@article {pmid42437603,
year = {2026},
author = {Yu, P and He, J and Chen, Y and Zhu, Y},
title = {Circadian Disruption Promotes Epileptic Seizures via the Ruminococcus gnavus-Arginine-NOX4-Ferroptosis Axis.},
journal = {Brain research bulletin},
volume = {},
number = {},
pages = {112037},
doi = {10.1016/j.brainresbull.2026.112037},
pmid = {42437603},
issn = {1873-2747},
abstract = {Circadian rhythm disruption (CRD) exacerbates epileptic seizures, yet the underlying molecular mechanisms remain unclear. Using a pentylenetetrazol (PTZ) kindling rat model combined with continuous light exposure, we found that CRD significantly shortened seizure latency and increased seizure frequency. 16S rRNA sequencing revealed that CRD substantially increased the abundance of Ruminococcus gnavus (R. gnavus) in the gut microbiota. Antibiotic-mediated microbiota depletion, fecal microbiota transplantation (FMT), and R. gnavus monocolonization experiments confirmed that R. gnavus enrichment is a critical factor driving seizure aggravation. Metabolomic analysis demonstrated that elevated R. gnavus suppressed the expression of argininosuccinate synthase 1 (ASS1), a key enzyme for arginine biosynthesis in the kidney, leading to impaired L-citrulline-to-L-arginine conversion and consequently decreased L-arginine levels in serum and hippocampal tissues. Arginine deficiency subsequently activated NADPH oxidase 4 (NOX4) upregulation in the hippocampus, triggering enhanced oxidative stress (elevated malondialdehyde (MDA) and reduced superoxide dismutase (SOD) activity), which ultimately induced ferroptosis (characterized by mitochondrial cristae reduction, acyl-CoA synthetase long-chain family member 4 (ACSL4) upregulation, and glutathione peroxidase 4 (GPX4) downregulation). Pharmacological intervention with the NOX4-specific inhibitor GLX351322 ameliorated oxidative stress, suppressed ferroptosis, and alleviated seizure severity. Importantly, L-arginine supplementation significantly prolonged seizure latency and reduced seizure frequency by reversing ferroptosis activation through downregulating NOX4-ACSL4 expression and upregulating GPX4 expression. This study unveils a complete signaling axis whereby CRD promotes epileptic seizures through the R. gnavus-ASS1-arginine-NOX4-ferroptosis cascade, providing novel therapeutic targets for clinical intervention.},
}

@article {pmid42439335,
year = {2026},
author = {Singh, S and Singh, S and Khandelwal, V and Bharti, U and Singh, PK},
title = {Gut Microbiota in Neuroinflammation, Neurodegenerative Disorders, and Neuropsychiatric Disorders: A Comprehensive Narrative Review.},
journal = {CNS & neurological disorders drug targets},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715273455874260702045636},
pmid = {42439335},
issn = {1996-3181},
abstract = {Neurodegenerative and neuropsychiatric illnesses are characterized by neuroinflammation, which is driven by microglial activation, cytokine production, and breakdown of the blood-brain barrier (BBB). It is currently known that the gut microbiota plays an important role in modulating neuroimmune signaling, which in turn may trigger anxiety-like behaviors and depressive phenotypes through the microbiota-gut-brain axis. This review aims to integrate the most recent mechanistic knowledge on treatment strategies targeting the gut microbiota to modulate neuroinflammation. This review article discusses preclinical and clinical studies that investigated microbial composition, metabolite profiles, and host-microbe interactions involved in neuroinflammatory processes. However, special attention was given to signaling via the vagus nerves and bile acids, as well as to tryptophankynurenine metabolism and short-chain fatty acids (SCFAs). To examine the potential connection between the two, researchers used animal models such as germ-free animals and antibiotic-injected mice for fecal microbiota transplantation (FMT). This article defines dysbiosis as amplifying neuroinflammatory responses by altering microglial phenotypes, disrupting the blood-brain barrier, and triggering the production of pro-inflammatory cytokines. In contrast, microbiome diversity rehabilitation through the use of probiotics, prebiotics, synbiotics, and dietary modifications reduces neuroinflammatory markers and enhances cognitive and behavioral status. Clinical trials have shown considerable promise in diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), autism spectrum disorder (ASD), and depression. However, variability in treatment protocols, treatment resistance, and host-specific factors continue to pose significant challenges. This narrative review integrates mechanistic insights into microglial activation, cytokine signaling, blood-brain barrier regulation, vagal pathways, tryptophan metabolism, and short-chain fatty acids with emerging clinical evidence and therapeutic strategies, including probiotics, prebiotics, dietary modulation, and personalized microbiome-based interventions. Despite promising therapeutic potential, microbiome engineering faces important challenges, including safety concerns, lack of standardized intervention protocols, and substantial inter-individual variability in host-microbiome responses, which currently limit clinical translation. This review focuses on both neurodegenerative and neuropsychiatric disorders, examining shared neuroinflammatory mechanisms mediated by the gut-brain axis and evaluating microbiotatargeted therapeutic strategies across these disease categories. The review discusses both preventive strategies, including dietary modulation, prebiotics, and lifestyle-based microbiome interventions, as well as therapeutic approaches such as microbiota-targeted treatments aimed at mitigating neuroinflammation and disease progression.},
}

@article {pmid42439648,
year = {2026},
author = {Parodi, E and Castello, LM and Bottino, P and Gotta, F and Novi, M and Orsello, M and Rocchetti, A and Prenna, S and Cantaluppi, V and Quaglia, M},
title = {Gut Microbiota Dysbiosis Is a Key Driver of Inflammaging in Chronic Kidney Disease.},
journal = {Cells},
volume = {15},
number = {13},
pages = {},
doi = {10.3390/cells15131171},
pmid = {42439648},
issn = {2073-4409},
mesh = {Humans ; *Dysbiosis/microbiology/complications ; *Renal Insufficiency, Chronic/microbiology ; *Gastrointestinal Microbiome ; Animals ; *Inflammation/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {The role of gut microbiota and intestinal dysbiosis in promoting inflammaging in chronic kidney disease (CKD) has been the focus of intense research over the last years. Some alterations at the phyla level, such as abundance of Proteobacteria and reduction in Firmicutes/Bacteroidites (F/B) ratio and saccarolytic populations, have been consistently reported in CKD. Other mechanisms include microbial translocation through a "leaky gut" and subsequent molecular mimicry, immune dysregulation (unbalance between T reg and Th17 subsets), and epigenetic interactions. Alterations of metabolic pathways and of bacterial metabolites, such as butyrate and other short chain fatty acids (SCFA), also appear to play a key role in modulating progression of CKD. On the other hand, microbiota-based therapy appears promising and includes diet, prebiotics, probiotics, synbiotics, postbiotics and fecal microbiota transplantation (FMT). Modulation of microbiota could correct critical alterations, such as F/B ratio and T reg/Th17 unbalance, blunting inflammaging and potentially reducing progression of CKD and cardiovascular disease. Despite current limitations, gut microbiota is emerging as a powerful environmental factor which could be harnessed to interfere with key mechanisms leading to inflammaging in CKD.},
}

Humans
*Dysbiosis/microbiology/complications
*Renal Insufficiency, Chronic/microbiology
*Gastrointestinal Microbiome
Animals
*Inflammation/microbiology
Fecal Microbiota Transplantation

@article {pmid42440795,
year = {2026},
author = {Shi, C and Gao, Y and Zhang, L and Chen, C and Su, L and Ren, K and Liu, Z and Liu, J},
title = {Gut-heart axis at high altitude: a dynamic mediator from hypoxic dysbiosis to adaptive cardioprotection.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1861538},
doi = {10.3389/fmicb.2026.1861538},
pmid = {42440795},
issn = {1664-302X},
abstract = {High-altitude hypoxia severely disrupts physiological homeostasis and markedly increases cardiovascular disease (CVD) risk through mechanisms that remain incompletely understood. Emerging evidence regards the gut microbiota as a crucial dynamic regulator within the gut-heart axis, constructing a bridge between the environmental hypoxic stress and the cardiovascular outcomes. This review has summarized the dynamic changes of the gut microbiota in high-altitude environments, from acute dysregulation to adaptive remodeling. We systematically delineate the pathogenic mechanisms whereby acute microbial imbalance drives CVD: at the metabolic level, there is a reduction in the production of short-chain fatty acids (SCFAs), accumulation of trimethylamine N-oxide (TMAO), buildup of hypoxia-induced energy metabolism intermediates (lactic acid and succinic acid), and dysregulation of secondary bile acid metabolism. At the immune inflammatory level, impaired intestinal barrier leads to lipopolysaccharide (LPS) translocation, combined with hypoxia-inducible factor-1α (HIF-1α) overexpression, collectively promoting the development of atherosclerosis, hypertension, and heart failure. The adaptive remodeling reduces vascular injury by enhancing myocardial energy metabolism mediated by SCFA, strengthening the intestinal barrier, regulating anti-inflammatory immunity, stabilizing blood pressure, and also reprogramming uric acid metabolism, thereby playing a role in cardiac protection. Finally, we propose microbiome-targeted intervention strategies, including high-fiber dietary modulation, probiotic/prebiotic/synbiotic supplementation, fecal microbiota transplantation, and metabolite-directed therapies, which provides new theoretical basis and precise therapeutic targets for the prevention of cardiovascular diseases in high-altitude environments.},
}

@article {pmid42441072,
year = {2026},
author = {Sun, Y and Zhang, X and Fan, Y and Liu, Y and Yang, D and Chen, X and Li, L},
title = {A chicken-origin Ligilactobacillus agilis R22 exerts probiotic features including growth-promotion and anti-Salmonella infection.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1862425},
doi = {10.3389/fmicb.2026.1862425},
pmid = {42441072},
issn = {1664-302X},
abstract = {INTRODUCTION: In the quest for the development of antibiotic alternatives, this study aimed to systematically evaluate the probiotic potential and mechanism of action of Ligilactobacillus agilis R22, a novel strain isolated from chickens.

METHODS: The in vitro probiotic properties of L. agilis R22, including growth ability, gastrointestinal tolerance, and antimicrobial activity, were initially assessed. Genomic and untargeted metabolomic analyses were conducted to explore its genetic and metabolic profiles. For in vivo evaluation, dietary supplementation of R22 was performed in broilers to assess growth performance, gut morphology, microbiota, and metabolites. Furthermore, a Salmonella enterica serovar Pullorum infection model in chicks and a fecal microbiota transplantation (FMT) experiment in mice were established to investigate its protective efficacy and underlying mechanisms.

RESULTS: L. agilis R22 exhibited robust growth, high tolerance to simulated gastrointestinal environments, and significant antimicrobial activity. Omics analyses revealed multiple probiotic-associated genes, an absence of virulence genes, and the capacity to synthesize essential nutrients for the host. In broilers, R22 supplementation significantly improved growth performance, intestinal morphology, and increased the levels of ghrelin and insulin-like growth factor-1. While the overall gut microbiota structure was not significantly altered, beneficial species and specific intestinal metabolites were enriched. In the S. Pullorum infection model, R22 effectively inhibited pathogen colonization in the gut and systemic dissemination to other organs, significantly mitigating pathological changes. Additionally, the FMT mouse model provided evidence that the in vivo protective effects of R22 are mediated by the gut microbiota it remodels.

DISCUSSION: The affected intestinal metabolites and the remodeled gut microbiota collectively contribute to the in vivo beneficial effects of L. agilis R22. Taken together, L. agilis R22 is a promising probiotic candidate that can be utilized in microbial feed additives.},
}

@article {pmid42442433,
year = {2026},
author = {Huang, K and Lu, J and Yu, Y and Xu, X and Wen, H and Wang, C and Xie, H and Sun, X and Tan, M and Han, L},
title = {Ferroptotic Vulnerability Drives Cardiac Fibrosis and Diastolic Dysfunction in Diabetic HFpEF via a Gut-Associated Proline-PPARγ Axis.},
journal = {Free radical biology & medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.freeradbiomed.2026.07.020},
pmid = {42442433},
issn = {1873-4596},
abstract = {BACKGROUND: Diabetic heart failure with preserved ejection fraction (HFpEF) is a metabolically driven syndrome characterized by diastolic dysfunction and progressive myocardial fibrosis, yet the cellular mechanisms linking metabolic stress to fibroblast maladaptation remain poorly defined.

RESULTS: Using a high-fat diet combined with low-dose streptozotocin (HFD+STZ)-induced diabetic HFpEF mouse model, we observed significant hyperglycemia, insulin resistance, preserved ejection fraction, and marked diastolic dysfunction accompanied by severe myocardial fibrosis. Notably, diabetic HFpEF mice exhibited gut microbiota remodeling characterized by enrichment of Akkermansia muciniphila and elevated circulating L-proline levels. Broad-spectrum microbiota depletion alleviated cardiac fibrosis and diastolic impairment, whereas fecal microbiota transplantation from diabetic HFpEF donors recapitulated the pathological phenotype. Mechanistically, L-proline supplementation aggravated cardiac remodeling and induced ferroptotic cell death in cardiac fibroblasts, as indicated by decreased GPX4 and SLC7A11 and increased ACSL4 and TFR1 expression. Single-cell transcriptomic analysis revealed that proline-associated metabolic reprogramming preceded ferroptosis activation along the fibroblast trajectory under diabetic stress. Importantly, pharmacological inhibition of ferroptosis or fibroblast-specific activation of PPARγ signaling markedly attenuated myocardial fibrosis and improved diastolic function in diabetic HFpEF mice. Consistently, patients with diabetic HFpEF displayed increased A. muciniphila abundance and elevated serum L-proline levels, supporting translational relevance.

CONCLUSIONS: Our findings identify cardiac fibroblast ferroptotic vulnerability as a key pathogenic mechanism in diabetic HFpEF and uncover a gut microbiota-associated proline-PPARγ-ferroptosis axis that drives myocardial fibrosis and diastolic dysfunction under diabetic metabolic stress. These results highlight a metabolically driven fibroblast-centered mechanism and provide potential therapeutic targets for diabetic HFpEF.},
}

@article {pmid42436017,
year = {2026},
author = {Wang, Q and Zhong, W and Huang, H and Yang, X and Liu, X and Ren, Y and He, F and Li, J},
title = {Harnessing microbial modulators to mitigate antibiotic-induced gut dysbiosis: from phytochemicals to faecal microbiota transplantation.},
journal = {Beneficial microbes},
volume = {},
number = {},
pages = {1-28},
doi = {10.1163/18762891-bja00123},
pmid = {42436017},
issn = {1876-2891},
abstract = {Antibiotics remain indispensable for the management of infectious diseases; however, their use inevitably perturbs the gut microbiota. Advances in metagenomics and multiomics approaches have demonstrated that antibiotic exposure profoundly disrupts microbial diversity and community structure, leading to the depletion of key commensals, the expansion of opportunistic pathogens, metabolic dysfunction, and the emergence of antimicrobial resistance. These alterations are increasingly associated with a broad spectrum of dysbiosis-related diseases (DRDs), encompassing metabolic, neuropsychiatric, and immune-mediated disorders. To mitigate or reverse antibiotic-induced microbial imbalances, various microbiota-targeted interventions have emerged as promising alternatives or complementary approaches. These include dietary phytochemicals (such as polyphenols, alkaloids, and organosulfur compounds), probiotics, prebiotics, synbiotics, postbiotics, bacteriophage therapy, and faecal microbiota transplantation (FMT). Evidence from in vitro and animal studies has provided mechanistic insights into how these interventions modulate microbial composition and function; however, clinical evidence varies across intervention type. This review summarizes the composition and functional roles of the gut microbiota, outlines the consequences of antibiotic exposure, and provides an overview of the underlying mechanisms, recent evidence, and potential applications of microbiota-targeted interventions in preserving intestinal homeostasis. This review aims to provide a theoretical basis and reference framework for the development of safer and more effective alternatives or adjuncts to antibiotic therapy.},
}

@article {pmid42430127,
year = {2026},
author = {Du, Z and Yao, H and Xi, C and Yuan, Q and Fu, P and Hu, J and Wu, G and Yang, W},
title = {Oral Lysozyme Attenuates Neuroinflammation and Brain Injury After Traumatic Brain Injury Through Gut Microbiota-Dependent Reprogramming of Tryptophan Metabolism.},
journal = {CNS neuroscience & therapeutics},
volume = {32},
number = {7},
pages = {e71025},
pmid = {42430127},
issn = {1755-5949},
support = {82401618//National Natural Science Foundation of China/ ; 82471407//National Natural Science Foundation of China/ ; 82171382//National Natural Science Foundation of China/ ; 2021QD026//Research Foundation of Huashan Hospital, Affiliated to Fudan University/ ; },
mesh = {Animals ; *Tryptophan/metabolism ; *Muramidase/administration & dosage ; *Brain Injuries, Traumatic/metabolism/drug therapy ; Male ; Administration, Oral ; *Gastrointestinal Microbiome/drug effects/physiology ; *Neuroinflammatory Diseases/metabolism/drug therapy ; Mice ; Humans ; Mice, Inbred C57BL ; *Neuroprotective Agents/administration & dosage ; },
abstract = {AIMS: Traumatic brain injury (TBI) induces secondary neuroinflammation and gut dysbiosis. This study investigated whether oral lysozyme confers neuroprotection after TBI through gut microbiota-dependent metabolic reprogramming of tryptophan metabolism.

