about 20% and risk factors include age >65 years and inflammatory bowel disease (IBD). Fecal microbiota transfer (FMT) has emerged as a highly effective treatment for recurrent C. difficile infection (rCDI), being successful in more than 90% of patients. This retrospective single-center study aimed to evaluate the effectiveness and safety of FMT in patients with rCDI at the University Hospital Zurich.

METHODS: Between 2012 and 2022, 84 patients underwent FMT for rCDI at our center, of which 83 were included in the final analysis. The median patient age was 71 years (22-97 years), and the majority of patients were female (67.5%). All patients had received multiple prior courses of antibiotic treatment for C. difficile infection.

RESULTS: The success rate following a single FMT was 92.8%, increasing to 97.6% with repeated procedures. Those rates were comparable in the IBD subgroup. FMT was well tolerated. Mild adverse events were reported in 14.5% of patients, most commonly reported adverse event being ongoing IBD activity (33.3%), and diarrhea (33.3%) followed by abdominal pain (25%). Serious adverse events occurred in 3.6% of patients mainly related to underlying conditions.

CONCLUSION: Our study confirms that FMT is a highly effective and well-tolerated treatment for rCDI, even in older patients with comorbidities. Importantly, FMT was successfully implemented without the use of a national stool bank, instead relying on locally processed related donor stool, highlighting its feasibility in resource-limited settings.

Humans
*Fecal Microbiota Transplantation/adverse effects/methods
Female
Male
*Clostridium Infections/therapy/microbiology
Aged
Middle Aged
Switzerland
Recurrence
Aged, 80 and over
*Clostridioides difficile
Adult
Treatment Outcome
Retrospective Studies
Young Adult
Feces/microbiology

@article {pmid42034536,
year = {2026},
author = {Yao, Y and Liu, Y and Li, Y and Lu, B and Cui, X and Pan, X},
title = {Re: Fecal Microbiota Transplantation plus Pembrolizumab and Axitinib in Metastatic Renal Cell Carcinoma: The Randomized Phase 2 TACITO Trial.},
journal = {European urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.eururo.2026.04.003},
pmid = {42034536},
issn = {1873-7560},
}

@article {pmid42035251,
year = {2026},
author = {Li, C and Wan, W and Li, C and Zhu, D and Li, J and Yang, S and Chen, W and Chen, H and Yu, C},
title = {The microbiota-gut-brain axis as a driver of secondary brain injury after aneurysmal subarachnoid hemorrhage: from bidirectional vicious cycle to therapeutic opportunities.},
journal = {Reviews in the neurosciences},
volume = {},
number = {},
pages = {},
pmid = {42035251},
issn = {2191-0200},
abstract = {Aneurysmal subarachnoid hemorrhage (aSAH) is a devastating stroke subtype with high morbidity and mortality, significantly contributed to by secondary brain injuries such as early brain injury and delayed cerebral ischemia. Despite advances in acute management, effective neuroprotective strategies remain an unmet need. The microbiota-gut-brain axis (MGBA), a pivotal bidirectional communication network, has recently emerged as a critical modulator of pathophysiology in acute brain injuries. However, its precise role and therapeutic potential in aSAH are not systematically defined. This review synthesizes clinical and preclinical evidence to move beyond correlation and delineate the spatiotemporal dynamics and the mechanisms that may underlie of MGBA dysregulation post-aSAH. We conceptualize a self-amplifying "brain-gut-brain" vicious cycle: the initial brain injury may disrupt intestinal barrier integrity and microbiota ecology via neuroendocrine and inflammatory pathways; in turn, gut-derived signals (e.g., altered microbial metabolites, endotoxin translocation) may propagate systemic inflammation and exacerbate neuroinflammation, blood-brain barrier disruption, and cerebral ischemia. We dissect this cycle by detailing the key molecular bridges (tryptophan metabolites, short-chain fatty acids, bile acids), signaling pathways (e.g., TLR4/NF-κB, NLRP3 inflammasome), and central effectors involved. Furthermore, we provide a critical, stratified evaluation of MGBA-targeting therapeutic strategies - including probiotics, prebiotics, fecal microbiota transplantation, and metabolite supplementation - assessing their mechanistic rationale, level of evidence, and translational challenges. Finally, we outline future directions emphasizing the need for defining therapeutic windows, establishing causal proof, and integrating MGBA modulation into multimodal neurocritical care. Harnessing the MGBA presents a novel and promising paradigm for developing adjunctive neuroprotective therapies to improve outcomes after aSAH.},
}

@article {pmid42036378,
year = {2026},
author = {Chen, D and Zhang, B and Wang, O and Zhang, X and Huang, J},
title = {[Effects of high-fat diet on gut microbiota in rats transplanted with gut microbiota from normal/high triglyceridemic individuals].},
journal = {Wei sheng yan jiu = Journal of hygiene research},
volume = {55},
number = {2},
pages = {261-268},
doi = {10.19813/j.cnki.weishengyanjiu.2026.02.014},
pmid = {42036378},
issn = {1000-8020},
mesh = {Animals ; *Diet, High-Fat/adverse effects ; *Gastrointestinal Microbiome ; Male ; Rats ; Rats, Sprague-Dawley ; *Triglycerides/blood ; Humans ; Feces/microbiology ; Fecal Microbiota Transplantation ; *Hypertriglyceridemia/microbiology ; },
abstract = {OBJECTIVE: Using sterile SD rats as a model, the fat accumulation and changes in the intestinal flora of rats transplanted with normal/high triglyceride(TG) population under high-fat diet were studied.

METHODS: 10-week-old male sterile rats were randomly divided into 3 groups according to body weight, with 6 rats in each group. The non-colonizing group was gavaged with normal saline, the normal lipid group was gavaged with normal TG(<1.7 mmol/L) human intestinal flora, and the high TG group was gavaged with high TG(≥1.7 mmol/L) human intestinal flora. Rats were given fecal bacterial solution by gavage at a dose of 1 mL per 100 g of body weight, every other day, for a total of 3 times, followed by 2 weeks of adaptive growth of the microbiota. After the transplanting was completed, a 9-week feeding experiment with high-fat diet(fat energy supply ratio 40.5%) was conducted. The body weight of the rats was measured weekly, and feces were collected every three weeks. After the experiment, liver, perirenal, subcutaneous and brown fat were weighed. The fat weight was used to represent the fat accumulation of the rats, and lipid indicators were determined. Liver HE staining was used to observe steatosis, and high-throughput sequencing was used to analyze the intestinal flora of the rats.

RESULTS: After the experiment, compared with the colonized normal TG population microbiota group, there were no significant differences in body weight, perirenal, subcutaneous and brown fat mass, and blood lipid levels in the colonized high TG microbiota group. Liver HE staining sections showed that both the colonized high TG and non-colonized dyslipidemia microbiota groups could observe more severe steatosis and obvious fat vacuums. The intestinal microbiota profiles of the two groups of rats colonized with different population microbiota showed different variation patterns at the phylum and genus levels. At 0 weeks of high-fat diet, the F/B ratios of the microbiota phylum in rats colonized with the feces of the high-TG population and those colonized with the feces of the normal TG population were 1.24 and 0.48, respectively. After 9 weeks of high-fat diet, The F/B ratios of the Firmicutes and Bacteroidetes phyla of the bacteria phyla in rats colonized with the feces of the high TG population and those colonized with the feces of the normal TG population were 3.37 and 0.81, respectively. In the fecal colonization group of rats in the high TG population under a high-fat diet, more obvious intestinal flora disorders occurred, the relative abundance of beneficial bacteria was inhibited, and the relative abundance of pathogenic bacteria increased.

CONCLUSION: Under high-fat diet, the colonization of intestinal flora in volunteers with different blood lipid levels has a certain relationship with the weight changes and fat accumulation of rats. The species composition and abundance of flora in different populations have undergone significant changes.},
}

Animals
*Diet, High-Fat/adverse effects
*Gastrointestinal Microbiome
Male
Rats
Rats, Sprague-Dawley
*Triglycerides/blood
Humans
Feces/microbiology
Fecal Microbiota Transplantation
*Hypertriglyceridemia/microbiology

@article {pmid42039746,
year = {2026},
author = {Tian, W and Peng, S and Xu, F and Kong, X and Li, Y and Zhang, W and Liu, Z and Zhang, H and Wang, J and Wang, L},
title = {Disruption of intestinal barrier and immune homeostasis links gut microbiota dysbiosis to aggravated experimental autoimmune myasthenia gravis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1726788},
pmid = {42039746},
issn = {2235-2988},
mesh = {Animals ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/immunology/microbiology ; Th17 Cells/immunology ; Rats ; Rats, Inbred Lew ; T-Lymphocytes, Regulatory/immunology ; Disease Models, Animal ; Cytokines/blood ; RNA, Ribosomal, 16S/genetics ; *Myasthenia Gravis, Autoimmune, Experimental/immunology/microbiology/pathology ; *Homeostasis ; Fecal Microbiota Transplantation ; *Intestinal Mucosa/immunology/microbiology ; Female ; },
abstract = {INTRODUCTION: Myasthenia Gravis (MG) is an acquired autoimmune disease. The imbalance between Th17 and Treg cells plays a crucial role in the pathogenesis of MG. A stable intestinal microbiota is essential for maintaining immune balance, a function primarily mediated by the Th17/Treg axis. This study aims to explore the role of gut microbiota in the pathogenesis of experimental autoimmune myasthenia gravis (EAMG) to identify potential new treatment strategies.

METHODS: An EAMG model was established in Lewis rats by immunization with the AChRα97-116 peptide segment. The composition and structure of the gut microbiota were analyzed by 16S rRNA sequencing. The serum levels of inflammatory cytokines (IFN-γ, TNF-α, IL-17, IL-10), AChR-Ab, and LPS were measured using the ELISA method. Colon tissues were subjected to Hematoxylin and eosin (H&E) staining, and Claudin-1 and Muc2 expression was analyzed via immunofluorescence. A microbiota disorder animal model was established by administering an antibiotic mixture via gavage, followed by fecal microbiota transplantation. Splenic CD3+CD4+IL-17A+ Th17 cells and CD3+CD4+CD25+Foxp3+ Treg cells were quantified by flow cytometry.

RESULTS: 1. Compositional and structural changes of the gut microbiota in EAMG. Compared with HC, the serum levels of IFN-γ, TNF-α, IL-17, and AChR-Ab in EAMG were significantly increased (P < 0.0001), while the serum level of IL-10 was significantly decreased (P < 0.0001), and the serum level of LPS was increased (P < 0.01). The protein levels of Claudin-1 (P < 0.001) and Muc2 (P < 0.05) in the colon were significantly reduced in EAMG. 2. Relative to rats receiving HC microbiota transplantation (HMb), those receiving EAMG microbiota transplantation (MMb) exhibited significantly elevated serum levels of AChR-Ab (P < 0.01), TNF-α (P < 0.05), IL-17 (P < 0.05), and LPS (P < 0.01), alongside significantly reduced colonic levels of Claudin-1 (P < 0.05) and Muc2 (P < 0.0001). 3. Compared with the EAMG group, the ABX + EAMG group (EAMG with microbiota dysbiosis) exhibited significantly lower colonic levels of Claudin-1 and Muc2 (P < 0.05), a significantly greater splenic Th17/Treg cell imbalance (P < 0.01), and significantly higher serum AChR-Ab levels (P < 0.01).

DISCUSSION: The gut microbiota is intricately linked to the progression of EAMG. Microbiota dysbiosis can exacerbate intestinal barrier damage in EAMG and may further influence the pathological changes of myasthenia by disrupting the Th17/Treg immune balance. These findings suggest a novel therapeutic strategy for the treatment of myasthenia gravis by re-establishing microbial homeostasis.},
}

Animals
*Gastrointestinal Microbiome/immunology
*Dysbiosis/immunology/microbiology
Th17 Cells/immunology
Rats
Rats, Inbred Lew
T-Lymphocytes, Regulatory/immunology
Disease Models, Animal
Cytokines/blood
RNA, Ribosomal, 16S/genetics
*Myasthenia Gravis, Autoimmune, Experimental/immunology/microbiology/pathology
*Homeostasis
Fecal Microbiota Transplantation
*Intestinal Mucosa/immunology/microbiology
Female

@article {pmid42039828,
year = {2026},
author = {Li, Z and Xie, C and Pan, C},
title = {The oral-gut-brain axis: how periodontitis influence depression.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1778744},
pmid = {42039828},
issn = {1664-302X},
abstract = {Depression has a high global prevalence and is a common mental-emotional disorder that severely jeopardizes human health. However, current treatment options remain limited, necessitating the exploration of novel pathological mechanisms and intervention targets. Recent studies indicate that periodontitis, as a prevalent chronic oral infectious disease, not only causes local microbial dysbiosis and inflammatory responses but may also influence central nervous system function through the "oral-gut-brain axis," thereby contributing to the pathogenesis and progression of neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis, as well as neuropsychiatric disorders like depression. This review systematically examines the impact of periodontitis on oral microbiota and its subsequent translocation and colonization in the gut microbiota through pathways including swallowing and bloodstream circulation, ultimately leading to structural and functional dysregulation of the gut microbiota. The interaction between oral and gut microbiota can influence the brain through the "gut-brain axis," including disturbances in neurotransmitter metabolism, activation of systemic immune responses, and direct or indirect effects of bacterial metabolites (such as short-chain fatty acids, lipopolysaccharides, etc.) on the blood-brain barrier and neural function. This suggests that periodontal health management may serve as a novel strategy for the prevention and treatment of depression. This article further summarizes the potential of oral interventions for periodontitis (such as mechanical debridement and local/systemic antimicrobial therapy), microbiota modulation methods (such as probiotics, prebiotics, and fecal microbiota transplantation), and multidisciplinary collaborative comprehensive treatment strategies in improving microbial homeostasis and alleviating depressive symptoms. Finally, this paper points out the current research limitations in mechanistic details, causal relationships, and clinical translation, while envisioning the feasibility and prospects of developing personalized treatment strategies by targeting the "oral-gut-brain axis" in the future.},
}

@article {pmid42040311,
year = {2026},
author = {Dong, B and Zhong, B and Zuo, J and Liao, L and Zeng, W and Xiong, M and Wei, Y and Zhang, D and Fan, X},
title = {Identification and Validation of Ferroptosis-Related Biomarkers and Therapeutic Targets in ARDS: A Bioinformatics and Experimental Study.},
journal = {Journal of inflammation research},
volume = {19},
number = {},
pages = {566825},
pmid = {42040311},
issn = {1178-7031},
abstract = {BACKGROUND: Acute respiratory distress syndrome (ARDS) is a severe inflammatory lung disease with high mortality and limited effective therapies. Recent studies link ferroptosis-an iron-dependent regulated cell death-to ARDS pathogenesis. This study aimed to identify/validate ferroptosis-related diagnostic biomarkers, therapeutic targets, and fecal microbiota transplantation (FMT)'s protective role in ARDS.

METHODS: Bioinformatic analyses of GEO datasets (GSE76293/GSE151263) included differential expression profiling, WGCNA, PPI network, and machine learning (LASSO/RF) to screen hub genes, with ROC analysis for diagnostic efficacy. An LPS-induced ARDS rat model with FMT intervention was validated via qRT-PCR, IHC, Western blot, and histological staining.

RESULTS: Thirty-seven ferroptosis-linked differentially expressed genes (FDEGs) were identified, enriched in ferroptosis, mitophagy, and immune pathways. Three hub genes (MAPK8, CREB1, GPX4) showed robust diagnostic utility (LASSO AUC=0.931; RF AUC=0.993 in GSE76293) and correlated with monocytes/neutrophils/activated NK cells. LPS suppressed their mRNA/protein levels in rats, reversed by FMT.

CONCLUSION: MAPK8, CREB1, and GPX4 are potential diagnostic biomarkers and therapeutic targets for ARDS. FMT protects against ARDS by reversing these genes' downregulation and suppressing ferroptosis, providing new insights into ARDS pathogenesis and ferroptosis-targeted interventions.},
}

@article {pmid42041380,
year = {2026},
author = {Alvaro, ME and Caserta, S and Martino, EA and Skafi, M and Bruzzese, A and Amodio, N and Lucia, E and Olivito, V and Labanca, C and Mendicino, F and Vigna, E and Morabito, F and Gentile, M},
title = {Gut Microbiota and Acute Myeloid Leukemia: State of the Art, Clinical Signals, and Translational Opportunities.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {4},
pages = {},
doi = {10.3390/antibiotics15040417},
pmid = {42041380},
issn = {2079-6382},
abstract = {Acute myeloid leukemia (AML) remains a highly morbid malignancy in which outcomes are constrained not only by disease refractoriness and relapse, but also by therapy-related toxicity-particularly infections, mucosal injury, and delayed hematopoietic reconstitution. The gut microbiota has emerged as a potentially modifiable layer of host vulnerability and resilience during AML treatment. Microbiome disruption is detectable already at diagnosis, even in antibiotic-naïve patients, and is often characterized by reduced community diversity, depletion of anaerobic taxa linked to short-chain fatty acids (SCFAs) production, and enrichment of pathobiont-associated profiles. During induction, cytotoxic therapy and antimicrobials precipitates diversity loss, domination events, and persistent shifts beyond discharge. Clinically, the most consistent translational signal is the association between baseline or early-treatment microbiome features and infectious outcomes, while emerging data suggest that diagnosis-time microbiome structure may also relate to hematologic recovery kinetics. Mechanistic models converge on pathways linking barrier integrity, microbial metabolites (notably butyrate and other SCFAs), immune calibration, and inflammatory translocation of microbial products. These insights support hypotheses: antimicrobial stewardship may preserve microbiome function; ecosystem repair strategies such as autologous fecal microbiota transfer (A-FMT) are feasible and can restore community structure; and metabolite or nutritional interventions merit evaluation in immunocompromised hosts. Regimen-specific microbiome effects and microbiome-drug interactions suggest that treatment choice could have downstream microbiome-mediated consequences. We synthesize evidence, outline interventional concepts, and define methodological priorities for next-generation trials assessing causality and clinical benefit. Progress will require longitudinal sampling, multi-omic integration (metabolomics, resistomics, and barrier/inflammatory biomarkers), and interventional designs linking microbiome dynamics to clinically meaningful outcomes.},
}

@article {pmid42032216,
year = {2026},
author = {Choi, Y and Ryu, S and Kang, A and Lee, W and Park, J and Kang, MG and Jang, KB and Kwon, Y and Kwak, MJ and Jeong, KC and Song, M and Kim, Y},
title = {Fecal virome transplantation alleviates weaning stress-induced behavioral alterations and intestinal health by reshaping the gut microbiome.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-49647-0},
pmid = {42032216},
issn = {2045-2322},
support = {RS-2025-16068814//National Research Foundation of Korea/ ; },
}