METHODS: In a severe TBI mouse model, neurological function, neuroinflammation, intestinal barrier integrity, and systemic immune homeostasis were assessed following oral lysozyme administration. Fecal untargeted metabolomics, antibiotic-mediated microbiota depletion, and fecal microbiota transplantation (FMT) were used to explore microbiota involvement. Cerebrospinal fluid (CSF) from 10 matched pairs of patients with severe TBI was analyzed for tryptophan pathway metabolites by liquid chromatography-mass spectrometry.

RESULTS: Lysozyme improved neurological outcomes, attenuated neuronal apoptosis and neuroinflammation, and restored peripheral CD4[+]/CD8[+] T cell homeostasis. Metabolomics revealed enrichment of fecal tryptophan metabolites (indole-3-carboxaldehyde, indolelactic acid, kynurenic acid [KYNA]) and a shift in cerebral kynurenine metabolism toward the KYNA branch. These associations were abolished by microbiota depletion and reproduced by FMT. Favorable clinical outcomes were associated with higher CSF KYNA and an elevated KYNA/QA ratio.

CONCLUSIONS: Oral lysozyme was associated with attenuated TBI-induced neuroinflammation and brain injury, potentially through gut microbiota-dependent tryptophan metabolism reprogramming. Concordance between preclinical and clinical metabolomic data supports lysozyme as a candidate microbiota-targeted therapeutic strategy. The KYNA/QA ratio warrants further validation as a prognostic indicator in larger, longitudinal cohorts.},
}

Animals
*Tryptophan/metabolism
*Muramidase/administration & dosage
*Brain Injuries, Traumatic/metabolism/drug therapy
Male
Administration, Oral
*Gastrointestinal Microbiome/drug effects/physiology
*Neuroinflammatory Diseases/metabolism/drug therapy
Mice
Humans
Mice, Inbred C57BL
*Neuroprotective Agents/administration & dosage

@article {pmid42431475,
year = {2026},
author = {Liu, S and Chen, Q and Bai, Y and Li, X},
title = {Harnessing the Microbiome for Head and Neck Cancer Therapy: From Mechanistic Insights to Translational Opportunities.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {105484},
doi = {10.1016/j.critrevonc.2026.105484},
pmid = {42431475},
issn = {1879-0461},
abstract = {The human microbiome, particularly the diverse microbial communities in the oral cavity and gut, plays a critical role in the pathogenesis, progression, and treatment response of head and neck squamous cell carcinoma (HNSCC). Emerging evidence indicates that specific microbial communities can bidirectionally modulate cancer therapeutic modalities. Moreover, interventions such as probiotics, prebiotics, and fecal microbiome transplantation have the potential to improve treatment efficacy and alleviate adverse effects. This review outlines the mechanisms underlying oral and gut microbiota in HNSCC development and progression, focusing on their bidirectional regulation of efficacy and toxicity across standard treatments, including surgery, radiotherapy, chemotherapy, targeted therapy, and immunotherapy. We emphasize that microbial signatures not only serve as predictive biomarkers and therapeutic targets but also constitute a fundamental component of personalized oncology in HNSCC, providing a comprehensive framework for integrating microbiota-based strategies into clinical practice.},
}

@article {pmid42431711,
year = {2026},
author = {Mao, G and Lan, H},
title = {Concomitant medication reporting should accompany fecal microbiota transplantation plus anti-PD-1 therapy in gastric cancer.},
journal = {Journal for immunotherapy of cancer},
volume = {14},
number = {7},
pages = {},
doi = {10.1136/jitc-2026-015908},
pmid = {42431711},
issn = {2051-1426},
mesh = {Humans ; *Stomach Neoplasms/therapy/drug therapy ; *Fecal Microbiota Transplantation/methods ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Combined Modality Therapy ; },
abstract = {This commentary discusses the phase I study of fecal microbiota transplantation plus anti-programmed cell death protein 1 therapy in refractory microsatellite-stable gastric cancer. We suggest that this strategy should be treated as a pharmacomicrobiomic intervention rather than only as an immunotherapy combination. Evidence from fecal microbiota transplantation trials and microbiome immunotherapy studies indicates that antibiotics, proton pump inhibitors, corticosteroids and other microbiome-modifying exposures may affect donor strain engraftment, immune activation, response assessment and safety. In China and other Asian settings, where acid suppression, Helicobacter pylori history, perioperative antibiotic use and nutritional interventions are common, standardized concomitant medication reporting would make future studies more interpretable and transferable.},
}

Humans
*Stomach Neoplasms/therapy/drug therapy
*Fecal Microbiota Transplantation/methods
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Programmed Cell Death 1 Receptor/antagonists & inhibitors
Combined Modality Therapy

@article {pmid42432504,
year = {2026},
author = {Wang, L and Liu, Z and Fan, F and Zhang, L and Li, J},
title = {Impact of fecal microbiota transplantation on lipid parameters in patients with metabolic syndrome: a meta-analysis.},
journal = {BMC gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12876-026-05037-4},
pmid = {42432504},
issn = {1471-230X},
support = {2023IR35//National High Level Hospital Clinical Research Funding (Interdepartmental Research Project of Peking University First Hospital)/ ; 2021YFC2500600/2021YFC2500601//National Key Research and Development Program of China/ ; National High Level Hospital Clinical Research Funding//State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University/ ; },
abstract = {BACKGROUND: Metabolic syndrome (MetS) is a global health challenge, with impaired lipid metabolism as a key feature. While fecal microbiota transplantation (FMT) shows promise as a MetS therapy, existing meta-analyses have reported conflicting results and focused mainly on glycemic parameters, leaving its impact on lipid metabolism largely unexplored. This meta-analysis systematically assessed the influence of allogenic FMT on lipid parameters in patients with MetS, unraveling its potential as an innovative therapeutic modality for this population.

METHODS: A meta-analysis was performed to explore the impact of allogenic FMT on lipid parameters (triglycerides, total cholesterol [TCHO], high-density lipoprotein cholesterol [HDL-C] and low-density lipoprotein cholesterol [LDL-C]) in patients with MetS. Terms regarding FMT and MetS were searched in PubMed/Medline, EMBASE, Web of Science, the Cochrane Library, and Scopus from the inception of the databases until 31 August 2023.

RESULTS: Nine randomized controlled trials (RCTs) were included and subgroup analyses according to follow-up durations were performed. This study was registered in PROSPERO (ID CRD42023389890). A total of 248 patients were included. Patients undergoing allogenic FMT manifested significantly lower TG level compared with control group (receiving placebo or autologous FMT, pooled MD -0.15 [95% CI: -0.29, -0.01]), as well as higher HDL-C level (MD 0.07 [95% CI: 0.02, 0.12]). Subgroup analysis confirmed that these effects were significant at 4 to 6 weeks post-FMT (TG: MD -0.16, 95% CI: -0.32, -0.01; HDL-C: MD 0.08, 95% CI: 0.02, 0.15). No significant difference was observed between allogenic FMT and control group concerning TCHO and LDL-C levels regardless of lengths of follow-up. In subgroup analysis, the results regarding TG and HDL-C remained consistent in the subgroup with 4 to 6 weeks of follow-up.

CONCLUSIONS: An overall reduction in TG level and elevation in HDL-C level was observed in patients with MetS receiving allogenic FMT. A potential optimal timeframe for FMT efficacy manifestation might be 4 to 6 weeks after first administration.

TRIAL REGISTRATION: This study is registered in PROSPERO and is available at https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023389890.},
}

@article {pmid42433272,
year = {2026},
author = {Valaei, A and Zahmatkesh, N and Aghaei, R and Maleki, M and Meskini, M and Siadat, SD},
title = {The role of the microbiota in hematological malignancies: A narrative review of mechanisms and therapeutic potential.},
journal = {New microbes and new infections},
volume = {72},
number = {},
pages = {101805},
pmid = {42433272},
issn = {2052-2975},
abstract = {The human microbiota, particularly the gut microbiome, plays a central role in maintaining immune homeostasis, regulating hematopoiesis, and modulating host metabolism through bioactive metabolites such as short-chain fatty acids (SCFAs), bile acids, and tryptophan-derived compounds. Disruption of this microbial ecosystem (dysbiosis) has emerged as a key contributor to the development and progression of hematological malignancies (HMs), including acute and chronic leukemias, lymphomas, and multiple myeloma. This narrative review synthesizes recent evidence (2022-2025) on the complex bidirectional interactions between the microbiota and HMs, highlighting their biological and clinical significance. Current evidence indicates that the microbiota influences hematological malignancies through multiple interconnected mechanisms, including immune regulation, inflammatory signaling, maintenance of hematopoietic homeostasis, and microbial metabolite-mediated modulation of the tumor microenvironment. Dysbiosis has been associated with disease progression, increased susceptibility to infections, impaired treatment tolerance, and inferior clinical outcomes. Conversely, chemotherapy, broad-spectrum antibiotics, and hematopoietic stem cell transplantation profoundly reshape microbial communities, further exacerbating dysbiosis and contributing to complications such as graft-versus-host disease following allogeneic transplantation. Emerging microbiota-targeted interventions, including dietary modulation, probiotics, prebiotics, and fecal microbiota transplantation, show promise for restoring microbial homeostasis and improving therapeutic outcomes. Furthermore, microbiome-derived biomarkers are increasingly being investigated for predicting treatment response, relapse risk, and immunotherapy efficacy. Despite these advances, important challenges remain, particularly in establishing causal relationships, standardizing microbiome profiling, and validating clinical applications through well-designed prospective and randomized studies. Overall, the accumulating evidence supports the microbiota as a critical determinant of hematological cancer biology and treatment response. Integrating microbiome-based diagnostics and therapeutic strategies into precision hematology may offer new opportunities to improve patient management and long-term clinical outcomes.},
}

@article {pmid42434323,
year = {2026},
author = {Deshpande, A and Hohmann, EL and Burns, C and Tomeo, NJ and Allegretti, JR},
title = {Practice Variations in the Management of Clostridioides difficile Infection: Findings From a Survey of US Physicians.},
journal = {Gastro hep advances},
volume = {5},
number = {9},
pages = {101025},
pmid = {42434323},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: In 2021, the American College of Gastroenterology and Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America released guidelines for Clostridioides difficile infection (CDI) management, with conflicting recommendations. We surveyed US gastroenterologists (GIs), infectious disease (ID) specialists, and primary care physicians (PCPs) on their use of clinical guidelines and attitudes toward gut microbial therapies for CDI.

METHODS: We conducted an online survey of 302 physicians (n = 101 GIs, 101 IDs, 100 PCPs; February 24 to March 13, 2023). Included GIs and IDs saw a minimum of 3 to 4 patients and PCPs 1 to 2 patients with CDI per month.

RESULTS: Physicians working in hospital/academic settings were more familiar with CDI guidelines than those working in independent/group practices. Half of GIs used American College of Gastroenterology guidelines; 98% of IDs followed Infectious Diseases Society of America and the Society for Healthcare Epidemiology of America guidelines. More PCPs reported that their institutions did not have set guidelines (40%). More GIs (51%) and IDs (74%) used the recommended multistep algorithm for CDI testing; PCPs were more likely to use a single diagnostic test (49%). GIs and IDs more often prescribed vancomycin taper (93% and 98%, respectively) and fidaxomicin (87% and 97%, respectively); PCPs were more likely to prescribe metronidazole (84%). Less than 10% of physicians felt very knowledgeable about donor-derived microbiome therapies. While 60% of GIs, 53% of IDs, and 50% of PCPs agreed donor-derived microbiome therapies are essential for CDI management, more than 50% cited the need for real-world evidence of safety and efficacy.

CONCLUSION: Education around CDI guidelines and standardized diagnostic and treatment algorithms are needed to ensure consistent CDI management.},
}

@article {pmid42434548,
year = {2026},
author = {Li, H and Wang, X and Yin, L and Li, Y and Fan, S and Zhang, H and Zhang, W and Ou, H and Wang, J},
title = {Abdominal massage alleviates IBS-D by modulating the gut microbiota and suppressing the LPS/TLR4/NF-κB/MLCK pathway.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1730607},
pmid = {42434548},
issn = {1664-302X},
abstract = {BACKGROUND: Diarrhea-predominant irritable bowel syndrome (IBS-D) is a common functional gastrointestinal disorder with complex and incompletely understood pathophysiology. This study aimed to investigate the therapeutic effects and underlying mechanisms of abdominal massage on diarrhea-predominant IBS-D using a rat model.

METHODS: IBS-D was induced in Sprague-Dawley rats through a combination of maternal separation and chronic stress. The experimental interventions consisted of abdominal massage and fecal microbiota transplantation (FMT) using donor microbiota obtained from IBS-D + abdominal massage rats. Assessments included fecal moisture content (FMC), Bristol stool scores, visceral hypersensitivity, intestinal motility, open field test, gut microbiota, short-chain fatty acids (SCFAs), inflammatory markers (LPS, TLR4/MyD88/NF-κB pathway), and intestinal barrier integrity (TEM, tight junction proteins, FITC-dextran permeability).

RESULTS: Abdominal massage significantly improved diarrheal symptoms, visceral hypersensitivity, gastrointestinal motility, and anxiety-like behaviors in IBS-D rats. It restored gut microbiota diversity, reduced SCFA levels, and suppressed the TLR4/MyD88/NF-κB pathway, leading to decreased pro-inflammatory cytokines and LPS levels. FMT replicated these effects, suggesting the role of gut microbiota modulation. Moreover, abdominal massage also ameliorated barrier dysfunction in IBS-D rats by restoring ultrastructure, modulating MLCK and junctional proteins, and reducing macromolecular permeability.

CONCLUSION: Abdominal massage alleviates IBS-D symptoms by modulating gut microbiota, inhibiting the TLR4/MyD88/NF-κB/MLCK signaling pathway, reducing inflammation, and restoring intestinal barrier function. These findings support its potential as a non-invasive therapeutic strategy for IBS-D.},
}

@article {pmid42434742,
year = {2026},
author = {Shen, C and Lou, R and Bai, F and Zhang, Y and Xu, T and Huang, Z},
title = {Integrative oncology in colorectal cancer: evidence-based strategies from prevention through survivorship.},
journal = {Frontiers in oncology},
volume = {16},
number = {},
pages = {1860619},
pmid = {42434742},
issn = {2234-943X},
abstract = {Colorectal cancer (CRC) is a leading global malignancy, with approximately 1.9 million new cases and over 900,000 deaths recorded in 2022, yet evidence-based integrative oncology strategies remain inconsistently incorporated into routine care. This narrative review synthesizes current evidence across the full CRC care continuum, from primary prevention through long-term survivorship. High-fiber diets, Mediterranean dietary patterns, calcium supplementation, regular physical activity, healthy weight maintenance, and berberine each demonstrate reproducible CRC risk reduction in large prospective cohorts and multicenter randomized controlled trials. The CHALLENGE trial (NEJM 2025) provides the first randomized phase 3 evidence that structured exercise after adjuvant chemotherapy reduces disease recurrence (HR 0.72) and death (HR 0.63) in colon cancer. Aspirin chemoprevention requires individualized risk-benefit assessment per 2022 US Preventive Services Task Force guidelines; preliminary CaPP3 trial data (conference presentation, June 2025; not yet peer-reviewed) suggest non-inferiority of low-dose aspirin (75-100 mg/day) to 600 mg/day in Lynch syndrome, pending formal publication. Fusobacterium nucleatum promotes colorectal carcinogenesis through five mechanistically distinct pathways: FadA-mediated Wnt/β-catenin activation, Fap2- and CbpF-mediated immune evasion via TIGIT and CEACAM1, succinate-HIF-1α-EZH2-mediated immune suppression, Hippo pathway-mediated suppression of pyroptosis, and autophagy-induced chemoresistance. Perioperative multi-strain probiotics significantly reduce postoperative infectious complications, and fecal microbiota transplantation shows preliminary promise for sensitizing microsatellite-stable CRC to immunotherapy. The 2022-2024 SIO-ASCO and ASCO-SIO clinical practice guidelines endorse mindfulness-based interventions, yoga, and acupuncture for anxiety, depression, fatigue, and cancer-related pain. Systematic integration of these interventions into multidisciplinary CRC care requires standardized implementation frameworks, CRC-specific clinical trials for mind-body modalities, and bioavailability-optimized phytochemical formulations.},
}

@article {pmid42434798,
year = {2026},
author = {Zhai, Z and Ma, S and Shang, S and Liang, X and Yin, S and Lin, H and Ding, R and Jiang, A and Zhang, R and Wu, M and Yu, J and Song, Q and Chen, D},
title = {The use of antibiotic, probiotic, and FMT in modulating Immunotherapy Efficacy and Survival: a systematic review and meta-analysis of clinical outcomes.},
journal = {The oncologist},
volume = {},
number = {},
pages = {},
doi = {10.1093/oncolo/oyag264},
pmid = {42434798},
issn = {1549-490X},
abstract = {BACKGROUND: Immune checkpoint inhibitors (ICIs) have been one of the important therapeutic approaches for patients with advanced malignancies; nevertheless, their clinical efficacy remains limited in many patients. Recently, the contribution of intestinal microbiota to improved antitumor immune responses has gradually been recognized.

METHODS: A comprehensive literature search was conducted in PubMed, Embase, and the Cochrane Library to identify relevant studies published up to June 15, 2026. We evaluated the influence of microbiota interventions with respect to efficacy and survival in cancer patients receiving ICIs from three perspectives: antibiotics, probiotics, as well as fecal microbiota transplantation (FMT). The main endpoint was objective response rate (ORR), and secondary endpoints were overall survival (OS) and progression-free survival (PFS).