@article {pmid42032281,
year = {2026},
author = {Tonkin-Hill, G and Shao, Y and Zarebski, AE and Mallawaarachchi, S and Xie, O and Mäklin, T and Thorpe, HA and Davies, MR and Bentley, SD and Lawley, TD and Corander, J},
title = {Strain-level transmission inference across multi-kingdom metagenomic data using TRACS.},
journal = {Nature microbiology},
volume = {},
number = {},
pages = {},
pmid = {42032281},
issn = {2058-5276},
support = {2025515//Department of Health | National Health and Medical Research Council (NHMRC)/ ; DE240100316//Department of Education and Training | Australian Research Council (ARC)/ ; 220540/Z/20/A//Wellcome Trust (Wellcome)/ ; 220540/Z/20/A//Wellcome Trust (Wellcome)/ ; 220540/Z/20/A//Wellcome Trust (Wellcome)/ ; 220540/Z/20/A//Wellcome Trust (Wellcome)/ ; },
abstract = {Coexisting strains of the same species within metagenomic data pose a substantial challenge to inferring transmission of pathogenic and commensal microbes. Here we present TRAnsmision Clustering of Strains (TRACS), a highly accurate algorithm for estimating genetic distances between strains at the level of individual single nucleotide polymorphisms, which is robust to intra-species diversity within the host. Analysis of faecal microbiota transplantation datasets and extensive simulations demonstrates that TRACS outperforms existing methods. We use TRACS to infer transmission networks in patients colonized with multiple strains, including severe acute respiratory syndrome coronavirus 2 amplicon sequencing data, deep population sequencing data of Streptococcus pneumoniae and single-cell genome sequencing data from patients infected with Plasmodium falciparum. Applying TRACS to gut metagenomic samples from a mother-infant cohort revealed species-specific transmission rates and identified increased the persistence of Bifidobacterium breve in infants, a finding previously missed owing to the presence of multiple strains. Our study shows that TRACS can be used across microbial kingdoms to uncover strain dynamics.},
}

@article {pmid42032982,
year = {2025},
author = {Huang, S and Yang, Q and Zhou, W},
title = {[Gut microbiota involved in cancer invasion and metastasis].},
journal = {Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences},
volume = {50},
number = {12},
pages = {2186-2200},
pmid = {42032982},
issn = {1672-7347},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Neoplasm Metastasis ; *Neoplasm Invasiveness ; *Neoplasms/microbiology/pathology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Epithelial-Mesenchymal Transition ; },
abstract = {The gut microbiota, as the "second genome" of the human body, plays a crucial role in maintaining the host's homeostasis and regulating the disease process. The latest research indicates that intestinal microecological imbalance is an important cause that triggers and accelerates tumor metastasis. The gut microbiota mainly promotes tumor invasion and metastasis through the following 2 mechanisms: 1) Contact-dependent mechanism, specific pathogenic bacteria directly adhere and invade tumor cells through surface proteins, inducing epithelial-mesenchymal transition and cytoskeleton remodeling; 2) non-contact-dependent mechanism, metabolites derived from the microbiota act on distant organs through the bloodstream, activating signaling pathways to construct pre-metastatic ecological niches and inducing systemic immunosuppression. Precise intervention strategies for the gut microbiota include supplementing specific probiotics with anti-cancer potential, selective antibiotics or phage therapy against specific pathogenic bacteria, fecal microbiota transplantation and microbial vaccines. Although preliminary studies have shown promising results, the high heterogeneity of the microbiota, the bidirectional action of metabolites, and the safety of long-term colonization remain bottlenecks for clinical translation. In the future, it is necessary to further clarify the key transfer-promoting microbiota and their characteristic metabolic and signaling mechanisms, promote the development of individualized and precise microbiota intervention strategies, and strengthen clinical translation research, in order to ultimately achieve the goal of effectively preventing and treating tumor metastasis by regulating the gut microbiota.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Neoplasm Metastasis
*Neoplasm Invasiveness
*Neoplasms/microbiology/pathology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Epithelial-Mesenchymal Transition

@article {pmid42029644,
year = {2026},
author = {Prince, AM and Zeltiņa, I and Reinis, A and Valciņa, O and Krūmiņa, A},
title = {HBV and the Microbiome-PubMed Database Literature Review.},
journal = {Infectious disease reports},
volume = {18},
number = {3},
pages = {},
doi = {10.3390/idr18030038},
pmid = {42029644},
issn = {2036-7430},
abstract = {OBJECTIVE: Hepatitis B virus (HBV) is a globally distributed infectious disease affecting the liver. This literature review aims to summarize all available relevant information on the PubMed database about HBV's connection to the microbiome and to consider possible treatment adjuncts.

MATERIALS AND METHODS: Database used: PubMed. Keywords used: "HBV", "Hepatitis B", "microbiome". In the PubMed database, 179 research publications were identified using these keywords; 69 studies were excluded as they were irrelevant or retracted. Of the remaining, 110 were analyzed in this literature review, and four additional literature sources were used to supply background information and context. Information was summarized. The analysed studies in total included 14,814 participants (excluding animal studies), of whom 8564 were HBV-infected individuals.

RESULTS: Results characterizing abundance or decrease in specific bacterial, viral, and fungal species are heterogeneous; multiple studies support that the HBV patient oral and fecal microbiome is different from that in healthy controls (HCs) and varies throughout disease progression. The HBV seems to transform the microbiome negatively, leading to dysbiosis and decreased microbial diversity in most studies. Evidence links HBV microbiome changes with influence on HbeAg seroconversion, HBV-DNA load, metabolic pathways, liver cirrhosis, and hepatocellular carcinoma. The research proposes that members of microbiota could potentially promote or protect against liver injury in HBV. Four studies proposed that the plasma virome in HBV patients was primarily composed of members of the Anelloviridae. One study researched a parasite (Entamoeba gingivalis) in HBV patients. Two studies analyzed HBV patients' fungal profiles.

CONCLUSIONS: Microbiota research, although promising, at the present moment is heterogeneous. HBV patients' microbiota is distinguishable from HCs, and multiple studies have tried to identify the HBV characteristic microbiome; however, more precise information is needed to draw conclusions. Fecal microbiota transplantation and probiotics have the potential to be therapy adjuncts for HBV patients, but more research is needed.},
}

@article {pmid42025145,
year = {2026},
author = {Liem, J and Chen, X and Lim, JJ and Mao, Q and Cui, JY and Lin, YS},
title = {Impact of the gut microbiome on hepatic cytochrome P450 3A4 (CYP3A4) in humanized pregnane X receptor-constitutive androstane receptor-CYP3A4/3A7 mice.},
journal = {Drug metabolism and disposition: the biological fate of chemicals},
volume = {54},
number = {5},
pages = {100284},
doi = {10.1016/j.dmd.2026.100284},
pmid = {42025145},
issn = {1521-009X},
abstract = {The interaction between the gut microbiome and drug metabolism is bidirectional and can influence the pharmacokinetics of certain drugs. In mice, the gut microbiome has been shown to influence Cyp3a11. However, evidence for microbial regulation of human cytochrome P450 3A4 (CYP3A4) is lacking. We aimed to bridge this gap by manipulating the microbiome of a humanized mouse model expressing CYP3A4, CYP3A7, pregnane X receptor and constitutive androstane receptor. Three groups of male and female humanized mice were studied: conventional (CV), germ-free (GF), and germ-free mice conventionalized (GFCV) using sex-matched pooled human fecal samples. The presence of microbiome upregulated CYP3A4 expression by 7.6-fold in male CV mice (P < .001) but downregulated CYP3A4 expression by 1.69-fold in female CV mice (P = .012) compared with GF mice. The human fecal microbiome transplant to sex-matched GF mice resulted in decreased microbial diversity (P < .05 in males and P < .01 in females) and was not effective in restoring CYP3A4 expression, suggesting complex underlying microbe-CYP3A4 interactions. We show that the hepatic CYP3A4 mRNA and protein expression were strongly correlated (R = 0.91; P = 2.6 × 10[-6]). A total of 57 bacterial species from the mouse gut microbiome were identified to be significantly correlated with CYP3A4 protein expression (P < .05). Five bile acids and no short-chain fatty acids were correlated with CYP3A4 protein expression. In summary, alterations in the gut microbiome influenced hepatic CYP3A4 in humanized mice in a sex-dependent manner, with distinct microbes strongly correlating with this regulatory pattern. SIGNIFICANCE STATEMENT: To the best of our knowledge, this study is the first to evaluate the expression of cytochrome P450 3A4 under different microbial conditions in a humanized mouse model, including conventionalization of germ-free mice using pooled sex-matched human feces. Alterations in the gut microbiome influenced hepatic cytochrome P450 3A4 in a sex-dependent manner and were strongly correlated with microbial species.},
}

@article {pmid42025824,
year = {2026},
author = {Lin, J and Zhu, Q and Wang, T and Sun, J and Yin, R and Zhang, Y and Dai, H and Qiao, S and Gao, S and Hu, S and Liu, H},
title = {Reconstitution of gut microbiota by medicinal plant isoflavones ameliorates heart failure with preserved ejection fraction.},
journal = {Pharmacological research},
volume = {228},
number = {},
pages = {108199},
doi = {10.1016/j.phrs.2026.108199},
pmid = {42025824},
issn = {1096-1186},
abstract = {Heart failure with preserved ejection fraction (HFpEF) is a heterogeneous syndrome with limited therapeutic options. Gut microbiota and microbiota-derived metabolites impact the progression and severity of HFpEF-related cardiometabolic dysfunctions. Here, we demonstrated that the isoflavone extract of Pueraria lobata (Iso-Pl), puerarin, or its microbial metabolite S-equol, improved left ventricular diastolic dysfunctions, reduced hypertension, and ameliorated metabolic disorders in an HFD and L-NAME-induced HFpEF mouse model. Antibiotic depletion and fecal microbiota transplantation experiments revealed an important contribution of gut microbiota to Iso-Pl efficacy. It reshaped gut microbiota composition and function, and reprogrammed microbial-mediated lysine and phenylalanine metabolism. Metabolomics analysis confirmed that Iso-Pl enhanced the production of beneficial metabolites, butyrate and S-equol, while reducing the lysine and phenylalanine-related trimethyllysine (TML) and phenylacetylglycine (PAGly) that have been reported to accumulate and aggravate HFpEF. Moreover, treatment with Iso-Pl, puerarin, and S-equol upregulated estrogen receptor β (ESR2) and activated the downstream eNOS-cGMP-PKG signaling axis in mice, while concurrently inhibiting the pro-inflammatory mitogen-activated protein kinase (MAPK) pathway. These activities collectively contributed to the alleviation of HFpEF by Iso-Pl. Collectively, our findings demonstrate that the cardioprotective effects of Iso-Pl are closely linked with the gut microbiota-dependent metabolic reprogramming and highlight P. lobata isoflavones as promising therapeutic agents for HFpEF.},
}

@article {pmid42025932,
year = {2026},
author = {Liu, Z and Zhang, T and Wang, S and Yin, H and Shao, X and Gao, L and Lu, X},
title = {Gut Microbiota: A Critical Regulator of Oxaliplatin-Induced Peripheral Neurotoxicity Development.},
journal = {Neurotoxicology},
volume = {},
number = {},
pages = {103460},
doi = {10.1016/j.neuro.2026.103460},
pmid = {42025932},
issn = {1872-9711},
abstract = {BACKGROUND: Oxaliplatin-induced peripheral neuropathy (OIPN) is a common dose-limiting toxicity that significantly affects patients' quality of life. Although neuroinflammation has been implicated, the precise contribution of the gut-nerve axis remains incompletely understood. This study aimed to investigate the role of gut microbiota and associated inflammatory signaling in OIPN.

METHODS: An OIPN model was established in Sprague Dawley rats. Gut microbiota depletion was achieved via antibiotic (ABX) treatment, and fecal microbiota transplantation (FMT) from healthy donors was performed to restore microbial communities. Mechanical allodynia and cold hypersensitivity were assessed using the von Frey filament test and the acetone test, respectively. Systemic inflammation was evaluated by measuring serum cytokine levels via enzyme-linked immunosorbent assay (ELISA). The composition of the gut microbiota was analyzed by 16S rRNA gene sequencing. Intestinal barrier integrity and local inflammation were assessed through histopathology, immunofluorescence, and quantification of tight junction proteins (ZO-1, occludin) and inflammatory markers (NF-κB, TNF-α) via quantitative polymerase chain reaction (qPCR) and Western blotting. Network pharmacology was employed to screen for potential common targets of oxaliplatin and neurotoxicity. Molecular alterations in the dorsal root ganglia (DRG) were examined using histology, qPCR, Western blotting, and immunofluorescence, with a focus on the TLR4/MyD88/NF-κB signaling pathway and pro-inflammatory cytokines.

RESULTS: Antibiotic-mediated depletion of gut microbiota significantly attenuated OXA-induced neuropathic pain and systemic inflammation, as evidenced by reduced levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1beta (IL-1β), whereas FMT reversed these protective effects. Analysis of 16S rRNA gene sequencing revealed that OXA altered gut microbiota composition, including reduced alpha diversity, altered beta diversity, a decreased Firmicutes/Bacteroidetes ratio, and taxonomic changes. These alterations were partially restored following FMT under the present experimental conditions. Functional prediction analysis indicated enrichment of the lipopolysaccharide (LPS) biosynthesis pathway. Consistently, OXA treatment was associated with elevated LPS levels in plasma and feces, which were reduced by ABX treatment and increased following FMT. OXA was also associated with impaired intestinal barrier integrity, as evidenced by decreased expression of ZO-1 and Occludin and increased inflammatory markers (NF-κB, TNF-α) in the colon, changes that were modulated by microbiota status. Network pharmacology analysis identified inflammation-related pathways and potential targets. In the DRG, OXA treatment was associated with neuronal injury, increased expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-8), and activation of the TLR4/MyD88/NF-κB signaling pathway, which were attenuated by antibiotic treatment and reappeared following FMT.

CONCLUSIONS: These findings support a microbiota-associated contribution to OIPN and suggest that gut microbiota may influence intestinal and peripheral inflammatory responses. Increased endotoxin burden and activation of TLR4-related signaling pathways may represent potential mechanisms linking the gut and nervous system in OIPN. Targeting the gut-nerve axis may offer a promising direction for future therapeutic strategies, although further studies are required to establish causality and identify specific microbial mediators.},
}

@article {pmid42026738,
year = {2026},
author = {Cao, B and Zhou, X and Cao, X and Shi, J and Liu, C and Yuan, B},
title = {Application of Gut Microbiota in the Treatment and Efficacy Evaluation of Tic Disorders: A Systematic Review.},
journal = {Journal of child and adolescent psychopharmacology},
volume = {},
number = {},
pages = {10445463261445906},
doi = {10.1177/10445463261445906},
pmid = {42026738},
issn = {1557-8992},
abstract = {OBJECTIVE: To systematically review existing evidence on the role of gut microbiota in the pathogenesis of tic disorders (TD) and to assess the therapeutic potential of microbiome-targeted interventions such as probiotics and fecal microbiota transplantation in the management of TD.

METHODS: A comprehensive search was conducted in PubMed, Web of Science, EMBASE, and The Cochrane Library (up to May 26, 2025). The review followed Preferred Reporting Items for Systematic Reviews and Meta-Analyses 2020 guidelines and was registered in PROSPERO (CRD420251067880).

RESULTS: Eleven studies were included, with four focusing on gut microbiome-based therapies and seven studies with gut microbiota and its metabolites as outcome indicators. At the genus level, children with TD exhibited specific alterations in gut microbiota: increased abundance of Bacteroides, Faecalibacterium, and Ruminococcus, alongside decreased levels of Bifidobacterium and Prevotella. This functional dysbiosis may trigger neuroinflammation via disrupted short-chain fatty acid metabolism and impaired intestinal barrier function, ultimately disturbing the glutamate and γ-aminobutyric acid neurotransmitter balance and leading to dysfunction in the cortico-striato-thalamo-cortical circuit. Meanwhile, probiotics as an intervention have been consistently reported to alleviate tic symptoms, although clinical evidence remains limited.

CONCLUSION: Gut microbiota may contribute to TD pathogenesis via immune modulation and neurotransmitter metabolism. While microbiota-based strategies show promise, heterogeneity and methodological limitations in current studies necessitate further high-quality research to validate mechanisms and support clinical application.},
}

@article {pmid42026772,
year = {2026},
author = {Gao, T and Zheng, M and Geng, F and Fu, Y and Yang, Y and Li, X and Wang, Y and Zhu, D and Wang, Z and Lu, L},
title = {Autonomic modulation following fecal microbiota transplantation in chronic insomnia.},
journal = {Postgraduate medicine},
volume = {},
number = {},
pages = {1-13},
doi = {10.1080/00325481.2026.2664261},
pmid = {42026772},
issn = {1941-9260},
abstract = {OBJECTIVE: To determine whether fecal microbiota transplantation (FMT) modulates autonomic function in chronic insomnia disorder and whether autonomic rebalancing mediates sleep improvement.

METHODS: This prespecified exploratory analysis was embedded within a multicenter, double-blind, randomized, placebo-controlled trial of FMT for chronic insomnia. The original trial was designed to evaluate the efficacy and safety of the FMT-based treatment protocol, with polysomnography-measured sleep efficiency at 1 month as the primary endpoint. Eighty adults were randomly assigned to receive either FMT (n = 40) or placebo capsules (n = 40). Overnight polysomnography was conducted at baseline and 1 month, and heart rate variability indices were derived to quantify autonomic regulation. Sleep outcomes included PSG-derived metrics and validated subjective questionnaires. Associations between changes in autonomic parameters and sleep outcomes were examined using correlation analyses. Mediation analysis was performed to evaluate whether autonomic changes statistically mediated FMT-associated improvements in sleep. Gut microbiota composition was profiled using 16S rRNA gene sequencing.

RESULTS: In the original trial, the FMT-based treatment met its prespecified primary endpoint, with significantly improved polysomnography-measured sleep efficiency at 1 month. In this exploratory analysis, FMT significantly reduced the LF/HF ratio (-0.10; 95% CI, -0.18 to -0.02; p = 0.010). A reduction in LF/HF was associated with longer TST (β = -0.41; p = 0.004). Mediation analysis showed that LF/HF accounted for 49.7% of the FMT effect on TST (ACME = 19.44 min; p = 0.018). FMT induced microbial compositional remodeling associated with the nocturnal LF/HF ratio, including enrichment of Lachnospira eligens, Christensenellaceae R-7 group, Ruminococcaceae, and Coprococcus, and depletion of Prevotella copri, Streptococcus, and Faecalibacterium.

CONCLUSIONS: These findings provide clinical exploratory evidence for autonomic system as a potential pathway through which microbiota-targeted interventions may alleviate insomnia. Further studies are needed to determine the durability and clinical significance of these findings.