RESULTS: The final analysis comprised 106 studies and categorized them into three groups: antibiotics (76 studies), probiotics (15 studies), and FMT (15 studies). Antibiotic use was correlated with compromised immunotherapy efficacy and unfavorable survival outcomes. In particular, antibiotics exposure was linked to a reduced ORR (Odds Ratio, OR = 0.60, 95% Confidence Interval, CI = 0.46-0.77, p < 0.001), shorter OS (Hazard Ratio, HR = 1.56, 95% CI = 1.44-1.69, p < 0.001), and shorter PFS (HR = 1.50, 95% CI = 1.32-1.70, p < 0.001). In contrast, probiotics showed a supportive and positive effect on immunotherapy outcomes, with improved ORR (OR = 1.95, 95% CI = 1.46- 2.62, p < 0.001) and better OS (HR = 0.56, 95% CI = 0.41- 0.78, p < 0.001) and PFS (HR = 0.53, 95% CI = 0.38-0.74, p < 0.001). FMT combined with immunotherapy achieved a favorable ORR of 0.30 (95% CI = 0.16-0.45, p < 0.001).

CONCLUSION: This meta-analysis synthesized evidence from studies on antibiotics, probiotics, and FMT use, suggesting gut microbiota offering potential approaches to enhance immunotherapy treatment effectiveness and clinical efficacy in individuals with advanced-stage solid cancers.},
}

@article {pmid42435313,
year = {2026},
author = {Hu, S and Zhang, X and Jiang, X and Du, L and Gao, X},
title = {Haematococcus pluvialis peptides ameliorated cyclophosphamide-induced immunodeficiency in mice by regulating intestinal barrier function.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.70884},
pmid = {42435313},
issn = {1097-0010},
support = {2024CXPT073//Key R&D Program of Shandong Province/ ; 2024ZLYS02//Key R&D Program of Shandong Province/ ; 2023KJ233//Outstanding Youth Innovation Team of Universities in Shandong Province/ ; WSJK2025MS203//Hainan Province Joint Project of Health and Medical Science and Technology Innovation/ ; },
abstract = {BACKGROUND: Immunodeficiency is a pathological state characterized by impaired functional integrity of the immune system, which contributes to the development of various diseases. Natural bioactive peptides are a promising option for improving immune function.

RESULTS: This study examined the therapeutic effects and underlying mechanisms of Haematococcus pluvialis peptides (HPP) against CTX-induced immunodeficiency in mice. The results demonstrated that HPP increased bodyweight, immune organ indices, and blood cell count - white blood cells (WBC), red blood cells (RBC), platelets (PLT), hemoglobin (HGB), lymphocytes (Lym), and granulocytes (Gran), as well as serum cytokine levels (interferon-gamma (IFN-γ), interleukin-2 (IL-2), and immunoglobulin A (IgA) - in immunodeficient mice. Haematococcus pluvialis peptides improved the villus length and crypt depth of the small intestine and increased intestinal levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and secretory immunoglobulin A (SIgA). Colonic levels of tight junction proteins - zonula occludens-1 (ZO-1) and occludin - were up-regulated. Fecal microbiota analysis suggested that HPP promoted the enrichment of beneficial bacterial genera (Ligilactobacillus, norank_f_Muribaculaceae, Alistipes) and suppressed pathogenic bacteria (Escherichia-Shigella and Klebsiella). Gut microbial metabolites analysis showed that HPP altered various fecal metabolites involved in lipids and lipid-like molecules, organoheterocyclic compounds, phenylpropanoids and polyketides, as well as organic acids and their derivatives. Fecal microbiota transplantation (FMT) experiments also validated the decisive role of gut microbiota in the immunomodulatory function of HPP.

CONCLUSION: These results offer novel insights into the protective efficacy and underlying mechanisms of HPP for alleviating immunodeficiency, establishing a robust theoretical basis for its application as a promising immunomodulatory agent. © 2026 Society of Chemical Industry.},
}

@article {pmid42116227,
year = {2026},
author = {Hron, BM and Zhang, YJ and Golden, C and Chalmers, C and Nemec, G and Delaney, E and Ozcan, E and Kim, M and Jalali, L and Solari, T and Brezsny-Feldman, J and Alm, EJ and Bry, L and Rosen, R},
title = {Association between blenderized tube feeds and differential oropharynx, stomach, and stool microbiome signatures relative to conventional formula feeds in children fed via enteral tube: A cross-sectional study.},
journal = {JPEN. Journal of parenteral and enteral nutrition},
volume = {50},
number = {5},
pages = {665-675},
doi = {10.1002/jpen.70097},
pmid = {42116227},
issn = {1941-2444},
support = {//Supported by National Institutes of Health R01 DK097112 (PI: Rosen) and K23 DK133679 (PI: Hron), NASPGHAN Astra- Zeneca Research Award (PI: Hron), NIH K12 5K12HD052896 (PI: Fleisher, awarded to Zhang); NASPGHAN Foundation/Reckitt/Mead Johnson Nutrition Young Investigator Development Award (PI: Zhang); AGA Research Scholar Award (PI: Zhang); Harvard Digestive Diseases Center Grants P30 DK034854 (NIH) and Massachusetts Life Sciences Center Capital Grant./ ; },
mesh = {Humans ; *Oropharynx/microbiology ; *Enteral Nutrition/methods ; Female ; Male ; *Stomach/microbiology ; Cross-Sectional Studies ; *Feces/microbiology ; Infant ; Child, Preschool ; Prospective Studies ; *Food, Formulated ; *Gastrointestinal Microbiome ; *Microbiota ; Gastroesophageal Reflux/prevention & control ; Intubation, Gastrointestinal ; },
abstract = {BACKGROUND: Blenderized gastrostomy tube feeds are associated with reduced gastrointestinal symptoms. We hypothesize that patients receiving blenderized tube feeds, compared with standard formula, will have less gastric-oropharyngeal microbial overlap, a possible biomarker of less gastroesophageal refluxate, and differences in beta diversity in the oropharynx, stomach, and stool.

METHODS: Children requiring enteral tube feeds for >3 months were prospectively recruited to provide saliva via posterior tongue swabs, gastric aspirates, and stool samples. Exclusion criteria were history of cystic fibrosis or solid organ transplant or antibiotic treatment course within 4 weeks. The primary exposure was diet category (formula vs. blenderized feeds). The primary outcome was Jaccard similarity between the gastric and oral microbiomes. Relationships of diet to Jaccard and relative bacterial abundance were analyzed by multivariate linear regression models adjusting for age, sex and proton pump inhibitor use.

RESULTS: Sixty (60.6%) children received blenderized tube feeds and 39 (39.4%) received formula. Beta diversity in the oral and rectal samples differed significantly between patients on blenderized versus formula feeds. Importantly, gastric and tongue microbiomes had significantly less overlap (by Jaccard distance) in patients receiving blenderized feeds, adjusting for covariates. Several key oral, gastric and stool commensal organisms were present in higher relative abundance in the blenderized versus formula group.

CONCLUSION: Oropharyngeal microbiomes are more distinct from the gastric microbiomes in patients receiving blenderized feeds, and the oropharyngeal and stool microbiomes demonstrated differential bacterial abundance compared with formula. Overall, these findings suggest a highly favorable microbial profile with blenderized feeds.},
}

Humans
*Oropharynx/microbiology
*Enteral Nutrition/methods
Female
Male
*Stomach/microbiology
Cross-Sectional Studies
*Feces/microbiology
Infant
Child, Preschool
Prospective Studies
*Food, Formulated
*Gastrointestinal Microbiome
*Microbiota
Gastroesophageal Reflux/prevention & control
Intubation, Gastrointestinal

@article {pmid42424947,
year = {2026},
author = {Zhang, B and Su, S and Lin, H and Zhu, M and Shao, G and Yao, R and Guan, W and Zhang, S},
title = {Brachyspira hyodysenteriae enriched by maternal deoxynivalenol exposure impairs lactation and offspring growth via the bacterial extracellular vesicle-mediated gut-mammary gland axis.},
journal = {Journal of hazardous materials},
volume = {514},
number = {},
pages = {142890},
doi = {10.1016/j.jhazmat.2026.142890},
pmid = {42424947},
issn = {1873-3336},
abstract = {Maternal exposure to deoxynivalenol (DON) disrupts gut homeostasis and impairs offspring health, but the mechanism linking DON to lactation dysfunction remains unclear. Here we show that DON impairs lactation performance in mice, as evidenced by reduced offspring growth, decreased milk fat and milk protein contents, and defective mammary gland function. DON also disrupts intestinal barrier integrity and reshapes the maternal gut microbiota, including enrichment of Brachyspira hyodysenteriae (B. hyodysenteriae), whose abundance is negatively associated with milk quality. Fecal microbiota transplantation (FMT) from DON-exposed dams reproduced the lactation phenotype in recipient mice. Extracellular vesicles (EVs) derived from DON-associated microbiota similarly transferred this defect. Among DON-enriched candidate bacteria, B. hyodysenteriae-derived EVs accumulated in mammary tissue, induced mammary inflammation and were sufficient to impair lactation performance in vivo. Mechanistically, B. hyodysenteriae-derived EVs acted through macrophages to suppress lactation-related programs in mammary epithelial cells. Pharmacological inhibition and genetic ablation experiments showed that NLRP3 and STING signaling contributed to this response, with EV-associated protein and DNA fractions preferentially linked to the NLRP3-IL-1β and STING-IFNB1 pathways, respectively. Together, these findings identify B. hyodysenteriae-derived EVs as microbial mediators of DON-induced gut-mammary communication and reveal a vesicle-dependent mechanism linking mycotoxin-induced dysbiosis to lactation dysfunction.},
}

@article {pmid42426884,
year = {2026},
author = {Lei, Y and Xu, Y and Yan, Y and Zhang, J and Zhang, T and Huang, J and Huang, Y and Zhong, J and Wang, X and Zhang, K and Chen, Y},
title = {Multi-omics and functional validation reveal that Methanobrevibacter-derived L-3-aminoisobutyrate alleviates subclinical mastitis in dairy goats via the HSPA1B-p65 signaling pathway.},
journal = {Microbiome},
volume = {},
number = {},
pages = {},
doi = {10.1186/s40168-026-02464-z},
pmid = {42426884},
issn = {2049-2618},
abstract = {BACKGROUND: Subclinical mastitis (SCM) is prevalent in dairy livestock and compromises milk quality and lactation performance. Although often attributed to bacterial infection, many cases lack identifiable pathogens, suggesting alternative mechanisms. While evidence supports a gut-mammary gland axis, the microbial drivers and microbiota-derived metabolites linking gut dysbiosis to SCM remain unclear. Here, we aimed to identify SCM-associated gut microbial markers, prioritize candidate therapeutic metabolites and define the underlying mechanism.

RESULTS: Based on differences in somatic cell count (SCC) and inflammatory phenotypes across a cohort of 167 mid-lactation Saanen dairy goats, we selected 6 healthy and 6 SCM goats for downstream analyses. By integrating metagenomics, metabolomics, cross-species fecal microbiota transplantation (FMT) and functional validation in vitro and in vivo, we found that SCM was accompanied by reduced milk yield and heightened inflammatory signatures. Compared with the Healthy group, SCM goats exhibited marked remodelling of the gut microbiota, with enrichment of opportunistic taxa (Eubacterium and Blautia) and a pronounced depletion of archaeal Methanobrevibacter spp. Notably, FMT from SCM donors recapitulated mammary inflammatory phenotypes in mice, supporting a causal contribution of gut dysbiosis to mammary inflammation. Joint metagenomic functional profiling and metabolomics further identified the branched-chain amino-acid-derived metabolite L-3-aminoisobutyrate (BAIBA) as significantly enriched in the gut of healthy goats. Moreover, Methanobrevibacter spp. harboured key enzyme genes (vorA, vorB and vorD) implicated in BAIBA biosynthesis. In an LPS-challenged MAC-T model, BAIBA attenuated mammary epithelial inflammation by activating endoplasmic reticulum protein quality control programmes and restoring HSPA1B expression, thereby suppressing NF-κB activation and reducing pro-inflammatory cytokine production. Finally, in naturally infected goats, intramammary administration of BAIBA lowered SCC, highlighting translational potential.

CONCLUSIONS: This study identifies BAIBA as a microbiota-derived metabolite that protects against SCM by restraining mammary inflammation via the HSPA1B-NF-κB axis, establishing a mechanistic gut-mammary link and highlighting a potential non-antibiotic intervention strategy. Video Abstract.},
}

@article {pmid42427207,
year = {2026},
author = {Huang, C and Chai, P and He, Y and Zhang, Y and Su, S and Liu, Z and Luo, Y and Liu, S and Hou, L and Zhang, J},
title = {Cyclocarya paliurus Polysaccharides Attenuate High-Fat Diet-Induced Metabolic Dysfunction via Gut Microbiota Remodeling.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70551},
pmid = {42427207},
issn = {1440-1746},
support = {S202117114001//Shanxi Undergraduate Training Program for Innovation and Entrepreneurship/ ; },
abstract = {BACKGROUND AND AIM: Alterations in gut microbiota composition are closely associated with obesity and metabolic disorders. Cyclocarya paliurus polysaccharides (CCPP) have been shown to improve lipid metabolism and modulate the gut microbiota; however, mechanistic evidence remains limited and may vary depending on preparation methods. This study investigated whether a crude polysaccharide-enriched Cyclocarya paliurus preparation alleviates high-fat diet-induced metabolic dysfunction and is associated with gut microbiota remodeling.

METHODS: Male C57BL/6 J mice were randomized into three groups: normal diet (ND), high-fat diet (HFD), and HFD supplemented with CCPP for 12 weeks. Serum metabolic parameters were measured; intestinal inflammatory cytokine transcripts were assessed by qRT-PCR; and cecal microbiota composition was analyzed by 16S rRNA gene sequencing. Additionally, fecal microbiota transplantation (FMT) was performed by transferring microbiota from CCPP-treated donors to antibiotic-pretreated HFD-induced recipients for 8 weeks.

RESULTS: CCPP attenuated HFD-induced body weight gain and reduced subcutaneous and visceral adipose tissue mass. CCPP significantly improved serum total cholesterol and low-density lipoprotein cholesterol (LDL-C) and reduced fasting glucose. Cecal 16S rRNA gene profiling showed that CCPP reshaped the gut dysbiosis associated with a HFD and enriched microbial taxa that are commonly linked to carbohydrate fermentation. These taxa specifically include Lachnospiraceae-related microbial taxa and Ileibacterium. Importantly, FMT from CCPP-treated donors recapitulated these metabolic improvements, confirming that the benefits of CCPP were microbiota-dependent.

CONCLUSION: CCPP mitigates obesity and metabolic dysfunction by remodeling the gut microbiota, particularly by enriching short-chain fatty acid-producing taxa. These findings highlight CCPP as a potential microbiota-targeted therapeutic agent for metabolic disorders.},
}

@article {pmid42427432,
year = {2026},
author = {Davar, D and Zarour, HM and Trinchieri, G},
title = {Toward a Dual-Axis Model of Microbiome Modulation in Cancer Immunotherapy: Pathobiont Elimination and Functional Ecosystem Restoration.},
journal = {Cellular and molecular bioengineering},
volume = {},
number = {},
pages = {},
pmid = {42427432},
issn = {1865-5025},
abstract = {PURPOSE: The gut microbiome is increasingly recognized as a modulator of cancer immunotherapy efficacy, including responses to immune checkpoint inhibitors (ICIs) and chimeric antigen receptor T-cell (CAR-T) therapy. Recent clinical trials of microbiome-targeted interventions such as fecal microbiome transplantation (FMT) and live biotherapeutic products (LBPs) suggest the potential to enhance antitumor immunity and improve clinical outcomes. Yet responses remain heterogeneous and are not fully explained by engraftment of donor taxa alone.

METHODS: We integrate evidence from interventional trials, observational cohort studies, and principles from gut microbial ecology to develop a model hypothesis on how microbiome-targeted therapies may shape response to immunotherapy, with potential to inform future trial design, analyses, and interpretation.

RESULTS: Drawing on the available evidence, we propose that therapeutic perturbation of the gut microbiome may augment immunotherapy efficacy through two parallel axes: (1) elimination of immunosuppressive pathobionts that restrain CD8+ T-cell activation and promote myeloid-mediated immunosuppression, and (2) functional restoration of the gut ecosystem through engraftment of taxa that provide metabolites, structural cues, and immunoregulatory signals required for effective antitumor immunity. The success of both axes appears to depend on ecological processes governed by predator-prey dynamics, including colonization resistance, resilience of the resident microbiota, and the ability of administered organisms to displace entrenched dysbiotic communities. This ecological lens may help to explain discrepancies across trial designs, donor types, and intervention modalities, and suggests that complete donor engraftment is neither necessary nor sufficient for clinical benefit.

CONCLUSIONS: A dual-mechanism model of pathobiont elimination and functional microbial restoration may help explain microbiome-mediated enhancement of cancer immunotherapy, highlighting a balanced immune permissive gut ecosystem as a key determinant of therapeutic success.},
}

@article {pmid42428309,
year = {2026},
author = {Chen, H and Zhang, S and Bai, Y and Yu, L and Gu, Y},
title = {Translating priority effects and niche engineering into rational microbiome therapeutics across the gut-lung axis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1871211},
pmid = {42428309},
issn = {1664-302X},
abstract = {The homeostasis of the human microbiome relies on "colonization resistance" governed by complex ecological rules. However, severe perturbations such as broad-spectrum antibiotics can dismantle this defense, shifting the microbial community into a "dysbiotic trap" driven by pathogen niche construction-an alternative stable state that is notoriously difficult to spontaneously reverse. This ecological mechanism explains the frequent failure of empirical therapies like fecal microbiota transplantation (FMT) and blind probiotic supplementation. Crucially, local ecological collapse triggers systemic cascades via the "gut-lung axis." The depletion of core gut metabolites, such as short-chain fatty acids, impairs the metabolic reprogramming and antimicrobial capacity of distal alveolar macrophages. This cascade drastically increases host susceptibility to respiratory infections. To break this clinical deadlock, microbiome medicine must transition from "empirical transplantation" to "rational microbiome engineering." This review systematically outlines the core pillars of this translational framework: achieving "precision niche clearing" via targeted bacteriophages; capturing optimal intervention windows to harness "priority effects"; and ultimately engrafting "synthetic microbial consortia" (SMCs) rationally designed upon metabolic cross-feeding principles. This strategy offers a promising avenue to durably shatter the dysbiotic deadlock and restore host immune homeostasis across the gut and systemic levels.},
}

@article {pmid42428310,
year = {2026},
author = {Li, X and Wang, W and Guo, Y and Feng, C and Fan, Y and Lu, Y and Lv, Y and Wang, Y and Pang, X},
title = {Advances in understanding intestinal microbiota mechanisms and intervention strategies for anxiety, depression, sleep disorders, and constipation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1838417},
pmid = {42428310},
issn = {1664-302X},
abstract = {Anxiety, depressive symptoms, sleep disorders, and chronic constipation frequently co-occur and collectively impose a substantial clinical burden. Although these conditions may involve partially overlapping neural, endocrine, immune, and metabolic processes, their shared pathophysiological basis has not been fully established. This narrative review examines the potential role of the microbiota-gut-brain axis in linking affective symptoms, sleep disturbances, and chronic constipation. Evidence from human observational studies, Mendelian randomization analyses, animal models, and preliminary interventional studies suggests that alterations in gut microbial composition and function may contribute to these clinical associations through microbial metabolites, immune signaling, neuroendocrine regulation, and neural pathways. The review also summarizes microbiota-targeted interventions, including probiotics, prebiotics, dietary modification, and fecal microbiota transplantation. However, substantial heterogeneity in study populations, microbial findings, experimental methods, and intervention protocols limits causal interpretation and clinical generalization. A more rigorous distinction among associative, mechanistic, genetic, and interventional evidence is therefore required when evaluating the therapeutic potential of microbiota-based strategies.},
}

@article {pmid42429144,
year = {2026},
author = {Wei, L and Kong, X and Li, Y and Wu, H and Gan, Y and Sun, F},
title = {Gut dysbiosis‑derived butyrate loss predicts feeding intolerance: Multiomics evidence guiding nurse‑driven microbiota‑supportive interventions (Review).},
journal = {Molecular medicine reports},
volume = {34},
number = {3},
pages = {},
doi = {10.3892/mmr.2026.13958},
pmid = {42429144},
issn = {1791-3004},
mesh = {Humans ; *Dysbiosis/microbiology/metabolism ; Multiomics ; *Gastrointestinal Microbiome ; *Butyrates/metabolism ; Critical Illness ; },
abstract = {Feeding intolerance (FI) is a common and debilitating challenge among critically ill patients that is linked to a pathway involving the collapse of the gut microbial ecology. The present review synthesizes multiomics evidence supporting a framework whereby critical illness‑associated gut dysbiosis results in a functional deficit of a microbially derived short‑chain fatty acid butyrate, a pivotal metabolite involved in maintaining intestinal barrier integrity, immuneoregulation and gastrointestinal motility. The loss of butyrate‑producing bacteria and their genetic pathways is strongly correlated with FI and may represent a contributory pathogenic mechanism. Key butyrate‑producing organisms diminished during this process include Faecalibacterium prausnitzii and Roseburia spp. Building upon this mechanistic framework, a pragmatic, nurse‑driven intervention model aimed at preserving and restoring microbial health in critically ill patients was proposed. This model is founded on four principal strategies: Minimizing iatrogenic harm (such as antibiotic/proton pump inhibitor stewardship), targeted microbiota nourishment (pre/synbiotics), cautious microbial restoration (probiotics/fecal microbiota transplantation) and innovative monitoring approaches. By integrating principles of microbial ecology with clinical nursing science, the present review provides a framework for developing nurse‑driven protocols designed to address the underlying pathophysiology of FI and improve patient outcomes.},
}

Humans
*Dysbiosis/microbiology/metabolism
Multiomics
*Gastrointestinal Microbiome
*Butyrates/metabolism
Critical Illness

@article {pmid42429615,
year = {2026},
author = {Jiang, K and Xiong, F and Peng, Y and Meng, L and Wang, X and Xu, Y and Tang, T and Gao, H},
title = {Intermittent Fasting Restores Cardiac Lipid Homeostasis in Diabetic Cardiomyopathy in Association With Akkermansia Muciniphila and 1-methyl-L-histidine.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e76528},
doi = {10.1002/advs.76528},
pmid = {42429615},
issn = {2198-3844},
support = {22274115//National Natural Science Foundation of China/ ; 21974096//National Natural Science Foundation of China/ ; LZ26C010002//Zhejiang Provincial Natural Science Foundation of China/ ; LQN26C010004//Zhejiang Provincial Natural Science Foundation of China/ ; },
abstract = {Diabetic cardiomyopathy (DCM) is a major cardiovascular complication of diabetes with limited effective interventions. Using a streptozotocin-induced insulin-deficient, type 1 diabetes-like DCM mouse model, we show that intermittent fasting (IF) improves cardiac function and attenuates myocardial remodeling. Antibiotic-mediated microbiota depletion largely abolished these benefits, whereas fecal microbiota transplantation from IF-treated donors recapitulated cardioprotection, supporting a causal role of the gut microbiota. Metagenomic profiling identified Akkermansia muciniphila (A. muciniphila) as a prominent IF-responsive taxon, and A. muciniphila supplementation alleviated cardiac injury without obvious improvement in glycaemia. Integrated serum and heart metabolomics identified 1-methyl-L-histidine as a microbiota-associated metabolite reduced in diabetes but restored by IF and A. muciniphila. In vitro and ex vivo assays further supported an L-anserine-linked microbial route for 1-methyl-L-histidine generation. Importantly, oral 1-methyl-L-histidine supplementation recapitulated key cardioprotective effects, remodeled cardiac lipid homeostasis, and reduced lipid peroxidation and oxidative injury. Together, these findings support a gut microbiota-metabolite-lipid axis associated with IF-related cardioprotection in DCM and highlight microbial metabolites as tractable targets to complement dietary intervention.},
}

@article {pmid42429658,
year = {2026},
author = {Wu, G and Wang, H and Zhou, Q and Fu, J and Zhang, F and Duan, Z and Wang, S and Huang, J and Zhou, H and Ma, Z and He, Y and Yin, J and Xu, K},
title = {Effects of gut microbiota on the susceptibility of ischemic stroke in mice.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0014926},
doi = {10.1128/msystems.00149-26},
pmid = {42429658},
issn = {2379-5077},
abstract = {UNLABELLED: Ischemic stroke is a highly prevalent disease with limited therapeutic options, and emerging evidence suggests that the gut microbiota influences stroke pathophysiology. However, whether the gut microbiota affects individual susceptibility to ischemic stroke remains unclear. Here, middle cerebral artery occlusion was performed to stratify mice into ischemic stroke-sensitive (SEN: reaching humane endpoints within day 1) and ischemic stroke-resistant (RES: surviving to day 7) groups based on post-stroke survival. SEN mice exhibited more severe brain injury than RES mice, accompanied by increased systemic inflammation and elevated intestinal permeability. Fecal microbiota from SEN or RES donors was transplanted into antibiotic-treated recipients. Mice receiving SEN microbiota developed significantly worse outcomes compared with those receiving RES microbiota. Multi-omic analyses of cecal contents, including 16S rRNA gene sequencing and liquid chromatography-mass spectrometry/mass spectrometry-based untargeted metabolomics, identified reduced butyrate-producing bacteria and altered glutathione metabolism as potential contributors to stroke susceptibility. Collectively, these findings demonstrate that gut microbiota and microbial metabolites modulate susceptibility to ischemic stroke.

IMPORTANCE: The role of the gut microbiota in determining susceptibility to ischemic stroke has remained poorly defined. This study demonstrates that microbiota dysbiosis and metabolite alterations functionally increase vulnerability to stroke injury, highlighting the gut microbiome as a potential target for risk stratification and preventive interventions. Modulating the gut microbiota may therefore represent a novel strategy for reducing stroke susceptibility.},
}

@article {pmid42242200,
year = {2026},
author = {Barlow, M and Bailey, S and Alessy, S and Al-Bawardy, B and Aldarweesh, S and Bawaked, RA and Alharith, H and Mahdi, A and Alaklabi, A and Mawardi, M and Althwanay, AM and Althumiri, NA and Alabbad, S and Bzeizi, KI and Rakic, S and Allehebi, A and Zivotic, P and Cetinkaya, V and AlJudaibi, B and Alqahtani, SA},
title = {Novel Technologies for Gastrointestinal Cancer Detection: A Systematic Review and Meta-Analysis of Diagnostic Accuracy.},
journal = {Clinical and translational gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ctg.0000000000001058},
pmid = {42242200},
issn = {2155-384X},
support = {P179873//World Bank Group/ ; },
abstract = {INTRODUCTION: Gastrointestinal (GI) cancers account for a quarter of all cancers and one-third of cancer-related deaths worldwide. Novel diagnostic approaches are crucial to enhance early detection and improve patient outcomes. This review systematically identified and evaluated novel GI cancer detection approaches.

METHODS: A systematic review was conducted using PubMed, EMBASE, Scopus, and the Cochrane Library on December 11, 2024, and updated on June 2, 2025. Cohort studies and randomized controlled studies, published in English, that evaluated a novel diagnostic approach for incident GI cancer in a clinical setting, included ≥300 participants, and reported diagnostic accuracy metrics were eligible for inclusion. Two reviewers independently screened studies and assessed risk of bias using the Quality Assessment of Diagnostic Accuracy Studies 2 tool.

RESULTS: Of 9,604 records screened, 72 studies were included: by site, 51 on colorectal, 1 on upper GI, 1 on esophageal, 7 on gastric, 9 on pancreatic, and 5 on hepatocellular carcinoma. Stool DNA testing in patients with a positive fecal immunochemical test showed the highest performance for colorectal cancer (area under the receiver operating characteristic curve [AUC] 0.94-0.98). The best performing technologies across other cancer types were Q-Cancer for pancreatic (AUC 0.89-0.92), the GALADUS model for hepatocellular carcinoma in cirrhotic patients (AUC 0.94), and an artificial intelligence model for esophageal cancer (AUC 0.87).

DISCUSSION: This review highlights several promising novel diagnostic approaches for GI cancer detection. External validation, population-level studies, and health economic evaluation are crucial to establish clinical utility across different settings and populations. Clinicians and policy makers must weigh the added value of novel technologies against current practice, regulatory requirements, clinical understanding, interpretation of results, and public trust.},
}

@article {pmid42420754,
year = {2026},
author = {Samulėnaitė, S and Mathis, V and Darcq, E and Burokas, A and Martín-García, E and Maldonado, R},
title = {Gut microbiota as a novel therapeutic target for eating disorders and obesity.},
journal = {British journal of pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bph.70547},
pmid = {42420754},
issn = {1476-5381},
support = {#2022/18-31//Fundació la Marató de TV3/ ; #PNSD-2019I006//Plan Nacional Sobre Drogas of the Spanish Ministry of Health/ ; #PNSD-2023I040//Plan Nacional Sobre Drogas of the Spanish Ministry of Health/ ; #2025//ICREA-Acadèmia/ ; #PNSD-2017I068//Ministerio de Sanidad, Servicios Sociales e Igualdad, Plan Nacional Sobre Drogas of the Spanish Ministry of Health'/ ; #PNSD-2022//Ministerio de Sanidad, Servicios Sociales e Igualdad, Plan Nacional Sobre Drogas of the Spanish Ministry of Health'/ ; #RD12/0028/0023//Instituto de Salud Carlos III, RETICS-RTA/ ; #2020-SGR//Generalitat de Catalunya, AGAUR/ ; PID2020- 120029GB-I00/MICIN/AEI//Ministerio de Ciencia e Innovación (MICIN), Agencia Estatal de Investigación (AEI)/ ; PDI2023-1511680B-C21//Ministerio de Ciencia e Innovación (MICIN), Agencia Estatal de Investigación (AEI)/ ; 01.2.2-LMT-K-718-03-0099//The European Regional Development Fund/ ; PCI2021-122073-2A//Spanish Ministerio de Ciencia e Innovación (ERA-NET)/ ; #HR22-00737//Caixa Health/ ; },
abstract = {The gut-brain axis constitutes a bidirectional communication network linking the intestinal microbiota and the central nervous system. Through this communication axis, the gut microbiota exerts a major influence on food intake under physiological and pathophysiological conditions. Exposure to a Western diet has been associated with dysbiosis of the gut microbiota, leading to profound changes in the gut-brain axis and promoting compulsive-like eating patterns. Alterations in the gut microbiota influence brain activity via multiple routes, including activation of vagal afferents, modulation of systemic immune and endocrine responses, and the action of microbiota-derived metabolites. Through these mechanisms, gut microbiota imbalance alters metabolic and reward-related brain processes that govern eating behaviour. Thus, gut microbiota interacts with homeostatic pathways by modulating satiety-related hypothalamic mechanisms, thereby influencing appetite and energy balance. In parallel, microbiota-dependent signalling affects hedonic feeding by shaping mesolimbic dopamine activity. Neuroinflammation is another key mechanistic interface within the gut microbiota-brain axis contributing to the development of metabolic disorders. Gut microbiota dysbiosis can increase intestinal permeability, facilitating the translocation of microbial components that promote systemic inflammation. Given this convergence between metabolic, inflammatory and reward mechanisms, modulation of the gut microbiota has emerged as a potential therapeutic approach for obesity and eating disorders. Prebiotics, probiotics, postbiotics, synbiotics and faecal microbiota transplantation are currently under investigation for their capacity to restore microbial balance and improve these metabolic and behavioural disorders. This review primarily focuses on the neurobehavioural regulation of feeding and its dysregulation, with particular emphasis on gut-brain axis mechanisms.},
}

@article {pmid42421228,
year = {2026},
author = {Serrano-García, L and Martínez-Salvador, E and Belda-Marco, A and Herrero-Oliva, C and Cortés, J and Llombart-Cussac, A and Fernández-Murga, L},
title = {Modulation of the response to immunotherapy in triple-negative breast cancer: the role of the microbiota and microbial metabolites in the tumor microenvironment.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2697600},
doi = {10.1080/19490976.2026.2697600},
pmid = {42421228},
issn = {1949-0984},
mesh = {Humans ; *Tumor Microenvironment/immunology ; *Triple Negative Breast Neoplasms/therapy/immunology/microbiology ; Female ; *Immunotherapy ; *Gastrointestinal Microbiome/immunology ; Animals ; },
abstract = {Triple-negative breast cancer is an aggressive and heterogeneous breast cancer subtype for which immune checkpoint inhibitors combined with chemotherapy have improved outcomes in selected patients. However, primary and acquired resistance remain common, underscoring the need to identify extrinsic, modifiable determinants of antitumor immunity. Increasing evidence indicates that the gut and tumor-associated microbiota shape systemic and intratumoral immune tone and influence the efficacy of cancer therapies. Beyond microbial composition, microbiota-derived metabolites-including short-chain fatty acids, indole-tryptophan derivatives, bile acids, polyamines, and other small molecules-can act as functional mediators linking microbial ecology to immune-cell programming and tumor biology. These metabolites modulate dendritic cell function, T-cell priming and fitness, myeloid polarization, inflammatory set points, and metabolic pathways within the tumor microenvironment, thereby potentially enhancing or constraining responses to chemoimmunotherapy. Importantly, while some studies propose intratumoral microbial effects, most clinically actionable evidence currently supports systemic gut-derived metabolites and immune tone modulation that secondarily shapes the TNBC tumor microenvironment. In this review, we synthesize current knowledge on (i) the immunobiology of triple-negative breast cancer (TNBC) relevant to microbiota-driven modulation, (ii) mammary and gut microbiome features reported in TNBC, and (iii) mechanistic pathways through which microbial metabolites may regulate antitumor immunity and immune checkpoint inhibitors (ICI) sensitivity. We also discuss methodological considerations for integrating microbiome profiling with metabolomics and immune phenotyping and evaluate emerging opportunities to leverage microbiota-derived metabolites as biomarkers and therapeutic targets. Finally, we highlight translational strategies-including diet, pre/probiotics, antibiotic stewardship, fecal microbiota transplantation, and metabolite-centric ("postbiotic") approaches-and outline priorities for TNBC-focused, prospective multi-omics studies to move from associative signatures toward actionable interventions.},
}

Humans
*Tumor Microenvironment/immunology
*Triple Negative Breast Neoplasms/therapy/immunology/microbiology
Female
*Immunotherapy
*Gastrointestinal Microbiome/immunology
Animals

@article {pmid42421565,
year = {2026},
author = {Molajafari, A and Ebrahim-Saraie, HS and Moghadam, MT and Hasannejad-Bibalan, M},
title = {A Comprehensive Study of Bidirectional Interactions Between the Human Microbiome and Blood Malignancies and Hematologic Conditions: Focus on Novel Therapeutic Strategies.},
journal = {Journal of clinical laboratory analysis},
volume = {},
number = {},
pages = {e70306},
doi = {10.1002/jcla.70306},
pmid = {42421565},
issn = {1098-2825},
abstract = {BACKGROUND: The human microbiota plays a key role in maintaining host homeostasis by regulating immune responses, metabolism, and hematopoiesis. Microbial dysbiosis has been increasingly associated with immune dysfunction, inflammation, and bone marrow abnormalities that may contribute to hematological diseases. This review summarizes current evidence on the role of the microbiota in normal hematopoiesis and its potential involvement in benign and malignant hematological disorders.