CLINICAL TRIAL REGISTRATION: ClinicalTrials.gov: NCT05917379 (June 23, 2023).},
}

@article {pmid42027687,
year = {2026},
author = {Wu, H and Yu, M and Huang, S and Peng, Y and Wei, G and Huang, C},
title = {The Gut-Brain Axis as a Mediator of Environmental Endocrine Disruptors in Attention-Deficit/Hyperactivity Disorder: A Systematic Review and Mechanistic Synthesis.},
journal = {Biological psychiatry global open science},
volume = {6},
number = {3},
pages = {100717},
pmid = {42027687},
issn = {2667-1743},
abstract = {The rising global prevalence of attention-deficit/hyperactivity disorder (ADHD) underscores the importance of environmental factors, particularly environmental endocrine-disrupting chemicals (EEDs), whose mechanistic links to ADHD remain unclear. The gut-brain axis, a key modulator of neurodevelopment, is susceptible to EEDs and is altered in ADHD, suggesting a potential mediating pathway. Following Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines and PROSPERO registration (CRD420251152480), we systematically searched PubMed, Web of Science, and Embase (January 2014-July 2025) for studies on EEDs, gut microbiota, and ADHD. Data from 127 included studies (observational, experimental, interventional) were narratively synthesized to evaluate the gut-brain axis as a mediator. We found 1) consistent epidemiological associations between prenatal/childhood EED exposure (e.g., phthalates, bisphenol A, pesticides) and increased ADHD risk; 2) a distinct gut microbial signature in ADHD featuring reduced alpha diversity, elevated Firmicutes/Bacteroidetes ratio, depletion of beneficial taxa (Lactobacillus, Bifidobacterium), and impaired short-chain fatty acid (SCFA) production; 3) evidence that EED exposure induces convergent gut dysbiosis; and 4) interventional studies indicating that modulating the microbiota (via probiotics, synbiotics, fecal microbiota transplantation) can ameliorate ADHD-related behaviors. These findings support a novel mechanistic model wherein EEDs disrupt gut microbiota homeostasis, thereby contributing to ADHD pathogenesis via immune-inflammatory, microbial metabolite (e.g., SCFA), and neuroendocrine pathways along the gut-brain axis. This review synthesizes evidence positioning the gut-brain axis as a critical mediator linking EED exposure to ADHD. It proposes a unifying etiological framework and highlights the microbiome as a promising target for preventive and therapeutic strategies. Future longitudinal and intervention studies are needed to establish causality.},
}

@article {pmid42029022,
year = {2026},
author = {Bornbusch, SL and Muletz-Wolz, CR},
title = {Applying microbial ecology frameworks to microbial therapies for wildlife.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0059825},
doi = {10.1128/msystems.00598-25},
pmid = {42029022},
issn = {2379-5077},
abstract = {Microbial ecology is increasingly incorporated into human and animal medicine via the study and purposeful manipulation of host-associated microbiomes. Microbial therapies-treatments with the aim of beneficially modulating microbiomes-are a burgeoning area of research and industry. These microbial therapies include prebiotic dietary items, live probiotics, and whole microbiota transplants (e.g., fecal microbiota transplants). Although microbial therapies for humans and domestic animals are now widely produced for commercial use and application, evidence supporting the efficacy of commercial microbial therapies is mixed. We suggest that microbial therapies are most effective when paired with concepts from ecology and rigorous empirical research. This is particularly relevant for the development and use of microbial therapies in wildlife animal species, in which we see large-scale variation in microbial communities across hosts of varying ecologies. Identifying and developing microbial therapies that can simultaneously be accessible and effective in a variety of hosts poses a novel challenge for microbial ecologists, animal scientists, and human and animal medical professionals. In addition to pre- and probiotics, we suggest that whole microbiota transplants provide a method of microbial supplementation that may better align with species-specific microbial ecology. Moving forward, emerging methods used in human medicine such as machine learning, network analysis, and microbiome engineering using high-throughput culturomics will likely be key to identifying and applying functionally relevant (e.g., disease suppressive) microbial taxa for wildlife therapies.},
}

@article {pmid42012708,
year = {2026},
author = {Kværner, AS and Birkeland, E and Avershina, E and Botteri, E and Bucher-Johannessen, C and Knudsen, MD and Hjartåker, A and Page, CM and Hov, JR and Song, M and Randel, KR and Hoff, G and Rounge, TB and Berstad, P},
title = {Alcohol consumption and colorectal carcinogenesis: an exploration of the gut microbial pathway as a potential mediator.},
journal = {European journal of nutrition},
volume = {65},
number = {4},
pages = {},
pmid = {42012708},
issn = {1436-6215},
abstract = {BACKGROUND: Alcohol consumption is one of the major risk factors of colorectal cancer (CRC), yet the mechanisms underlying this relationship, particularly the role of gut microbes, are not fully understood.

OBJECTIVE: To study associations of alcohol intake with the gut microbiome and colorectal lesions among CRC screening participants. Of particular interest was the potential role of gut microbes in mediating the association between alcohol intake and colorectal lesions.

METHODS: Screening participants with a positive faecal immunochemical test at ages 55–77 were eligible for the CRCbiome study. Alcohol intake was assessed using a validated, semi-quantitative food frequency questionnaire and linked with shotgun metagenome based gut microbial profiles to study associations with screen-detected colorectal lesions. The potential role of alcohol-associated gut microbes in mediating the association between alcohol intake and colorectal lesions was examined using causal mediation analysis.

RESULTS: Of 1468 participants with dietary data, 414 were diagnosed with advanced lesions. Alcohol intake was positively associated with advanced lesions in a dose-dependent manner (ptrend = 0.008), with odds ratio of 1.09 (95% confidence interval, 1.00, 1.19) per 10 g/day increase. Compared to non-consumers, those consuming alcohol were characterized by a distinct microbial profile, manifested as modest, but consistent, shifts in α- and β-diversity, and differentially abundant bacteria. A causal mediation analysis showed that 12% of the association between alcohol intake and advanced lesions was mediated by alcohol-associated gut bacteria.

CONCLUSION: Alcohol consumption was associated with a distinct microbial profile, which partly explained the association between alcohol intake and advanced colorectal lesions. Trial registration: The BCSN is registered at clinicaltrials.gov (National clinical trial (NCT) no. 01538550).

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00394-026-03960-6.},
}

@article {pmid42016722,
year = {2026},
author = {Hansen, SH and Bhattacharjee, N and Hu, C and Maseng, MG and Grannö, O and Bang, C and Olbjørn, C and Perminow, G and Valeur, J and Bengtson, MB and Frigstad, SO and Andersen, S and Aabrekk, TB and Detlie, TE and Franke, A and Kristensen, VA and Halfvarson, J and Høivik, ML and Iyer, RK and Hov, J},
title = {Bacterial clusters are associated with the risk of severe disease progression in inflammatory bowel disease irrespective of conventional disease categories.},
journal = {Microbiome research reports},
volume = {5},
number = {1},
pages = {4},
pmid = {42016722},
issn = {2771-5965},
abstract = {Background: Inflammatory bowel diseases (IBDs) are complex conditions marked by chronic inflammation in the gastrointestinal tract. Traditional classification separates IBD into Crohn's disease and ulcerative colitis, but this division may not fully capture disease heterogeneity. Here, we examine whether microbiome-driven subtyping can describe novel clinical IBD phenotypes. To achieve this, we applied unsupervised clustering to fecal microbiota profiles from the population-based Inflammatory Bowel Disease in South-Eastern Norway III (IBSEN III) cohort. Methods: A Gaussian Mixture Model (GMM) was used to cluster participants with IBD based on microbiome composition and examine associations between clusters and clinical outcomes, including inflammatory markers and disease severity during the first year after inclusion. Results: Three microbiome-based clusters were identified: CLO (dominated by Clostridia UCG-014), ALF (Agathobacter, Lachnoclostridium, and Faecalibacterium), and RUM (Ruminococcus gnavus). Participants in the RUM cluster had a higher risk of future severe disease than those in the CLO cluster, even among participants with remission-to-mild disease at inclusion (21% vs. 6%, P < 0.00001). This association could not be explained by antibiotic use or baseline disease severity. Cluster membership alone performed comparably to fecal calprotectin in distinguishing severe disease, and a combined model significantly improved accuracy (P < 0.0001). Conclusion: Our findings demonstrate a connection between microbiome composition and the risk of severe disease development, which is partly independent of inflammation levels at the time of sampling. Microbiome-informed subgrouping could lead to more personalized treatment strategies. Further validation is needed to determine the clinical utility of these clusters.},
}

@article {pmid42018414,
year = {2026},
author = {Boumasmoud, M and León-Sampedro, R and Beusch, V and Benz, F and Arnoldini, M and Hall, AR},
title = {Interspecies interaction controls Escherichia coli growth in human gut microbiome samples.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {17},
pages = {e2527793123},
doi = {10.1073/pnas.2527793123},
pmid = {42018414},
issn = {1091-6490},
support = {310030_192428//Swiss NSF/ ; },
mesh = {Humans ; *Escherichia coli/growth & development ; *Gastrointestinal Microbiome/physiology ; Feces/microbiology ; },
abstract = {Gut microbial community composition varies from one person to another. Potentially, this means the ecological interactions experienced by individual strains or species also vary among microbiomes of different people. However, testing this directly in human microbiomes and identifying ecological drivers involved are challenging. Here, we use replicated anaerobic microcosms to quantify variability of population growth for a key commensal species among microbiome samples from different individuals and to identify underlying intra- and interspecific interactions. In a reciprocal transplant experiment, both absolute and relative growth performance of different Escherichia coli strains varied among gut microbiome samples from healthy individuals. This was partly explained by intraspecific competition: growth performance of individual E. coli strains was associated with displacement of resident conspecifics. However, the determinants of E. coli growth varied among samples. In one microbiome sample with a distinctive taxonomic composition, culture acidification by resident microbes impaired growth of all E. coli strains. We identified a strain of Clostridium butyricum contributing to this effect and showed that transferring it into other microbiomes predictably altered pH, fermentation product profiles (butyrate accumulation and acetate/lactate depletion), and population growth of other species including E. coli, thereby reshaping overall taxonomic composition. Our results suggest natural interindividual gut microbiome variation translates to variable ecological interactions with incoming bacteria, but these dynamics can be manipulated by a generalizable interspecies interaction.},
}