METHODS: A narrative literature review was conducted through comprehensive searches of major scientific databases without time restrictions using the keywords Microbiome, Dysbiosis, Hematopoiesis, Anemia, Immune Thrombocytopenia, Congenital Neutropenia, Thrombosis, Lymphoma, Leukemia, and Multiple Myeloma. Relevant experimental, clinical, and review articles were screened and synthesized.

RESULTS: Available evidence suggests that the microbiota may influence hematopoietic stem cell function, immune cell development, and hematopoietic homeostasis. Microbial dysbiosis has been proposed to be associated with benign hematological disorders, including anemia, immune thrombocytopenia, congenital neutropenia, and thrombosis, as well as hematological malignancies such as leukemia, lymphoma, and multiple myeloma. Certain bacterial and viral infections may also influence disease progression and therapeutic responses. Microbiota-targeted interventions, including probiotics, prebiotics, dietary interventions, fecal microbiota transplantation, and other microbiome-based therapies, have shown potential as adjunctive therapeutic strategies.

CONCLUSIONS: Current evidence suggests that microbiota dysbiosis may contribute to the pathogenesis of various hematological disorders. A better understanding of host-microbiota interactions may support the development of novel biomarkers and microbiota-based therapeutic approaches, although further clinical studies are required to confirm their efficacy and safety.},
}

@article {pmid42422736,
year = {2026},
author = {Kaur, P and Rivera-Nieves, J},
title = {A standardized fecal microbiota transplantation protocol enables consistent, microbiota-driven colitis in IL-10-deficient mice.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1842264},
pmid = {42422736},
issn = {1664-302X},
abstract = {Gut microbiota dysbiosis is a central feature of inflammatory bowel disease (IBD), yet experimental systems that enable controlled investigation of microbiota-driven inflammation remain limited. In interleukin-10-deficient (Il10[-/-]) mice, intestinal inflammation is strictly dependent on the presence of commensal microbiota; however, disease onset and severity are highly variable, reflecting differences in microbial composition across environments. To overcome this limitation, pharmacologic approaches such as piroxicam administration have been widely used to synchronize disease, but these methods introduce epithelial injury and non-microbiota-dependent inflammatory pathways that confound mechanistic interpretation. Here, we describe a standardized fecal microbiota transplantation (FMT) protocol that enables controlled microbiota-driven induction of colitis in Il10[-/-] recipient mice without the use of chemical triggers. In this model, recipient mice aged 8-10 weeks receive fecal microbiota via oral gavage from either colitic Il10[-/-]; Itgb7[-/-] double knockout (DKO) donor mice or non-colitic young Il10[-/-] controls. The DKO donors exhibit impaired mucosal immune regulation and reduced IgA responses, features associated with the emergence of a colitogenic microbial community. Repeated FMT administration over 9 weeks promotes uniform disease induction and reduces variability in disease kinetics across experimental cohorts. Importantly, this approach preserves microbiota-driven disease mechanisms while improving experimental consistency compared with conventional spontaneous Il10[-/-] models and avoids the confounding effects of pharmacologic synchronization. The protocol is compatible with downstream histological, immunological, and microbiome analyses and provides a practical platform for investigating host-microbiota interactions and microbiome-targeted therapeutic strategies in IBD.},
}

@article {pmid42422874,
year = {2026},
author = {Jiang, Q and Zhu, X and Yin, L},
title = {The role of gut microbiota dysbiosis in the pathogenesis of hyperuricemic nephropathy.},
journal = {Frontiers in molecular biosciences},
volume = {13},
number = {},
pages = {1872377},
pmid = {42422874},
issn = {2296-889X},
abstract = {Hyperuricemic nephropathy (HN) is a renal complication associated with sustained hyperuricemia and urate-related renal injury. Emerging evidence suggests that gut microbiota dysbiosis may participate in HN pathogenesis by influencing uric acid metabolism, intestinal urate excretion, gut barrier integrity, microbial metabolite production, and gut-kidney immune crosstalk. However, the strength of evidence varies substantially across proposed mechanisms, with many findings derived from animal models, in vitro experiments, CKD studies, or human studies of hyperuricemia and gout rather than HN-specific clinical cohorts. This review summarizes current clinical and experimental evidence linking gut microbiota dysbiosis with HUA, gout, CKD, and HN, critically evaluates proposed mechanistic pathways, and discusses microbiota-targeted interventions including probiotics, prebiotics, dietary strategies, fecal microbiota transplantation, and metabolite-based approaches. Particular emphasis is placed on distinguishing association from causality and identifying translational gaps that should be addressed in future HN-specific studies.},
}

@article {pmid42414480,
year = {2026},
author = {Nieri, R and Severino, A and Foglio, E and De Maio, F and Santoni, D and Sardaro, MLS and Fancello, G and Masucci, L and D'Aiello, A and Morini, S and Tarquini, D and Gervasoni, J and Santucci, L and Leoni, O and Mammi, C and Pedicino, D and Mangoni, A and Amato, KR and Russo, MA and Crea, F and Liuzzo, G and Limana, F},
title = {Human gut microbiota from acute coronary syndrome patients promotes plaque vulnerability in a mouse model of atherosclerosis.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-61047-y},
pmid = {42414480},
issn = {2045-2322},
support = {2017WJBKKW//Ministero dell'Università e della Ricerca, PRIN 2017/ ; 2017WJBKKW//Ministero dell'Università e della Ricerca, PRIN 2017/ ; },
abstract = {Gut microbiota has been implicated in atherosclerosis and plaque destabilization. However, the relationship between microbiota composition and plaque vulnerability remains incompletely understood. This study tested whether fecal microbiota from patients with acute coronary syndrome (ACS) versus chronic coronary syndrome (CCS) differentially associates with atherosclerotic plaque phenotype in a fecal microbiota transplantation (FMT) model. Female ApoE[-]/[-] mice underwent antibiotic-mediated microbiota depletion followed by repeated FMT from ACS (n = 9) or CCS (n = 11) donors. Mice were fed a standard diet or a 1% choline-enriched diet for 12 weeks. Atherosclerosis burden and plaque vulnerability were assessed by Oil Red O morphometry (necrotic core area, fibrous cap thickness, cap-to-core ratio) and immunostaining (including MMP2). Serum trimethylamine N-oxide (TMAO) levels were quantified by UPLC-MS/MS, and fecal microbiota composition was analyzed by 16 S rRNA gene sequencing at study end. Choline supplementation increased circulating TMAO levels in all experimental groups. However, TMAO concentrations did not differ between ACS- and CCS-FMT recipient mice and did not correlate with lesion size or plaque vulnerability parameters. Despite comparable TMAO levels, choline-fed ACS-FMT recipient mice developed a more vulnerable plaque phenotype than CCS-FMT recipients, characterized by larger necrotic cores, thinner fibrous caps, a reduced cap-to-core ratio, increased intraplaque MMP2 expression, and elevated pro-inflammatory cytokines and chemokines. In addition, 16 S rRNA gene sequencing identified distinct microbial taxa associated with plaque vulnerability-related features. In this ApoE[-]/[-] FMT model, donor coronary syndrome status is associated with differential plaque vulnerability features and distinct gut microbiota signatures, independently of circulating TMAO levels.},
}

@article {pmid42415721,
year = {2026},
author = {Hou, H and Li, Y and Tang, W and Gao, Y and Tian, Y and Chen, F and Zhang, L and Zhang, J and Xu, X and Li, Y and Li, Y and Wang, Q and Liu, L and Teng, T and Wu, H and Zhou, X},
title = {Gut microbiota-targeted interventions for depression in adolescents and young adults: Mechanisms, evidence strength and clinical strategies-A narrative review.},
journal = {General psychiatry},
volume = {39},
number = {4},
pages = {e70036},
pmid = {42415721},
issn = {2517-729X},
abstract = {Depression in adolescents and young adults is common, associated with substantial functional impairment and characterised by limited treatment efficacy. The microbiota-gut-brain (MGB) axis has emerged as a potential therapeutic target for depression. This narrative review synthesises preclinical and clinical evidence on a range of MGB axis interventions aimed at alleviating depressive symptoms in youth, including probiotics, prebiotics, synbiotics, postbiotics, faecal microbiota transplantation (FMT) and lifestyle strategies such as dietary modification and structured exercise. In animal models, these interventions consistently produce antidepressant effects, accompanied by reduced inflammatory signalling, normalisation of hypothalamic-pituitary-adrenal axis activity and upregulation of neurotrophic and serotonergic pathways. In humans, particularly among younger cohorts, the evidence is heterogeneous. Some probiotic or synbiotic regimens have yielded modest improvements in depressive symptoms in preliminary trials, whereas stand-alone prebiotics have shown inconsistent or null effects; clinical evidence for postbiotics and FMT remains preliminary. Lifestyle interventions that target the MGB axis, such as Mediterranean-style diets and structured exercise programmes, have been associated with improved mood and, in some studies, reductions in inflammatory biomarkers. Compared with studies in adults, research in this population remains limited by small sample sizes, greater methodological heterogeneity and less consistent findings and also suggests the presence of age-specific pathways. Current evidence indicates that interventions targeting the MGB axis should be approached cautiously and considered only as adjunctive strategies for the treatment of depression in this population. Future work requires rigorously designed, strain- and protocol-specific clinical trials with standardised procedures, careful safety monitoring and biomarker-guided personalised approaches.},
}

@article {pmid42418807,
year = {2026},
author = {Tahmasebi, H and Bahar, A and Khazaei, M and Arabestani, MR},
title = {The Dual Role of the Gut Microbiota in Cancer Chemoresistance.},
journal = {MicrobiologyOpen},
volume = {15},
number = {4},
pages = {e70357},
doi = {10.1002/mbo3.70357},
pmid = {42418807},
issn = {2045-8827},
mesh = {Humans ; *Drug Resistance, Neoplasm ; *Neoplasms/drug therapy/microbiology ; *Gastrointestinal Microbiome ; *Antineoplastic Agents/therapeutic use/metabolism/pharmacology ; Probiotics ; Fecal Microbiota Transplantation ; Animals ; },
abstract = {Chemoresistance is one of the primary reasons that cancer chemotherapy fails to deliver successful treatment outcomes and contributes to poor overall survival rates for patients with cancer. New research has begun to shed light on the effects of the gut microbiome (GM). This new research will examine how certain microorganisms (referred to as "bad bacteria") can contribute to cancer treatment failure, as well as how others (such as Bifidobacterium, Akkermansia, and Lactobacillus) can enhance treatment success. This review will focus on the molecular mechanisms underlying these effects, including drug metabolism by microorganisms, modulation of the immune system by microorganisms, regulation of cellular apoptosis by microorganisms, and metabolic crosstalk between tumor tissue and the microbiome. Finally, we will look at new therapies under development that leverage knowledge of the microbiome to combat chemoresistance, including fecal microbiota transplantation, targeted probiotic and prebiotic supplementation, and dietary modifications. By studying the complex interactions among the host, the microbiome, and chemotherapeutic agents, we hope to demonstrate how microbiome-centered approaches can tailor and enhance an individual's cancer treatment while transforming the GM from a passive participant to an active target in cancer therapy.},
}

Humans
*Drug Resistance, Neoplasm
*Neoplasms/drug therapy/microbiology
*Gastrointestinal Microbiome
*Antineoplastic Agents/therapeutic use/metabolism/pharmacology
Probiotics
Fecal Microbiota Transplantation
Animals

@article {pmid42418904,
year = {2026},
author = {Yu, J and Wan, Y and Peng, Y and Liang, S and Chan, FKL and Ng, SC and Tun, HM},
title = {Multi-cohort evidence for impaired microbial support of the methionine cycle in children with autism spectrum disorder.},
journal = {Psychiatry research},
volume = {364},
number = {},
pages = {117317},
doi = {10.1016/j.psychres.2026.117317},
pmid = {42418904},
issn = {1872-7123},
abstract = {The contribution of gut microbiota to outcomes of autism spectrum disorders (ASD) has been increasingly appreciated in recent years. With the accumulating evidence on ASD-driven alterations of the gut microbiota, heterogeneities arise across different reports. To account for variabilities in gut microbiota, clinical representations of ASD and data processing approaches, as well as limitations in sample sizes among the existing gut microbiota studies for ASD, the present multi-cohort analysis applied a standard bioinformatic and statistical pipeline on the publicly available gut metagenomic sequencing data for 674 samples, including 326 TD and 348 ASD individuals, collected from eight studies across three main geographical regions. Throughout the analysis, we identified taxonomic profiles of the gut microbiota exhibited more pronounced dysbiosis associated with ASD and between-study variations compared to functional profiles. Differentially abundant taxonomic and pathway markers were identified and validated for their consistent response to ASD across different studies. Co-occurring deficits in microbial pathways for salvaging adenosylcobalamin and S-adenosyl-L-methionine and biosynthesis of methionine in children with ASD point to a reduced microbial support for the host methionine cycle. Species from Faecalibacterium, Bacteroides, Blautia and Bifidobacterium were identified as microbial contributors to ASD-deficient microbial pathways, particularly those related to the methionine cycle. Therefore, the generalisable ASD-deficient contributors to the methionine cycle, such as Blautia wexlerae, Bacteroides stercoris and Streptococcus thermophilus, could be further investigated for their role in therapeutic applications for ASD.},
}

@article {pmid42419261,
year = {2026},
author = {Valles-Colomer, M and Foster, JA},
title = {Decoding the microbiome: Insights into FMT for depression.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1154-1156},
doi = {10.1016/j.chom.2026.06.004},
pmid = {42419261},
issn = {1934-6069},
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Major Depressive Disorder/therapy/microbiology ; *Microbiota ; Animals ; },
abstract = {While fecal microbiota transplantation (FMT) emerges as a promising microbiome-targeted treatment approach, its application in major depressive disorder (MDD) remains investigational. In this issue of Cell Host & Microbe, Wang et al. provide insights into the potential underpinnings of FMT in MDD and offer a step toward decoding the molecular pathways accompanying clinical response.},
}

*Fecal Microbiota Transplantation
Humans
*Major Depressive Disorder/therapy/microbiology
*Microbiota
Animals

@article {pmid42419268,
year = {2026},
author = {Sen, P and Kaulmann, D and Youngster, I and Abdeen, SK and Elinav, E},
title = {Advances and challenges in microbiome transplantation.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1202-1219},
doi = {10.1016/j.chom.2026.06.006},
pmid = {42419268},
issn = {1934-6069},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/adverse effects/trends ; *Clostridium Infections/therapy/microbiology ; *Microbiota ; Animals ; Clostridioides difficile ; Gastrointestinal Microbiome ; },
abstract = {Over the past two decades, the microbiome has emerged as a central modifier of host health, whose manipulation may prevent or treat disease. Fecal microbiome transplantation (FMT) transfers stool from healthy donors to recipients to restore microbial structure and function. It is universally accepted as therapy for recurrent Clostridioides difficile infection (rCDI) and is studied across metabolic, neurological, oncological, and autoimmune disorders. However, challenges remain, including donor selection, possible transmission of infectious or non-communicable risks, and limited understanding of mechanisms driving benefits. This review summarizes FMT designs, mechanisms, indications, and obstacles. It discusses emerging strategies such as the use of microbial consortia and extra-intestinal microbiome transplantation and suggests that a better understanding of FMT functions, limitations, and off-target effects may enable safer, more generalizable modulation of microbiome-regulated diseases. Such a mechanistic understanding may manifest as refined donor screening, standardized protocols, tracked outcomes, and identified microbes and metabolites inducing durable clinical benefits.},
}

Humans
*Fecal Microbiota Transplantation/methods/adverse effects/trends
*Clostridium Infections/therapy/microbiology
*Microbiota
Animals
Clostridioides difficile
Gastrointestinal Microbiome

@article {pmid42419269,
year = {2026},
author = {Engevik, MA and Hecht, AL and Allegretti, JR and Kashyap, PC},
title = {Ecological and dietary strategies to constrain Clostridioides difficile.},
journal = {Cell host & microbe},
volume = {34},
number = {7},
pages = {1220-1240},
doi = {10.1016/j.chom.2026.05.023},
pmid = {42419269},
issn = {1934-6069},
mesh = {Humans ; *Clostridioides difficile/physiology/pathogenicity/growth & development ; *Clostridium Infections/microbiology/prevention & control ; Fecal Microbiota Transplantation ; *Diet ; Animals ; Gastrointestinal Microbiome ; Microbiota ; Feces/microbiology ; Biofilms/growth & development ; },
abstract = {Clostridioides difficile exemplifies a pathogen that leverages its metabolic plasticity to exploit nutrients that become available during community disruption, including host and microbiota-derived metabolites and substrates enriched in modern diets. These ecological dynamics underpin the high and growing burden of C. difficile infection (CDI), including recurrent disease and the rising prevalence of community-associated CDI. Fecal microbiota transplantation and standardized stool-derived products consistently re-establish colonization resistance through convergent functions that include secondary bile acid restoration, nutrient niche exclusion, and suppression of opportunistic pathogens. These principles have provided a valuable roadmap for rational consortia design. In this review, we synthesize current ecological mechanisms governing C. difficile colonization, persistence, and recurrence, highlight missing dimensions in diet intervention studies and mucosal colonization by C. difficile, and propose an ecology-informed, artificial intelligence-enabled precision framework that integrates host susceptibility, exposures, diet, community function, and pathogen features to guide personalized prevention and treatment.},
}

Humans
*Clostridioides difficile/physiology/pathogenicity/growth & development
*Clostridium Infections/microbiology/prevention & control
Fecal Microbiota Transplantation
*Diet
Animals
Gastrointestinal Microbiome
Microbiota
Feces/microbiology
Biofilms/growth & development

@article {pmid42419591,
year = {2026},
author = {Kim, S and Seo, H and Jo, S and Rahim, MA and Hossain, MS and Shuvo, MSH and Jeong, SY and Lee, MY and Kim, KH and Lee, N and Won, JH and Song, HY and Yoon, SY},
title = {Oral Sodium Butyrate Supplementation, Gut Microbiome Modulation, and Reduced Acute Graft-versus-Host Disease After Allogeneic Hematopoietic Stem Cell Transplantation.},
journal = {Transplantation and cellular therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jtct.2026.07.006},
pmid = {42419591},
issn = {2666-6367},
abstract = {BACKGROUND: Acute graft-versus-host disease (aGVHD) remains a major cause of morbidity and mortality after allogeneic hematopoietic stem cell transplantation (allo-HSCT). Disruption of the gut microbiome during transplantation has been implicated in the pathogenesis of aGVHD, yet clinically applicable strategies to modulate the microbiome in immunocompromised patients remain limited.

OBJECTIVES: To evaluate the association between oral sodium butyrate supplementation and the incidence and severity of aGVHD, and to investigate its impact on gut microbiome recovery following allo-HSCT.

STUDY DESIGN: In this prospective, single-center study, 39 consecutive patients undergoing allo-HSCT received oral sodium butyrate (1,200 mg/day) from neutrophil engraftment to day +100. Outcomes were compared with 18 historical controls treated at the same institution without butyrate supplementation. The primary endpoint was the cumulative incidence of grade II-IV aGVHD by day +100. Secondary endpoints included lower gastrointestinal aGVHD and microbiome characteristics assessed using shotgun metagenomic sequencing. Competing risk analyses were performed to account for death as a competing event.

RESULTS: Butyrate supplementation was associated with a lower incidence of grade II-IV aGVHD (30% vs 53%, p=0.028) and grade III-IV aGVHD (5% vs 34%, p=0.002). Lower gastrointestinal aGVHD occurred in 5% of the butyrate group compared with 40% of historical controls (p<0.001). In multivariable competing risk analysis, butyrate supplementation remained independently associated with reduced grade II-IV aGVHD (adjusted HR 0.31, 95% CI 0.11-0.89; p=0.029) and lower gastrointestinal aGVHD (adjusted HR 0.07, 95% CI 0.02-0.30; p<0.001). Microbiome analysis demonstrated improved recovery of gut microbial diversity at day +100 in the butyrate group, with enrichment of commensal taxa and restoration of fecal butyrate levels.

CONCLUSIONS: Oral sodium butyrate supplementation was associated with reduced incidence and severity of aGVHD, particularly involving the gastrointestinal tract, along with improved microbiome recovery. These findings suggest a potential role for postbiotic-based microbiome modulation in GVHD prevention and warrant validation in randomized controlled trials.},
}

@article {pmid42420318,
year = {2026},
author = {Nie, H and Wang, N and Mao, H and Wei, Y and Qian, J and Chen, R and Yuan, Q and Xiao, Y and Zhang, L and Yan, F},
title = {Periodontitis aggravates bone loss through gut microbiota alterations in ovariectomized mice.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01084-7},
pmid = {42420318},
issn = {2055-5008},
support = {0224C032//High-Level Hospital Construction Project of Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Institute of Stomatology, Nanjing University/ ; 82270979//National Natural Sciences Foundation of China/ ; JSDW202246//Jiangsu Province Key discipline cultivation unit/ ; },
abstract = {Epidemiological evidence suggests a bidirectional relationship between periodontitis and osteoporosis, yet the underlying mechanisms remain unclear. In this study, using a mouse model combining ovariectomy-induced osteoporosis and ligature-induced periodontitis, we demonstrated that periodontitis significantly aggravated both alveolar and femoral bone loss, impaired intestinal barrier integrity, and elevated systemic inflammation. Gut microbiota and metabolomic analyses revealed that periodontitis induced distinct alterations in gut microbial composition and intestinal metabolic profiles, potentially contributing to systemic inflammation and bone metabolic dysregulation. Furthermore, fecal microbiota transplantation demonstrated that gut microbiota from periodontitis donors aggravated bone loss and inflammation in recipient mice, whereas microbiota from donors that received periodontal treatment partially alleviated inflammatory responses and skeletal deterioration. Collectively, these findings suggest that periodontitis may aggravate osteoporosis via gut microbiota-mediated mechanisms, highlighting the importance of maintaining oral health to mitigate the adverse impact of periodontitis on systemic bone metabolism.},
}

@article {pmid42420462,
year = {2026},
author = {Desharnais, L and Swaby, A and Messaoudene, M and Doré, S and Yu, MW and Fiset, B and Breton, V and Ponce, M and Hu, Y and Wilson, L and Sorin, M and Wang, Y and Dewar, K and Pollak, M and Elkrief, A and Routy, B and Walsh, LA and Quail, DF},
title = {Diet-microbiome synergy underlies obesity-associated immunotherapy efficacy.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {42420462},
issn = {1476-4687},
abstract = {Physiological host factors, such as the gut microbiome and obesity, independently influence anti-tumour immunity and responses to immune checkpoint inhibitors (ICIs)[1], with high body mass index (BMI) having an unexpected link with greater ICI efficacy[2-6]. However, how these factors interact across diverse dietary contexts remains unclear. Here, using 12 mouse diet models that reflect a spectrum of obesity biology, we characterize diet-driven metabolic, immune and gut microbiota features associated with ICI sensitivity. We find that obesity-associated ICI responses are poorly correlated with metabolic dysfunction and are instead dependent on the diet-gut axis. Obesogenic diets promote a robust and persistent gut microbial ecosystem that is capable of restoring ICI sensitivity following a short-term diet switch or fecal microbiota transplants (FMTs) from non-responder models. Monocolonization of germ-free mice with favourable bacteria such as Lactobacillus johnsonii, together with an obesogenic diet, synergistically promotes tumour regression through an enrichment of microbiota-derived aromatic amino acid metabolites. Moreover, human-to-mouse FMT from donors with a high BMI enhanced ICI efficacy compared with donors with a normal BMI, and an obesogenic diet restored sensitivity following FMT from a non-responder patient. Our study provides insight on epidemiological associations between BMI and ICI efficacy, and suggests that immunomodulatory synergy between diet and the gut microbiota could be leveraged to improve ICI outcomes and FMT interventions.},
}

@article {pmid42128989,
year = {2026},
author = {Takata, E and Lee, JJ and Lightner, AL},
title = {Needles for healing: stem cells, platelet-enriched plasma, and fat injection in perianal fistulizing Crohn's disease.},
journal = {Techniques in coloproctology},
volume = {30},
number = {1},
pages = {},
pmid = {42128989},
issn = {1128-045X},
mesh = {Humans ; *Crohn Disease/complications ; *Rectal Fistula/therapy/etiology ; *Wound Healing ; *Platelet-Rich Plasma ; *Mesenchymal Stem Cell Transplantation/methods ; *Adipose Tissue/transplantation ; },
abstract = {Perianal fistulizing Crohn's disease affects a third of patients with Crohn's disease and represents one of the most challenging complications to manage. This severe phenotype is characterized by aggressive disease behavior, high recurrence rates, frequent hospitalizations and surgical interventions, and profound impairment of quality of life, particularly affecting social and sexual function. The complex pathophysiology involves genetic susceptibility, immune dysregulation with elevated inflammatory cytokines, epithelial-to-mesenchymal transition, myofibroblast activation, and impaired wound healing mechanisms. Despite advances in anti-inflammatory and immunomodulatory therapies, current medical and surgical approaches achieve long-term fistula healing in only approximately 50% of patients. More than 90% of patients undergo multiple operative interventions, often with limited efficacy and risk of fecal incontinence. Anti-tumor necrosis factor agents, particularly infliximab, remain the cornerstone of medical therapy, yet more than 50% of patients lose response over time. Combination approaches with setons and biologics improve outcomes but remain suboptimal for many patients.These persistent limitations have prompted increasing interest in regenerative strategies aimed at restoring tissue integrity and enhancing local healing mechanisms. Mesenchymal stem cell therapy, particularly adipose-derived stem cells, has emerged as a promising approach, with clinical trials demonstrating complete fistula healing in the majority of cases and a favorable safety profile, but there are limitations with logistics of cell handling and negative late phase pivotal trials. This review evaluates the current landscape of novel regenerative therapies for perianal fistulizing Crohn's disease, including mesenchymal stem cell preparations, extracellular vesicle-based approaches, and adjunctive techniques.},
}

Humans
*Crohn Disease/complications
*Rectal Fistula/therapy/etiology
*Wound Healing
*Platelet-Rich Plasma
*Mesenchymal Stem Cell Transplantation/methods
*Adipose Tissue/transplantation

@article {pmid42407345,
year = {2026},
author = {Shi, Y and Xue, Q and Yuan, Y and Li, Y and Zhu, X and Niu, D and Jin, C},
title = {WD-3 improves anti-PD-L1 therapy by remodeling the tumor immune microenvironment through gut microbiota.},
journal = {Immunobiology},
volume = {231},
number = {4},
pages = {153215},
doi = {10.1016/j.imbio.2026.153215},
pmid = {42407345},
issn = {1878-3279},
abstract = {BACKGROUND: Gastric cancer (GC) ranks as the fifth most prevalent malignancy globally. Emerging evidence implicates gut microbiome as a key modulator of anti-tumor immunity and immunotherapy response. Traditional Chinese Medicine (TCM) presents a promising yet underexplored avenue for microbiome modulation.

METHODS: 16S rDNA sequencing of fecal samples was used to detect changes of gut microbiota in advanced GC patients. GC models were established in huPBMC-NOG-dKO mice after fecal microbiota transplantation (FMT) to investigate the potential synergy between Number 3 Prescription (WD-3) and anti-PD-L1 monoclonal antibody (mAb) in treatment of non-responders.

RESULTS: In this study, WD-3 combined with αPD-L1 showed additive benefit after the FMT of non-responders in the humanized mouse model model. WD-3 combination therapy correlated with reduced proportion of Treg cell infiltration in tumors. WD-3 combination was also associated with increased species richness and improved gut microbiota community structure compared to αPD-L1 alone, with increased relative abundances of Enterobacteriaceae and Lachnospiraceae.

CONCLUSION: Our data provide correlative evidence that WD-3 supplementation combined with αPD-L1 treatment may attenuate GC progress in the FMT mouse model, indicating association with the modulation of gut microbiota. These findings aim to provide treatment strategies for the clinical treatment of advanced GC.},
}

@article {pmid42410815,
year = {2026},
author = {Liao, DX and Zhang, S and Cao, D and Cai, X and Sun, HL and Jin, WD and Fu, T},
title = {Fecal microbiota transplantation for chronic constipation following bowel surgery in an elderly patient: A case report.},
journal = {Medicine},
volume = {105},
number = {27},
pages = {e49600},
doi = {10.1097/MD.0000000000049600},
pmid = {42410815},
issn = {1536-5964},
mesh = {Humans ; *Constipation/therapy/etiology ; Male ; *Fecal Microbiota Transplantation/methods ; Aged ; Chronic Disease ; Treatment Outcome ; Dysbiosis/therapy ; Colorectal Surgical Procedures ; *Postoperative Complications/therapy ; },
abstract = {RATIONALE: Chronic constipation is a common gastrointestinal disorder traditionally managed with laxatives and surgical interventions. Nevertheless, a subset of elderly patients remains unresponsive to conventional treatments. Additionally, chronic constipation is linked to an increased risk of mortality from cardiovascular events and a heightened incidence of colorectal cancer.

PATIENT CONCERNS: A 65-year-old male with a medical history of sigmoidostomy, enterostomy, and jejunostomy presented with an 11-year history of intermittent abdominal distension, pain, and constipation refractory to standard treatments including lactulose, castor oil, and glycerin enemas.

DIAGNOSES: The patient was diagnosed with severe chronic constipation associated with surgically altered anatomy and intestinal dysbiosis.

INTERVENTIONS: After thorough discussion, fecal microbiota transplantation (FMT) was implemented as a therapeutic intervention.

OUTCOMES: The patient's abdominal distension and pain were significantly alleviated within 1 week and completely resolved 6 months post-FMT. No recurrence was observed during the subsequent follow-up period.

LESSONS: This case demonstrates that FMT can serve as an effective therapeutic intervention for elderly patients with surgically altered anatomy and intestinal dysbiosis, particularly those showing reduced response to conventional laxative treatments for chronic constipation.},
}

Humans
*Constipation/therapy/etiology
Male
*Fecal Microbiota Transplantation/methods
Aged
Chronic Disease
Treatment Outcome
Dysbiosis/therapy
Colorectal Surgical Procedures
*Postoperative Complications/therapy

@article {pmid42410982,
year = {2026},
author = {Alanazi, A},
title = {Organ-Specific Human Microbiomes and Dysbiosis: Mechanistic Links to Disease and Emerging Therapeutic Strategies.},
journal = {Journal of clinical laboratory analysis},
volume = {},
number = {},
pages = {e70307},
doi = {10.1002/jcla.70307},
pmid = {42410982},
issn = {1098-2825},
abstract = {BACKGROUND: The human microbiome is a dynamic and diverse community of microorganisms that affects susceptibility to illness and promotes wellness. Dysbiosis, or disruption of this delicately regulated microbial ecology, has been identified as a major factor in the emergence and development of systemic and organ-specific disorders.

OBJECTIVE: With an emphasis on dysbiosis-driven illness processes and therapeutic intervention implications, this study attempts to critically analyze host-microbiome interactions across key human organ systems.

METHODS: Using predetermined microbiome-related keywords, a systematic literature search (2001-2025) was carried out in PubMed, Scopus, Web of Science, and Google Scholar. To assess microbiome formation, organ-specific distribution, disease correlations, and therapeutic implications, English-language peer-reviewed original papers, meta-analyses, and clinical or validated animal studies were chosen and methodically compiled.

RESULTS: Microbiome dysbiosis is linked to cardiovascular, metabolic, inflammatory, neurological, hepatic, renal, and cancer-related illnesses by interfering with immune modulation, metabolic balance, and epithelial barrier integrity, according to evidence from human and verified animal research. Modified production of short-chain fatty acids, immunological signaling imbalance, chronic inflammation, and communication between the gut-organ axis are examples of mechanistic linkages. Immune and metabolic indicators improved condition-specifically with interventions such as probiotics, fecal microbiota transplantation, and diet-based regulation.

CONCLUSION: Collectively, current evidence supports the microbiome as a modifiable determinant of disease risk and therapeutic response, underscoring its translational potential for precision medicine.},
}

@article {pmid42411731,
year = {2026},
author = {Liang, B and Zou, J and Mao, X and Xie, N and Liang, Z},
title = {Systematic Review and Meta-Analysis of the Efficacy of Fecal Microbiota Transplantation in Parkinson's Disease: An Exploration Based on UPDRS and Cognitive Scores.},
journal = {Revista de neurologia},
volume = {81},
number = {6},
pages = {50106},
doi = {10.31083/RN50106},
pmid = {42411731},
issn = {1576-6578},
mesh = {Humans ; *Parkinson Disease/therapy/psychology ; *Fecal Microbiota Transplantation ; Randomized Controlled Trials as Topic ; Treatment Outcome ; Cognition ; Severity of Illness Index ; },
abstract = {BACKGROUND: Parkinson's disease (PD) is a common neurodegenerative disorder that has been increasingly linked to gut-brain axis dysfunction. Fecal microbiota transplantation (FMT), a microbiome-targeted intervention, has shown theoretical and preliminary clinical potential in PD, but randomized clinical evidence remains limited. This review aimed to systematically evaluate the effects of FMT on motor, non-motor, and cognitive outcomes in patients with PD.

METHODS: A Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA)-compliant systematic review and meta-analysis of randomized controlled trials (RCTs) comparing FMT with placebo or conventional care in PD was conducted. Two reviewers independently screened studies, extracted data, and assessed risk of bias. Pooled analyses were performed using a random-effects model, and the certainty of evidence was evaluated using the Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) approach.

RESULTS: Five RCTs involving 226 participants were included. No statistically significant differences were observed between the FMT and control groups in Movement Disorder Society Unified Parkinson's Disease Rating Scale (MDS-UPDRS) Parts I-III, Montreal Cognitive Assessment (MoCA), or Mini-Mental State Examination (MMSE) scores at any assessed follow-up time, with heterogeneity generally low to moderate across outcomes.