Humans
*Escherichia coli/growth & development
*Gastrointestinal Microbiome/physiology
Feces/microbiology

@article {pmid42019770,
year = {2026},
author = {Xie, M and Kong, L and Hou, L and Chen, Y and Hou, J},
title = {Atopic Dermatitis: Multi-omics Insights into Microbiota-Driven Modulation of the Gut-Skin Axis.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {108504},
doi = {10.1016/j.micpath.2026.108504},
pmid = {42019770},
issn = {1096-1208},
abstract = {Atopic dermatitis (AD) is a heterogeneous inflammatory skin disease resulting from complex interactions among host genetics, immune dysregulation, and microbial imbalance. Recent advances in multi-omics technologies have revealed distinct AD endotypes characterized by specific genetic variants, microbial enterotypes, and metabolite profiles. Emerging evidence highlights the gut-skin axis as an important regulatory pathway, in which alterations in gut microbiota influence the production of key microbial metabolites, including short-chain fatty acids (SCFAs) and tryptophan-derived aryl hydrocarbon receptor (AHR) ligands, thereby modulating Th2-dominant inflammatory responses. Integrated analyses combining metagenomics, metabolomics, and single-cell transcriptomics have further identified endotype-specific signatures, such as Bacteroides-enriched profiles associated with lipopolysaccharide-driven inflammation and Prevotella-dominant clusters linked to enhanced AHR activation and epithelial barrier repair. These findings provide a basis for precision stratification and the development of targeted therapeutic strategies, including genotype-guided biologics, microbiota modulation, engineered probiotics, phage therapy, and fecal microbiota transplantation. This review summarizes current evidence integrating host genetics, microbiota networks, and multi-omics biomarkers to provide a comprehensive framework for understanding AD endotypes and to highlight potential avenues for precision diagnosis and targeted interventions.},
}

@article {pmid42022531,
year = {2026},
author = {Wang, Y and Fu, J and Zhan, J and Liang, Y and Chen, R and Su, L and Zhou, Q and Zhang, Y and Cong, W and Xu, F},
title = {Panax ginseng-Polygonum cuspidatum is beneficial for alleviating atherosclerosis in ApoE[-/-] mice by modulating the composition of gut microbiota and related metabolites.},
journal = {Frontiers in cardiovascular medicine},
volume = {13},
number = {},
pages = {1773819},
pmid = {42022531},
issn = {2297-055X},
abstract = {BACKGROUND: Atherosclerosis (AS) is a central pathological driver underlying most cardiovascular diseases. Gut microbiota and related metabolites participate in regulating atherosclerosis. Panax ginseng and Polygonum cuspidatum (GP) herb pair has traditionally been used for cardiovascular diseases. Some active compounds in GP have shown anti-atherosclerotic effects and the effects of GP still needs more evidence-based supports. Therefore, this study aims to investigate the potential effects of GP on atherosclerosis and explore the underlying mechanisms.

METHODS: Fifty C57BL/6J ApoE[-/-] mice were randomly assigned to five groups: model, statin, low-dose GP, medium-dose GP and high-dose GP. They were fed a high-fat diet (HFD) to induce atherosclerosis. Ten wild-type C57BL/6J mice were given chow diet and served as controls. After 12-week intervention, their aortic tissues were collected for Oil Red O staining, colon tissues for Alcian staining and immunofluorescence, and serum samples for measurement of lipid levels and inflammatory cytokines. Then, their fecal DNA was extracted for metagenomic sequencing, while cecum and ileocecal valves were for untargeted metabolomics. Finally, fecal microbiota transplantation was performed to assess the contribution of gut microbiota to observed effects. Twenty additional ApoE[-/-] mice were randomized to two groups: FMT-Mod and FMT-GPH, given feces from the model or high-dose GP group.

RESULTS: Atherosclerotic plaques accumulated in the aorta and aortic sinus after HFD, while statin and high-dose GP alleviated this burden. TC, TG, LDL-C, MCP-1, MCP-3 and IL-2 showed significant increase after HFD, while statin and GP decreased LDL-C, MCP-1 and MCP-3. The goblet cells, ZO-1 and Occludin decreased after HFD, while statin and GP increased them, indicating that the intestinal barrier integrity was improved. Additionally, the composition of gut microbiota was modulated by GP. Some candidate taxa were identified, such as Bifidobacteriales, Bacteroidetes and Escherichia coli. Twenty-two metabolites were differentially abundant among the control, model and GP groups. Nineteen of them were modulated by HFD and reversed by GP, including 1-methylnicotinamide, dopamine and lysoPA (0:0/18:0). Mice given fecal transplants from the high-dose GP group showed less aortic plaques, lower levels of some lipid and inflammatory cytokines, more goblet cells, more expression of ZO-1 and Occludin, and more 1-methylnicotinamide than those given fecal transplants from the model group.

CONCLUSION: This study suggests that GP is beneficial for alleviating atherosclerosis in HFD-induced ApoE[-/-] mice, potentially by modulating the composition of gut microbiota and related metabolites.},
}

@article {pmid42023455,
year = {2026},
author = {Borrego-Ruiz, A and Borrego, JJ},
title = {The Gut Microbiome in Sleep Disorders: A Review of Recent Evidence.},
journal = {Actas espanolas de psiquiatria},
volume = {54},
number = {2},
pages = {586-601},
doi = {10.62641/aep.v54i2.2123},
pmid = {42023455},
issn = {1578-2735},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Sleep Wake Disorders/microbiology/therapy/physiopathology ; Dysbiosis/complications/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {Alterations in the gut microbiome have been shown to influence sleep through gut-brain interactions. However, the interplay between the gut microbiome and sleep disorders remains insufficiently understood. This narrative review provides an overview of recent evidence on the role of the gut microbiome in sleep disorders, examining host-microbial regulation of the sleep cycle, the relationship between gut microbiome dysbiosis and sleep disorders, the influence of the gut microbiome on sleep-related breathing disorders, sleep deprivation, and sleep fragmentation, as well as microbial therapeutic approaches to sleep disorders. Through its effects on bacterial metabolites, immune responses, and neuronal signaling, the gut microbiome might be potentially involved in the regulation of sleep-wake cycles. Disturbances in sleep have been associated with shifts in gut microbiome composition, but this relationship remains incompletely understood and it suggests a bidirectional nature. Evidence indicates that interventions targeting the gut microbiome, such as the use of psychobiotics and fecal microbiota transplantation, may have potential for improving sleep outcomes, but further research is needed to determine their actual effectiveness. Understanding the full range of factors influencing the gut microbiome and their interactions with other variables will be essential for elucidating the mechanisms behind gut-sleep interactions. Thus, future studies should focus on clarifying causality, identifying key biomarkers, and developing microbial-based interventions to establish effective therapeutic strategies.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Sleep Wake Disorders/microbiology/therapy/physiopathology
Dysbiosis/complications/microbiology
Fecal Microbiota Transplantation

@article {pmid42023457,
year = {2026},
author = {Li, J and Liu, J and Chen, M and Wang, Y and Zhou, C},
title = {Observation of the Therapeutic Effect of Washed Microbiota Transplantation on Childhood Autism Spectrum Disorder.},
journal = {Actas espanolas de psiquiatria},
volume = {54},
number = {2},
pages = {263-275},
doi = {10.62641/aep.v54i2.2120},
pmid = {42023457},
issn = {1578-2735},
mesh = {Humans ; *Autism Spectrum Disorder/therapy/microbiology ; Male ; Female ; Child ; *Fecal Microbiota Transplantation/methods ; Retrospective Studies ; Child, Preschool ; Gastrointestinal Microbiome ; Feces/microbiology ; Treatment Outcome ; },
abstract = {BACKGROUND: This retrospective study evaluated the efficacy and safety of washed microbiota transplantation (WMT) via trans colonic endoscopic administration tube for children with autism spectrum disorder (ASD).

METHODS: The clinical data of 19 children with ASD treated between November 2021 and December 2023 were analysed. The data included scores on the Autism Behaviour Checklist (ABC), Childhood Autism Rating Scale (CARS) and PedsQL™ 3.0 Gastrointestinal Symptoms Scales (PedsQL-GI) before treatment and one and six months post-WMT, as well as faecal 16S rRNA sequencing results (vs. healthy controls).

RESULTS: ABC, CARS and PedsQL-GI scores improved significantly over time (all p < 0.001, large effect sizes). CARS and PedsQL-GI scores decreased notably at one and six months after treatment. ABC scores reduced significantly only at six months posttreatment. PedsQLGI scores at six months posttreatment further declined relative to those atone month posttreatment, whereas ABC and CARS scores remained stable. Subgroup analysis showed greater score reductions in the high-score ASD and constipation subgroups than in other patients. Faecal microbiota analysis revealed structural differences between ASD and healthy children. WMT altered gut flora structure and increased beneficial bacteria (e.g., Faecalibacterium).