CONCLUSIONS: Based on current evidence from five small RCTs, FMT did not demonstrate a statistically significant benefit for motor, daily living, or cognitive outcomes in PD. However, these findings should be interpreted cautiously, given the limited sample size, short follow-up duration, and between-study differences in intervention protocols. Larger, well-designed RCTs with standardized FMT protocols and longer follow-up are needed. The PROSPERO Registration: This systematic review was registered in the PROSPERO database under registration number CRD420251121443, https://www.crd.york.ac.uk/PROSPERO/view/CRD420251121443.},
}

Humans
*Parkinson Disease/therapy/psychology
*Fecal Microbiota Transplantation
Randomized Controlled Trials as Topic
Treatment Outcome
Cognition
Severity of Illness Index

@article {pmid42412324,
year = {2026},
author = {Adiga, U and Vasishta, S and Adiga, S and Augustine, AJ},
title = {Targeting the Gut-Heart Axis in Atherosclerosis: Microbial Metabolites, Molecular Mechanisms, and Precision Therapeutics.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {42412324},
issn = {1867-1314},
abstract = {Despite advances in lipid-lowering and anti-inflammatory medications, atherosclerotic cardiovascular disease (ASCVD) continues to be the leading cause of morbidity and mortality worldwide. Recent studies have identified the gut microbiota as a key modulator of cardiovascular health via the gut-heart axis. This review investigates the molecular processes by which microbial metabolites affect atherogenesis. Proatherogenic substances like trimethylamine-N-oxide (TMAO), which are produced from dietary precursors through gut microbial and hepatic metabolism, aggravate foam cell production, platelet aggregation, and vascular inflammation. Short chain fatty acids (SCFAs), such as butyrate and propionate, have been shown to protect against atherosclerosis by activating G-protein-coupled receptors, regulating gene expression, and improving endothelial function. Additionally, secondary bile acids, tryptophan derivatives, and phenylacetylglutamine have emerged as important microbial metabolites involved in vascular disease. The review also summarizes various therapeutic strategies such as use of probiotics, prebiotics, postbiotics, precision microbiome editing (using bacteriophages and CRISPR-Cas systems), and fecal microbiota transplantation (FMT) for targeting gut-heart axis. Multi-omic systems combined with artificial intelligence can now detect disease-specific microbial signatures, improving risk stratification and paving the way for precision microbiome-based therapeutics. However, challenges such as determining causality, regulatory intricacies, and inter-individual variability in host-microbiome interactions remain. Despite these obstacles, the gut-heart axis provides a disruptive paradigm in preventive cardiology by emphasizing tailored microbiome therapies as a complement to traditional ASCVD care.},
}

@article {pmid42412955,
year = {2026},
author = {Lv, J and Waza, AA},
title = {Recurrent urinary tract infections in older adults: A systematic review of current challenges and emerging therapeutic strategies.},
journal = {Acta pharmaceutica (Zagreb, Croatia)},
volume = {76},
number = {2},
pages = {1-25},
doi = {10.2478/acph-2026-0017},
pmid = {42412955},
issn = {1846-9558},
mesh = {Humans ; *Urinary Tract Infections/diagnosis/epidemiology/therapy/microbiology/drug therapy ; Aged ; Recurrence ; *Anti-Bacterial Agents/therapeutic use/administration & dosage ; Female ; Prevalence ; Age Factors ; Risk Factors ; },
abstract = {As global life expectancy continues to rise, urinary tract infections (UTIs) have become an increasing concern in older adults. The higher prevalence in this population is attributed to anatomical and physiological changes of the urinary tract, hormonal imbalances, immunosenescence, and the presence of comorbidities. These factors, combined with a distinct microbiological profile and rising antimicrobial resistance, create significant clinical challenges in diagnosis and treatment. We conducted a systematic review of clinical trials and observational studies on the epidemiology, pathogenesis, diagnosis, and management of recurrent urinary tract infections (rUTIs) in older adults. The prevalence of rUTIs increases with age, disproportionately affecting women, with 53 % of those over 55 years experiencing recurrences within one year. Healthcare-associated UTIs (HAUTIs) account for 20-30 % of nosocomial infections, primarily impacting older adults. The host microbiome seemed crucial in UTI pathogenesis, with Escherichia coli being the leading causative agent due to its ability to adhere, colonise, and evade the immune response. In elderly patients, atypical presentations - such as delirium, functional decline, or nonspecific abdominal symptoms - complicate diagnosis, underscoring the critical need to differentiate symptomatic infections from asymptomatic bacteriuria (ASB) to prevent misdiagnosis and overtreatment. Effective management requires accurate diagnosis, appropriate antibiotic selection, and careful monitoring of adverse effects, especially in patients with comorbidities. Emerging therapies, including faecal microbiota transplantation, bacteriophages, probiotics, and proanthocyanidins, offer promising adjuncts. While long-term antibiotic prophylaxis is effective, it increases the risk of bacterial resistance, particularly in catheterised patients. Behavioural modifications, such as increased fluid intake, aid pathogen clearance, and topical estrogen therapy in postmenopausal women provides additional preventive benefit. Managing recurrent UTIs in ageing populations requires addressing microbiological, diagnostic, and antimicrobial resistance challenges. Despite resistance levels, the first-line treatment, nitrofurantoin, remains a viable therapeutic option, particularly in developed countries. An integrated approach combining individualised care, healthcare provider training, and rational antimicrobial use is essential to improving patient outcomes and quality of life. Future strategies should focus on novel antimicrobials targeting bacterial virulence factors, vaccines against uropathogens, and advanced diagnostic technologies.},
}

Humans
*Urinary Tract Infections/diagnosis/epidemiology/therapy/microbiology/drug therapy
Aged
Recurrence
*Anti-Bacterial Agents/therapeutic use/administration & dosage
Female
Prevalence
Age Factors
Risk Factors

@article {pmid42413478,
year = {2026},
author = {Newsome, RC and Jobin, C},
title = {Microbiota and immunotherapy: The birth of a new paradigm?.},
journal = {Cell metabolism},
volume = {38},
number = {7},
pages = {1269-1272},
doi = {10.1016/j.cmet.2026.06.007},
pmid = {42413478},
issn = {1932-7420},
abstract = {Emerging data suggest fecal microbiota transplantation (FMT) may improve cancer patients' responses to immune checkpoint blockade not only by enriching beneficial bacteria but also by depleting harmful taxa. Here, we discuss the "supplementation" and new "depletion" FMT paradigms in cancer management and highlight key knowledge gaps to be addressed to move this field forward.},
}

@article {pmid42413716,
year = {2026},
author = {Gu, M and Wang, Z and Huang, F and Li, Y and Liu, Z and Huang, Z and Chang, P},
title = {Gut microbiota and metabolites in remodeling the tumor microenvironment and regulating immunotherapeutic efficacy in colorectal cancer.},
journal = {Life sciences},
volume = {},
number = {},
pages = {124581},
doi = {10.1016/j.lfs.2026.124581},
pmid = {42413716},
issn = {1879-0631},
abstract = {AIMS: Immune checkpoint inhibitors (ICIs) benefit patients with mismatch repair-deficient/microsatellite instability-high (dMMR/MSI-H) colorectal cancer (CRC), but efficacy remains limited in proficient mismatch repair/microsatellite-stable (pMMR/MSS) tumors. This review evaluates how the gut microbiota and microbial metabolites influence CRC development, the tumor microenvironment, and immunotherapy responses, with emphasis on strategies for pMMR/MSS CRC.

MATERIALS AND METHODS: We reviewed and critically evaluated recent preclinical, translational, and clinical evidence on microbiota-associated metabolic regulation, chronic inflammation, DNA damage, epigenetic reprogramming, microbial biomarkers, and microbiota-targeted interventions.

KEY FINDINGS: Microbial effects are context dependent and cannot be classified simply as beneficial or harmful. Short-chain fatty acids, tryptophan derivatives, and secondary bile acids influence epithelial integrity, immune-cell function, tumor metabolism, and epigenetic regulation. Akkermansia muciniphila, Bifidobacterium, and Lactobacillus strains are promising candidates for improving ICI responses. Notably, tumor-associated bacteria, including Fusobacterium nucleatum and selected Bacteroides taxa, may exert context-dependent and potentially opposing effects depending on strain, metabolite output, host background, and treatment setting. Emerging strategies include dietary modulation, fecal microbiota transplantation, probiotics, engineered bacteria, and rational combination therapies.

SIGNIFICANCE: The gut microbiota is a modifiable component of ICI resistance rather than a sole determinant. Future studies should establish causal mechanisms and develop reproducible, function-based biomarkers through longitudinal multi-omics analyses and prospective clinical validation.},
}

@article {pmid42413732,
year = {2026},
author = {Paul, P and Kaul, R and Ayyan, M and Lakshmanan, AP and Chaari, A},
title = {Gut Microbiome-Modulating Therapeutics and Lipid Profile in Metabolic Syndrome: A Systematic Review and Meta-Analysis of Clinical Trials.},
journal = {Clinical nutrition ESPEN},
volume = {},
number = {},
pages = {103461},
doi = {10.1016/j.clnesp.2026.103461},
pmid = {42413732},
issn = {2405-4577},
abstract = {OBJECTIVES: To evaluate the effects of gut microbiome-modulating interventions (probiotics, prebiotics, synbiotics, and fecal microbiota transplantation) on lipid profile parameters in adults with metabolic syndrome (MetS).

DESIGN AND DATA SOURCES: Systematic review and random-effects meta-analysis with univariate meta-regression of controlled clinical trials indexed in PubMed, Web of Science, and Scopus through June 2025.

ELIGIBILITY CRITERIA: Controlled clinical trials in adults with MetS diagnosed according to ATP III, IDF, or WHO criteria reporting at least one lipid outcome (total cholestrol (TC), low-density lipoprotein cholestrol (LDL-C), high desntiry lipoprotein cholestrol (HDL-C), or triglycerdies (TG)). Studies without control groups, insufficient data, or populations not meeting full MetS criteria were excluded.

DATA EXTRACTION AND SYNTHESIS: Two reviewers independently screened and extracted data. Risk of bias was assessed using the Cochrane RoB 2 tool. Random-effects meta-analysis (DerSimonian-Laird) generated pooled mean differences (MDs) with 95% confidence intervals (CIs). Heterogeneity was assessed using I[2] statistics. Meta-regression evaluated moderators including age, baseline BMI, intervention dose, duration, and geographic region.

RESULTS: Nineteen studies comprising 21 trial comparisons and 897 participants were included. Microbiome-modulating interventions were associated with reductions in TC (MD -8.97 mg/dL; 95% CI -12.55 to -5.38) and TG (MD -11.33 mg/dL; 95% CI -19.25 to -3.40), while HDL-C showed no significant change. LDL-C was also reduced in the primary pooled analysis (MD -5.05 mg/dL; 95% CI -9.57 to -0.53); however, this finding should be interpreted cautiously because of substantial between-study heterogeneity (I[2] = 73.8%) and loss of statistical significance in sensitivity analyses. Greater lipid reductions were generally observed in trials using higher probiotic doses and longer intervention durations, although moderator effects were not consistent across all lipid outcomes.

CONCLUSIONS: Microbiome-modulating interventions are associated with modest improvements in selected lipid parameters in adults with metabolic syndrome, particularly TC and TG. Evidence for LDL-C reduction is less robust because of substantial heterogeneity and sensitivity to analytical assumptions. Larger, well-standardized clinical trials are required to confirm lipid-specific effects, identify responsive populations, and determine the clinical relevance of these interventions.},
}

@article {pmid42414020,
year = {2026},
author = {Clister, D and Chandra, QM and Tan, MW and Gunawan, MC and Bibi, A and Ahmed, A and Bastian, M and Meesakul, P and Cao, S and Kim, B and Nurkolis, F and Syahputra, RA},
title = {Microbiome-Based Precision Interventions in Type 2 Diabetes Mellitus: Mechanisms, Modulators, and Translational Opportunities.},
journal = {The Journal of nutrition},
volume = {156},
number = {7},
pages = {101596},
doi = {10.1016/j.tjnut.2026.101596},
pmid = {42414020},
issn = {1541-6100},
abstract = {Type 2 diabetes mellitus (T2DM) is a complex metabolic disease driven by insulin resistance, chronic low-grade inflammation, and impaired glucose regulation. Although pharmacological options have advanced, sustained glycemic control remains elusive due to heterogeneity in disease progression and therapeutic response. Precision medicine offers a framework to individualize interventions, with the gut microbiota emerging as a central determinant of host metabolic and immune regulation. Dysbiosis has been implicated in T2DM through altered microbial metabolites-including short-chain fatty acids, bile acids, branched-chain amino acids, and indole derivatives-that shape insulin sensitivity, inflammatory pathways, and glucose homeostasis. This review critically examined microbiome-targeted strategies such as probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and personalized nutrition, alongside advances in metagenomics and machine learning for biomarker discovery. By integrating mechanistic and translational insights, we highlight opportunities and challenges in implementing microbiome-based precision interventions, underscoring their potential to transform T2DM management.},
}

@article {pmid42402612,
year = {2026},
author = {Cao, L and Zhang, G and Zhang, G and Zhang, F and Li, W and Song, Q and He, J and Zhao, J and Zhang, Z},
title = {Cichorium intybus L. polysaccharide improves growth performance and colonic barrier function in weaned piglets via the microbiota-HDCA-TGR5-Akt-NF-κB signaling axis: validation by FMT and in vitro models.},
journal = {Journal of animal science and biotechnology},
volume = {17},
number = {1},
pages = {},
pmid = {42402612},
issn = {1674-9782},
support = {32302766//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Weaning stress predisposes piglets to intestinal barrier disruption and gut dysbiosis, which contribute to post-weaning diarrhea and poor feed efficiency. Chicory (Cichorium intybus L.) polysaccharide (CLP) is a fructan-rich prebiotic candidate; however, how CLP reshapes the microbiota-metabolite network to protect the colon remains unclear.

METHODS: In Exp. 1, 96 weaned piglets [Duroc × (Landrace × Yorkshire), 28 days old, 8.03 ± 0.2 kg] were fed a basal diet (CON group) or a 0.5% CLP supplemented diet (CLP group). In Exp. 2, fecal microbiota from piglets were transplanted into dextran sulfate sodium (DSS)-induced mice to confirm the causal role of the CLP-remodeled microbiota. Metagenomic and untargeted metabolomic analyses were employed to identify key microbial species and functional metabolites. In Exp. 3, Caco-2 cells were treated with varying concentrations of hyodeoxycholic acid (HDCA) for 24 h to functionally validate the regulatory effects on TGR5 and FXR expression levels.

RESULTS: The results showed that dietary CLP significantly decreased the feed to gain ratio, diarrhea rate and histology index (P < 0.05), but increased goblet cell numbers (P < 0.05). Metagenomic sequencing revealed that CLP significantly increased microbial α-diversity and remodeled the community structure, specifically enriching beneficial microbes, such as Blautia sp., Eubacterium sp., and Ruminococcus sp. To test microbiota causality, fecal microbiota from CON or CLP piglets was transplanted into antibiotic treated mice followed by DSS challenge. The CLP modified microbiota alleviates DSS induced colitis, upregulated Occludin and ZO-1 expression, and reduced colonic IL-1β and TNF-α levels. Mechanistically, the CLP remodeled microbiota promoted the accumulation of HDCA, which functioned as a signaling ligand to activate the colonic TGR5 receptor. This activation subsequently suppressed the phosphorylation of Akt (P < 0.05), leading to the inhibition of the NF-κB signaling pathway through the reduced phosphorylation of IκBα and the p65 subunit (P < 0.05), thereby effectively abrogating the inflammatory response.

CONCLUSION: Dietary CLP supplementation mitigates weaning induced intestinal injury and inflammation by remodeling the colonic microbiota, specifically enriching HDCA-producing species. The subsequent activation of the HDCA-TGR5-Akt signaling axis inhibits the NF-κB pathway, thereby improving host immune responses and intestinal barrier function.},
}

@article {pmid42403915,
year = {2026},
author = {Wang, T and Chen, L and Lei, C and Song, X and Tuohongerbieke, A and Feng, J and Gasparetto, R and Zhang, X and McClain, CJ and Tan, Y and Deng, Z},
title = {Intestinal neutral ceramidase exacerbates MASH pathogenesis.},
journal = {eGastroenterology},
volume = {4},
number = {2},
pages = {e100417},
pmid = {42403915},
issn = {2976-7296},
abstract = {BACKGROUND: Metabolic dysfunction-associated steatotic liver disease and its more severe manifestation, metabolic dysfunction-associated steatohepatitis (MASH), are intimately linked to genetic factors, gut microbiota and barrier alteration. Ceramidases and ceramides are associated with MASH, yet the role of intestinal neutral ceramidase in MASH development remains unclear.

METHODS: Murine models with intestinal epithelial cell (IEC)-specific depletion of neutral ceramidase (Asah2[ΔIEC]) or aryl hydrocarbon receptor (AhR [ΔIEC]) were subjected to either a Western diet (WD) at 6 weeks old for 10-12 months to induce MASH, or a hydrogenated vegetable oil, sucrose, palmitate and cholesterol (HSPC) diet to accelerate MASH progression. Fecal microbiota transplantation was performed in germ-free mice.

RESULTS: MASH is associated with the induction of neutral ceramidase, which reshapes the intestinal microbiota and metabolite profiles, leading to increased production of 2-hydroxyhippuric acid (2-HHA). We identified 2-HHA as an inhibitor of AhR signalling, a pathway that normally promotes intestinal fucosylation. Elevated 2-HHA suppresses AhR activity, reduces fucosylation and contributes to MASH and associated airway inflammation in mice fed WD or HSPC diet. Notably, IEC-specific deletion of neutral ceramidase decreases 2-HHA levels, restores AhR signalling, enhances fucosylation and protects against MASH. Consistently, intestinal AhR deficiency exacerbates MASH by reducing intestinal fucosylation, whereas supplementation with fucoidan increases fucosylation, improves barrier function and attenuates MASH.