CONCLUSIONS: Preliminary findings suggest that WMT may improve gastrointestinal and core symptoms in children with ASD, especially those in high-score subgroups. Caution is needed given this study's small sample size, and large prospective studies are required for validation.},
}

Humans
*Autism Spectrum Disorder/therapy/microbiology
Male
Female
Child
*Fecal Microbiota Transplantation/methods
Retrospective Studies
Child, Preschool
Gastrointestinal Microbiome
Feces/microbiology
Treatment Outcome

@article {pmid42023591,
year = {2026},
author = {Lei, P and Qi, Z and Ma, Q and Zhao, B and Wen, B and Jiang, W and Xi, W and Liu, Y and Xun, Y and Zhang, S and Wang, Y and Guo, Y and Wang, W and Ma, X and Jia, M and Fan, Y},
title = {Gut microbiota reshapes host energy metabolism to modulate depressive behaviors.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2662556},
doi = {10.1080/19490976.2026.2662556},
pmid = {42023591},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome/physiology ; Humans ; *Energy Metabolism ; Male ; Animals ; *Major Depressive Disorder/microbiology/metabolism/therapy ; Mice ; Female ; Fecal Microbiota Transplantation ; *Bacteria/classification/genetics/metabolism/isolation & purification ; Middle Aged ; Adult ; Mice, Inbred C57BL ; Disease Models, Animal ; Metabolomics ; Mitochondria/metabolism ; },
abstract = {Disturbances in energy metabolism are a key pathophysiological feature of major depressive disorder (MDD). The gut microbiota, as a critical regulator of host metabolism, may influence systemic energy homeostasis and contribute to depression. To investigate this, we performed a multi-omics analysis integrating targeted metabolomics and shotgun metagenomics on samples from 100 MDD patients and 68 healthy controls. MDD patients exhibited significant disruptions in central energy pathways (glycolysis, TCA cycle, and ornithine cycle), which correlated with symptom severity and cognitive impairment. We identified 36 bacterial species whose abundances were linked to mitochondrial fatty acid synthesis, ketogenesis, and amino acid metabolism, and were associated with altered levels of core metabolites like lactate and L-glutamic acid. Mediation analysis established a "gut microbiota-energy metabolites-depressive phenotype" axis, where metabolites mediated the effects of specific bacteria (e.g., Dorea_formicigenerans) on symptoms. To validate causality, we used a chronic social defeat stress mouse model with simultaneous autologous fecal microbiota transplantation (FMT). FMT effectively reshaped the gut microbiota, ameliorated depression-like behaviors, and reversed the stress-induced shift toward anaerobic glycolysis in serum and the central nervous system. Critically, FMT restored mitochondrial morphology and structural integrity in the prefrontal cortex and hippocampus, renormalizing the relationship between metabolism and behavior. Our findings elucidate the gut microbiota's role in MDD pathogenesis via host energy metabolism regulation and posit early autologous FMT as a novel strategy to correct central energy imbalances.},
}

*Gastrointestinal Microbiome/physiology
Humans
*Energy Metabolism
Male
Animals
*Major Depressive Disorder/microbiology/metabolism/therapy
Mice
Female
Fecal Microbiota Transplantation
*Bacteria/classification/genetics/metabolism/isolation & purification
Middle Aged
Adult
Mice, Inbred C57BL
Disease Models, Animal
Metabolomics
Mitochondria/metabolism

@article {pmid42025006,
year = {2026},
author = {Song, H and Wang, J and Hao, Y and Li, X and Yan, S and Han, S and Zhao, J and Han, Y and Sun, S and Chen, X and Purba, MA and Chen, H and Li, C},
title = {Gut microbiota dysbiosis induced by tibial dyschondroplasia in turn accelerates disease pathogenesis through the gut-bone axis in broilers.},
journal = {Poultry science},
volume = {105},
number = {7},
pages = {106927},
doi = {10.1016/j.psj.2026.106927},
pmid = {42025006},
issn = {1525-3171},
abstract = {Tibial dyschondroplasia (TD) is a common and economically significant skeletal disorder in broilers, characterized by unmineralized, avascular cartilage plugs protruding into the metaphyseal region. Despite some evidence connecting the gut microbiota to skeletal disorders, the specific microbial drivers of TD pathogenesis remain unclear. In this study, we performed fecal microbiota transplantation in both healthy and TD model broilers to assess the influence and contribution of gut microbiota dysbiosis to TD pathogenesis. The broilers were allocated into 4 groups: CON (normal control group broilers), TD (TD model broilers), TDRN (TD model broilers that received FMT from normal broilers) and NRTD (normal broilers that received FMT from TD model broilers). Results demonstrated that FMT successfully transferred the TD phenotype from diseased to healthy broilers (NRTD group), whereas transplantation from healthy donors did not reverse the TD phenotype in TD broilers (TDRN group). This to some extent indicates that gut microbiota as a critical pathogenic driver. Microbiome analysis revealed significant depletion of Lactobacillus and enrichment of Streptococcus and Escherichia-Shigella in all TD-affected groups (TD, TDRN, NRTD) compared to controls (P < 0.05). Metabolomic profiling identified seven stably dysregulated metabolites. Among them, chenodeoxycholic acid showed a strong positive correlation with Lactobacillus abundance and tibial mineral content, while 2-methoxyestradiol (an estrogen metabolite) exhibited inverse associations. Collectively, these findings provide evidence that gut microbiota dysbiosis causally contributes to TD and define the Lactobacillus-chenodeoxycholic acid axis and estrogen metabolism as promising targets for preventive and management strategies against TD in broilers.},
}

@article {pmid41807473,
year = {2026},
author = {Cheng, L and Li, Y and Zhang, Y and Qin, C and Yang, L and Yan, X and Nie, G},
title = {Cetobacterium somerae as a microbial correlate of improved muscle quality after intestinal microbiota transplantation in Yellow River carp (Cyprinus carpio).},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {41807473},
issn = {2055-5008},
support = {U22A20532//National Natural Science Foundation of China/ ; HARS-22-16-S//Special Fund for Henan Agriculture Research System/ ; },
mesh = {Animals ; *Carps/microbiology/growth & development ; *Gastrointestinal Microbiome ; Animal Feed/analysis ; *Fecal Microbiota Transplantation ; *Muscles ; *Muscle, Skeletal ; },
abstract = {Dietary faba bean enhances fish muscle quality but concurrently reduces growth performance. The gut microbiota critically modulates muscle growth and quality. However, the specific microbial taxa, metabolites, and regulatory mechanisms responsible remain to be elucidated. This study established a differential gut microbiota model in faba-bean-fed Yellow River carp (Cyprinus carpio), used whole-intestinal microbiota transplantation (WIMT) to directly test its effect on muscle quality, and supplemented the key bacterium and its metabolite to confirm their contribution. After a 6-week faba bean diet, growth performance declined, whereas muscle texture improved (P < 0.05). This improvement was concomitant with a higher abundance of the genera Aeromonas and Cetobacterium in the gut. Following 8 weeks of daily WIMT from faba-bean-fed donors, Yellow River carp maintained normal growth performance (P > 0.05) and simultaneously showed improved muscle texture, characterized by more small-diameter fibers, lower fat content, and higher collagen levels (P < 0.05), recapitulating the donor's key muscle phenotype. Meanwhile, WIMT reshaped the gut microbiome composition and its metabolic profile, and the marker species Cetobacterium somerae and its metabolite acetic acid showed associations with improvements in muscle quality. Further in vivo validation indicated that C. somerae reduced fat deposition and improved muscle texture, an effect possibly linked to activation of the AMPK-PGC-1α-FoxO pathway, and its metabolite acetic acid mirrored these changes. This study reveals the direct impact of gut microbiota on muscle quality through WIMT in Yellow River carp, provides novel evidence of the fish gut-muscle axis, and offers a scientific basis for improving muscle quality.},
}

Animals
*Carps/microbiology/growth & development
*Gastrointestinal Microbiome
Animal Feed/analysis
*Fecal Microbiota Transplantation
*Muscles
*Muscle, Skeletal

@article {pmid42011573,
year = {2026},
author = {Zheng, X and Ye, DD and Weng, XY and Huang, ZW and Li, YH and Zhang, LS and Chen, MY and Liu, FY and Zhu, JY and Dong, MG and Zheng, XB and Huang, XQ},
title = {[Therapeutic effects of Baitouweng Decoction on ulcerative colitis mice with dampness-heat syndrome via inhibiting CaSR-Gq/11-MAPK signaling pathway based on fecal microbiota transplantation].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {51},
number = {5},
pages = {1259-1272},
doi = {10.19540/j.cnki.cjcmm.20251210.706},
pmid = {42011573},
issn = {1001-5302},
mesh = {Animals ; *Fecal Microbiota Transplantation ; Mice ; *Drugs, Chinese Herbal/administration & dosage ; *Colitis, Ulcerative/drug therapy/metabolism/genetics/therapy/microbiology ; Male ; *Receptors, Calcium-Sensing/metabolism/genetics ; Gastrointestinal Microbiome/drug effects ; Humans ; *MAP Kinase Signaling System/drug effects ; Female ; Disease Models, Animal ; },
abstract = {This study aimed to investigate whether Baitouweng Decoction(BTD) exerts pharmacodynamic effects on ulcerative colitis(UC) mice with dampness-heat syndrome in the large intestine by modulating the gut microbiota and its metabolites to inhibit the calcium sensing receptor(CaSR)-G-protein alpha subunit Q/G-protein alpha subunit 11(Gq/11)-mitogen activated protein kinase(MAPK) signaling pathway. In the experiment, mice were divided into the following groups: a normal group, a model group, a Baitouweng Decoction fecal microbiota transplantation(BTD-FMT) group, a normal-FMT group, and a normal-FMT + Akkermansia muciniphila group. Except for the normal group, a UC with dampness-heat syndrome model was established in all mice. The corresponding fecal supernatant or Akkermansia muciniphila was administered on days 9, 11, 13, 15, 17, 19, and 21. Items below were recorded: body weight, diet, dampness-heat syndrome modeling conditions, and disease activity index(DAI) scores. The distribution and fluorescence intensity of fluorescein isothiocyanate(FITC)-Dextran in the gut were detected using a small animal 3D live imaging system. Pathological changes in the colon and tongue tissues were observed using hematoxylin-eosin(HE) staining. The mRNA expression of inflammatory factors and Muc2 in colon tissue was measured by quantitative real-time PCR(qRT-PCR). The expression levels of forkhead box protein p3(Foxp3) and retinoic acid related orphan receptor γt(RORγt) in colon tissue were analyzed by immunohistochemistry. Goblet cell and mucin expression were analyzed by alcian blue-periodic acid-Schiff(AB-PAS) staining. Western blot was employed to detect the expression of Zonula occludens-1(ZO-1), Occludin, Claudin-1, CaSR, G-protein alpha subunit αQ(Gnaq), G-protein alpha subunit 11(Gna11), extracellular signal-regulated kinase 1/2(ERK1/2), c-Jun N-terminal kinase(JNK), mitogen-activated protein kinase p38(p38 MAPK, p38), phosphorylated extracellular signal-regulated kinase 1/2(p-ERK1/2), phosphorylated c-Jun N-terminal kinase(p-JNK), and phosphorylated mitogen-activated protein kinase p38(p-p38 MAPK, p-p38) in colon tissue. The results indicated that compared with the normal group, model mice with dampness-heat syndrome showed significant increases in rectal temperature, water intake, DAI scores, total movement trajectories/distance traveled in the open field test, and dampness-heat syndrome scores. Compared with the model group, BTD-FMT exerted therapeutic effects on UC mice with dampness-heat syndrome, which were evidenced by significantly ameliorated dampness-heat symptoms and tongue tissue pathology, reduced DAI scores, restored colon length, decreased colon histopathological scores, and modulated immune responses. Furthermore, BTD-FMT downregulated the mRNA expression of tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), and interleukin-6(IL-6) while upregulating interleukin-10(IL-10) and interleukin-4(IL-4) expression. Barrier protein levels were appropriately upregulated, alleviating increased intestinal barrier permeability. Additionally, the expression balance between Foxp3 and RORγt was restored, the goblet cell repair and mucin expression were promoted, and the expression of key proteins in the CaSR-Gq/11-MAPK signaling pathway was suppressed in colon tissue. In terms of therapeutic effect, BTD-FMT was superior to normal-FMT. Supplementation with Akkermansia muciniphila partially mimicked the therapeutic effects of BTD-FMT and achieved a synergistic effect when combined with normal-FMT. In conclusion, BTD exerts anti-inflammatory and intestinal mucosal barrier repair effects in UC mice with dampness-heat syndrome via gut microbiota and metabolite modulation, and the CaSR-Gq/11-MAPK signaling pathway inhibition. Akkermansia muciniphila enhances the effect of normal-FMT.},
}

Animals
*Fecal Microbiota Transplantation
Mice
*Drugs, Chinese Herbal/administration & dosage
*Colitis, Ulcerative/drug therapy/metabolism/genetics/therapy/microbiology
Male
*Receptors, Calcium-Sensing/metabolism/genetics
Gastrointestinal Microbiome/drug effects
Humans
*MAP Kinase Signaling System/drug effects
Female
Disease Models, Animal

@article {pmid42012958,
year = {2026},
author = {Green, ER and Negretti, NM and Brunner, TH and Shealy, NG and Moser, FA and Drury, SL and Traina, KA and Reyes Ruiz, VM and Yang, TS and Lehmann, CJ and Byndloss, MX and van de Plas, R and Zackular, JP and Light, SH and Sucre, JMS and Skaar, EP},
title = {The intestinal microbiota impacts nutritional immunity and resistance to Acinetobacter baumannii pneumonia.},
journal = {Proceedings of the National Academy of Sciences of the United States of America},
volume = {123},
number = {17},
pages = {e2534432123},
doi = {10.1073/pnas.2534432123},
pmid = {42012958},
issn = {1091-6490},
support = {R01 AI101171/AI/NIAID NIH HHS/United States ; R01 AI138581/AI/NIAID NIH HHS/United States ; K22 AI166265/AI/NIAID NIH HHS/United States ; R01 HL168556/HL/NHLBI NIH HHS/United States ; K08 HL143051/HL/NHLBI NIH HHS/United States ; R35 GM146969/GM/NIGMS NIH HHS/United States ; R35 GM138369/GM/NIGMS NIH HHS/United States ; R01 DK131104/DK/NIDDK NIH HHS/United States ; R01 AI168302/AI/NIAID NIH HHS/United States ; T32 HL094296/HL/NHLBI NIH HHS/United States ; T32 GM150375/GM/NIGMS NIH HHS/United States ; T32 ES007028/ES/NIEHS NIH HHS/United States ; T32 GM008554/GM/NIGMS NIH HHS/United States ; R01 AI138581/AI/NIAID NIH HHS/United States ; R01 AG078803/AG/NIA NIH HHS/United States ; U54 DK134302/DK/NIDDK NIH HHS/United States ; 1AY2AX000077//HHS | NIH | Advanced Research Projects Agency for Health (ARPA-H)/ ; GT15104//HHMI (HHMI)/ ; 2022-A-19568//Pew Charitable Trusts (Pew)/ ; 022792//Burroughs Wellcome Fund (BWF)/ ; },
mesh = {*Acinetobacter baumannii/immunology/pathogenicity ; Animals ; *Gastrointestinal Microbiome/drug effects/immunology ; Mice ; *Acinetobacter Infections/immunology/microbiology ; Humans ; Anti-Bacterial Agents/pharmacology/adverse effects ; Dysbiosis/microbiology/immunology ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; Female ; Male ; *Pneumonia, Bacterial/microbiology/immunology ; Neutrophils/immunology ; Disease Models, Animal ; },
abstract = {Broad-spectrum antibiotics are frequently administered to intensive care unit patients as part of empiric care. This treatment has been associated with subsequent infections by the emerging nosocomial pathogen Acinetobacter baumannii; however, the mechanisms underlying this linkage remain unclear. Here, we observe an association between antibiotic treatment and microbiota disruption that precedes A. baumannii infection in a hospitalized patient cohort and demonstrate in a murine model that broad-spectrum antibiotic administration drives susceptibility to intranasal infection with this pathogen. Reconstitution of the intestinal microbiota by fecal microbiota transplant restores control of A. baumannii bloodstream dissemination, implicating microbiota dysbiosis as a key driver of pulmonary disease. Using single-cell RNA sequencing, we determine that antibiotic pretreatment reduces the abundance of transcripts related to phagocyte effector functions in the lung, including nutritional immunity pathways that restrict pathogen access to essential nutrient metals. Depletion studies identify neutrophils and inflammatory monocytes as central mediators of microbiota-dependent protection, and loss of the nutritional immunity components lipocalin-2 or calprotectin abrogates the effects of antibiotics on infected mice, demonstrating a causal relationship between microbiota dysbiosis and impaired phagocyte-mediated nutritional immunity. Together, these findings provide a mechanism for the increased severity of A. baumannii pneumonia following antibiotic exposure and highlight the intestinal microbiota as a potential therapeutic target to prevent nosocomial infections with this and other healthcare-associated pathogens.},
}

*Acinetobacter baumannii/immunology/pathogenicity
Animals
*Gastrointestinal Microbiome/drug effects/immunology
Mice
*Acinetobacter Infections/immunology/microbiology
Humans
Anti-Bacterial Agents/pharmacology/adverse effects
Dysbiosis/microbiology/immunology
Mice, Inbred C57BL
Fecal Microbiota Transplantation
Female
Male
*Pneumonia, Bacterial/microbiology/immunology
Neutrophils/immunology
Disease Models, Animal

@article {pmid42013837,
year = {2026},
author = {Zheng, M and Yan, H and Hao, W and An, H and Chen, X and Wu, Q and Ge, X and Ye, H and Zhou, M and Zhou, G and Yang, X and Hu, M and Zhang, P and Pan, W and Tang, R and Zheng, K and Huang, XF and Yu, Y},
title = {Gut microbiota-derived ergothioneine alleviates antipsychotic-induced synaptic and cognitive impairments.},
journal = {Cell host & microbe},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.chom.2026.03.020},
pmid = {42013837},
issn = {1934-6069},
abstract = {Chronic antipsychotic use is associated with neuronal damage and cognitive impairment, with the gut microbiome increasingly implicated. However, the specific microbial metabolites and mechanisms involved remain unknown. Here, we demonstrate that chronic olanzapine treatment induces gut microbial dysbiosis, compromises intestinal barrier integrity, and causes cognitive deficits in mice. Multi-omics analyses reveal profound depletion of the microbiota-associated metabolite ergothioneine in blood and brain, a finding validated in the blood of olanzapine-treated patients and risperidone- and clozapine-treated mice. This deficiency correlates with a loss of ergothioneine-producing bacteria (Cyanobacteria and subordinate taxa). Fecal microbiota transplantation from olanzapine-treated mice confers cognitive impairment, while ergothioneine supplementation mitigates it. Mechanistically, ergothioneine attenuates hippocampal oxidative stress and inhibits the redox-sensitive phosphatase protein tyrosine phosphatase 1B (PTP1B). Furthermore, hippocampal neuronal-specific PTP1B deletion abolishes olanzapine-induced synaptic and cognitive deficits. Our findings identify depletion of microbiota-derived ergothioneine as a mechanism underlying antipsychotic-induced cognitive impairment, highlighting therapeutic strategies to mitigate this side effect.},
}