CONCLUSIONS: These findings identify intestinal neutral ceramidase as a key driver of MASH through a microbiota-2-HHA-AhR axis that impairs intestinal fucosylation and barrier function, highlighting a potential therapeutic target.},
}

@article {pmid42404763,
year = {2026},
author = {Wang, X and Piao, Y and Xia, B and Chu, W and Yao, X and Li, W},
title = {Diet, gut microbiota, and the gut-brain axis: mechanistic interactions and therapeutic implications in neuropsychiatric disorders.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1834069},
pmid = {42404763},
issn = {2235-2988},
mesh = {Humans ; *Diet ; *Gastrointestinal Microbiome/physiology ; *Mental Disorders/therapy/microbiology ; *Brain ; Animals ; Dysbiosis ; *Brain-Gut Axis/physiology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {The gut microbiota is a dynamic trans-kingdom ecosystem that contributes to host immunological, metabolic, and neuroendocrine homeostasis through the microbiota-gut-brain axis (MGBA). Diet is one of the major environmental factors shaping this axis, as it influences microbial composition, microbial production of neuroactive metabolites, and intestinal barrier integrity. Dysbiosis has been increasingly associated with neurological, psychiatric, and neurodevelopmental disorders, including Alzheimer's disease, Parkinson's disease, depression, autism spectrum disorder, and attention-deficit/hyperactivity disorder. Experimental studies have identified several potential mechanisms linking gut microbiota to brain function, including immune modulation, vagus nerve signaling, microbial metabolite production, and blood-brain barrier regulation. However, translating these findings into clinical practice remains challenging because human studies are affected by genetic heterogeneity, dietary variation, medication use, lifestyle factors, and disease-specific confounders. In this review, we summarize current evidence on the interactions among diet, gut microbiota, and brain function, with particular emphasis on microbial metabolites, immune mediators, and barrier-related mechanisms. We also critically discuss microbiota-targeted interventions, including precision nutrition, probiotics, and fecal microbiota transplantation, highlighting both their therapeutic potential and their current limitations. A more cautious and mechanistically integrated understanding of the MGBA may support the development of personalized strategies for neuropsychiatric disease prevention and management.},
}

Humans
*Diet
*Gastrointestinal Microbiome/physiology
*Mental Disorders/therapy/microbiology
*Brain
Animals
Dysbiosis
*Brain-Gut Axis/physiology
Probiotics/therapeutic use
Fecal Microbiota Transplantation

@article {pmid42404795,
year = {2026},
author = {Tang, J and Chen, L and Wang, Q and He, X and Hang, D and Chen, G and Feng, L},
title = {Optimized fecal microbiota transplantation using membrane-filtered bacterial concentrates as adjunctive therapy for mild-to-moderate ulcerative colitis: a retrospective cohort study.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1805799},
pmid = {42404795},
issn = {1664-302X},
abstract = {BACKGROUND AND AIMS: Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach for ulcerative colitis (UC). This single-center retrospective cohort study evaluated the clinical effectiveness and safety of an optimized FMT protocol, in which donor bacteria were concentrated by tangential-flow micropore membrane filtration and delivered after pre-FMT antibiotic preconditioning, as adjunctive therapy in adults with mild-to-moderate UC.

METHODS: We analyzed prospectively collected data from 156 patients with mild-to-moderate active UC treated between December 2022 and December 2024. Treatment allocation was determined by a shared clinical decision between the gastroenterologist and patient based on disease severity, prior medication exposure, and patient preference. Patients were grouped into four pre-specified treatment strata: aminosalicylates alone (Group A, n = 42), aminosalicylates plus corticosteroids/immunosuppressants (Group B, n = 38), aminosalicylates plus FMT (Group FMT1, n = 40), and aminosalicylates plus corticosteroids/immunosuppressants plus FMT (Group FMT2, n = 36). Donor stools were processed using a validated tangential-flow 0.22-μm membrane filtration workflow that retains and concentrates viable bacteria in the retentate while clearing soluble metabolites and host debris in the permeate. Confounding was addressed using multivariable logistic regression and inverse probability of treatment weighting (IPTW) as a sensitivity analysis. The primary outcome was clinical response at 12 weeks; effect sizes are reported as risk differences with 95% confidence intervals.

RESULTS: Clinical response rates at 12 weeks were 31.0% (Group A), 52.6% (Group B), 72.5% (Group FMT1), and 77.8% (Group FMT2). Clinical remission rates were 19.0%, 34.2%, 55.0%, and 61.1%, respectively. FMT-containing regimens were associated with higher response and remission than aminosalicylates alone (risk difference for response: 41.5%, 95% CI 22.7-60.3% for FMT1 vs. A; 46.8%, 95% CI 28.0-65.6% for FMT2 vs. A; both P < 0.001). Microbiome analysis using 16S rRNA gene sequencing showed that responders had increased Bacteroides-related amplicon sequence variants and increased alpha diversity comparable to donor profiles, while non-responders maintained dysbiotic profiles. Adverse events were mild and comparable across all groups.

CONCLUSIONS: In this retrospective cohort, an optimized FMT protocol using membrane-filtered bacterial concentrates was associated with higher rates of clinical response, clinical remission and endoscopic improvement at 12 weeks compared with conventional therapy, with an acceptable short-term safety profile. Given the observational design, these findings should be interpreted as hypothesis-generating and require confirmation in randomized controlled trials.},
}

@article {pmid42404992,
year = {2026},
author = {Szilagyi, A and Galiatsatos, P and Margolese, N and Hilzenrat, N},
title = {Microbiome alternative treatments for hepatic encephalopathy: Reassessment of the potential use of lactose in lactase non-persistent cirrhosis patients.},
journal = {Canadian liver journal},
volume = {9},
number = {2},
pages = {319-327},
pmid = {42404992},
issn = {2561-4444},
abstract = {BACKGROUND: Hepatic encephalopathy is secondary to liver failure and is prevalent in 20%-40% of cirrhosis patients. The cause involves ammonia toxicity, gut-brain interactions, and inflammation usually involving the microbiome. The aim was to review succinct management of microbiome disturbances. The purpose includes an argument for further research into the possible selective benefit of lactose and dairy products in managing chronic hepatic encephalopathy in lactose maldigesters.

METHODS: Articles from 1970 to June 2025 were sought on PubMed and Google Scholar, as well as individual articles, regarding using altered microbiome and hepatic encephalopathy management.

RESULTS: Non-digestible disaccharides and synthetic polymers, often combined with non-absorbable antibiotic rifaximin, have been found to benefit hepatic encephalopathy. It is of note that after a few reports, lactose was abandoned as a potential treatment in lactase non-persistent cirrhotic patients. After abandonment for unclear reasons, colonic adaptation in lactase non-persistent populations was clearly defined to be associated with microbiome changes similar to other non-absorbable disaccharides.

CONCLUSIONS: While current treatment is acceptable to most patients, the potential role of lactose and dairy products likely deserves further studies in patients with lactase non-persistence. The process of colonic adaptation may favour improvement in hepatic encephalopathy by altering the bacterial milieu. Use of dairy foods could also improve nutrition in cirrhosis. As such, use of lactose or dairy products could have a wide application since cirrhosis is common in parts of the world where lactose maldigestion is also widespread.},
}

@article {pmid42405758,
year = {2026},
author = {Zhang, S and Tu, J and Hong, W and Liu, J and Xue, C and Dong, N},
title = {Gut microbiota as key mediators of animal acclimation to temperature changes: mechanisms and interventions.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0241225},
doi = {10.1128/aem.02412-25},
pmid = {42405758},
issn = {1098-5336},
abstract = {With the intensification of global climate change, temperature fluctuations profoundly affect animal physiology and health. Research has shown that the gut microbiota, as a critical bridge between the host and its environment, helps animals adapt to temperature changes by regulating intestinal barrier stability, immune function, and energy metabolism. This adaptive capacity underscores the indispensable role of gut microbiota in temperature change responses. In cold environments, animals increase food intake and activate brown adipose tissue to maintain body temperature, but prolonged exposure causes metabolic overload and gut microbiota imbalance. Chronic cold reduces beneficial bacteria and increases pro-inflammatory species, impairing intestinal barrier integrity and inducing systemic inflammation, ultimately leading to metabolic disorders and immunosuppression. Similarly, heat exposure leads to pathogenic overgrowth and immune dysfunction, reducing microbial diversity and increasing the abundance of harmful bacteria, ultimately impairing animal health. Furthermore, the gut-brain axis plays a central role in coping with environmental stress, as temperature change alters microbial composition and metabolites, impacting neurotransmitter synthesis and release, thereby regulating physiological states and emotional responses. Finally, targeted microbial interventions-such as fecal microbiota transplantation (FMT), probiotics, prebiotics, synbiotics, and postbiotics-are discussed as effective strategies to restore gut microbiota homeostasis, enhance host resilience to temperature change, and improve animal health under temperature fluctuations.},
}

@article {pmid42405768,
year = {2026},
author = {Berryhill, BA and Gil-Gil, T and Burke, KB and Fontaine, J and Brink, CE and Harvill, MG and Goldberg, DA and Navas, JN and Grabowicz, M and Konstantinidis, KT and Levin, BR and Woodworth, MH},
title = {Enteric populations of Escherichia coli are likely to be resistant to phages due to O antigen expression.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0038626},
doi = {10.1128/msphere.00386-26},
pmid = {42405768},
issn = {2379-5042},
abstract = {Metagenomic data provide evidence that bacteriophage (phage) abound in the enteric microbiomes of humans. However, the contribution of these viruses in shaping the bacterial composition of the gut microbiome and how these phages are maintained remain unclear. We performed experiments with 756 combinations of 54 Escherichia coli and nine phage isolates from four fecal microbiota transplantation (FMT) doses and five laboratory phages as samples of non-dysbiotic human enteric microbiota. We also developed a mathematical model of the population and evolutionary dynamics of bacteria and phage. Our experiments predict that as a consequence of the production of the O antigen, most of the E. coli in the human enteric microbiome will be resistant to infections with the array of co-occurring phages. Our modeling suggests that phages are maintained in these enteric communities due to the high rates of transition between the O antigen-resistant and -sensitive states. Based on our observations and predictions from this theory, we postulate that the phage found in the human gut are likely to play a little role in shaping the strain composition of E. coli of healthy individuals. Although we only investigated E. coli, the mechanism of resistance described here is shared among most of the gram-negative bacteria. Evidence is provided that, as a consequence of O antigen-mediated resistance, the genetically diverse array of bacteriophage in the gut microbiome of humans plays little or no role in determining the densities and distribution of the genetically diverse strain E. coli in this habitat. Our mathematical model predicts and our experiments support the hypothesis that the phage present in the gut microbiome are maintained by replication on the minority of sensitive bacteria generated by the leakiness of O antigen-mediated resistance.IMPORTANCEBacteriophages (phages) are abundant in the human gut, yet whether these viruses shape the bacterial communities living there remains unresolved. Using Escherichia coli and phages isolated from the stool of healthy fecal microbiota transplantation (FMT) donors, together with a mathematical model, we show that the vast majority of gut E. coli are resistant to co-occurring phages because they express the O antigen, a surface structure that masks the receptors phages use to attach. Despite this widespread resistance, phages persist by replicating on a small, continually regenerated subpopulation of sensitive cells, a phenomenon we term leaky resistance. These findings suggest that phages play a little role in determining which E. coli strains dominate the healthy human gut. Because the O antigen is broadly expressed across gram-negative bacteria, this mechanism likely extends well beyond E. coli and helps explain why isolating therapeutic phages against many pathogens is difficult.},
}

@article {pmid42401711,
year = {2026},
author = {Huang, L and Lu, C and Hu, Y and Chen, J and Chen, A and Zhong, C and Chen, D and Qin, Z and He, X and Wu, L},
title = {Washed microbiota transplantation is associated with short-term changes in selected spirometric parameters in patients with abnormal spirometry.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-60829-8},
pmid = {42401711},
issn = {2045-2322},
support = {2026P-ZD004//Guangzhou Clinical High-Tech Major and Specialized Technology Project/ ; 82505713//the National Natural Science Foundation of China/ ; 2025A1515011113//the Basic and Applied Basic Research Fund of Guangdong Province/ ; 2025KTSCX058//the Characteristic Innovation Project of Regular Colleges and Universities in Guangdong Province/ ; },
abstract = {Gut microbiota may modulate pulmonary inflammation through the gut-lung axis. This study investigated the association between washed microbiota transplantation (WMT) and short-term changes in pulmonary function, inflammatory markers, and gut microbiota in patients with abnormal spirometric patterns. A total of 110 patients who underwent fecal microbiota transplantation, also referred to as WMT, were consecutively screened between March 2023 and January 2025. Of these, 47 patients with paired baseline and post-WMT spirometric data were included in the primary spirometric analysis. According to baseline spirometric patterns, WMT recipients were classified into an abnormal spirometric-pattern group (DG, n = 19) and a normal spirometric-pattern WMT-recipient group (HC, n = 28; HC denotes WMT recipients with normal spirometry rather than healthy community controls). In addition, 43 patients receiving conventional treatment without WMT were included as a non-WMT comparison group (CON). The WMT group underwent multi-course interventions with longitudinal monitoring of pulmonary function parameters, inflammatory markers, breath-holding time (BHT), and 36-Item Short Form Health Survey scores (SF-36). Gut microbiota composition and predicted functional profiles were analyzed using 16S rRNA gene sequencing. After one WMT course, DG patients showed increases in forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1). Compared with the non-WMT comparison group, the change in FVC was greater in WMT recipients, whereas the between-group difference in FEV1 change was not statistically significant. Other spirometric indices, BHT, inflammatory markers, SF-36 scores, and microbiome-related findings were considered exploratory. Exploratory 16S rRNA gene sequencing identified differences in selected gut microbial taxa between WMT recipients with abnormal and normal spirometric patterns, including differences in Firmicutes, Faecalibacterium, and Alistipes. Predicted functional profiling suggested changes in glycerolipid metabolism-, Nod-like receptor signaling-, and bacterial chemotaxis-related functional potentials. WMT was associated with short-term changes in selected spirometric parameters, particularly FVC and FEV1, in patients with abnormal spirometric patterns. Changes in inflammatory markers, BHT, SF-36 scores, and microbiome-related findings were exploratory and hypothesis-generating. Further randomized, disease-specific studies with standardized pulmonary function testing and mechanistic validation are needed.},
}

@article {pmid42398209,
year = {2026},
author = {Zhang, C and Jiang, Y and Li, X and Wan, Z and Li, M and Xu, Q and Wang, W and Huo, J},
title = {Run Chang Tong Mi tea alleviates functional constipation through regulating gut microbiota and SCF/c-kit pathway.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {159},
number = {},
pages = {158519},
doi = {10.1016/j.phymed.2026.158519},
pmid = {42398209},
issn = {1618-095X},
abstract = {BACKGROUND: Functional constipation (FC) is a gastrointestinal motility disorder related to intestinal transit function and hormonal imbalance and has been reported to be associated with an imbalance in the gut microbiota. Clinically, Run Chang Tong Mi tea (RCTM) can effectively alleviate the constipation symptoms of patients with FC. However, the mechanism by which RCTM improves FC and its regulation of intestinal homeostasis remain unclear.

PURPOSE: This study aims to investigate the potential mechanism of RCTM alleviates FC by improving intestinal motility and mucosal secretion function through gut microbiota and its metabolites.

METHOD: The FC rat model was established by loperamide hydrochloride. The treatment effect of RCTM was evaluated by assessing stool frequency, fecal water content, time to first black stool, and small bowel transit rate. The histological changes of colon were observed by HE staining. Serum and colonic hormone levels were measured by ELISA. Immunohistochemistry was performed to assess the expression of tight junction proteins associated with the intestinal barrier. Western blotting and RT-qPCR were used to analyze the expression of SCF/c-kit pathway and intestinal barrier related proteins and mRNA, 16S rDNA sequencing was used to analyze the composition of intestinal microbiota, and GC/MS was used to detect SCFAs levels. By transplanting RCTM-treated fecal bacteria into FC rats, the relationship between the disturbance of gut microbiota, the onset of FC and the effect of RCTM intervention was further clarified.

RESULTS: RCTM can effectively restore the gastrointestinal motility and repair the damaged intestinal barrier in FC rats. RCTM promoted the secretion of excitatory hormones and neurotransmitters in the gastrointestinal tract, and regulated the mRNA and protein content of SCF/c-kit pathway. Furthermore, RCTM restored gut microbiota disorder and SCFAs content. More importantly, RCTM-FMT effectively alleviated constipation symptoms and increased gastrointestinal hormone and neurotransmitter levels, effects that were associated with alterations in the abundance of Lachnospiraceae and Lactobacillus as well as enhanced SCFA production. Moreover, RCTM-FMT improved intestinal barrier function, which was associated with decreased abundances of Escherichia-Shigella and Dubosiella.

CONCLUSION: Our findings indicate that RCTM alleviated constipation in rats with FC, and this amelioration was associated with modulation of the gut microbiota, elevation of SCFAs, and restoration of the SCF/c-kit pathway.},
}

@article {pmid42401355,
year = {2026},
author = {El-Sehrawy, AAMA and Farah, H and Oripov, F and Shakhmurova, G and Hussein, FM and Maharana, L and Singh, R and Tailor, NK},
title = {Estrobolome and the Endocrine-Microbiome Axis in Breast and Endometrial Carcinogenesis.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {105471},
doi = {10.1016/j.critrevonc.2026.105471},
pmid = {42401355},
issn = {1879-0461},
abstract = {The estrobolome, the community of gut microbial genes involved in estrogen metabolism, may influence hormone bioavailability and cancer risk, although human evidence remains largely associative. This review summarizes evidence that bacterial β-glucuronidases, sulfatases, and hydroxysteroid dehydrogenases regulate enterohepatic estrogen recycling, while microbial metabolism also shapes receptor signaling, genotoxic estrogen metabolites, inflammation, and immune responses. Observational studies link gut microbial composition and function with breast and endometrial cancer, but causality remains unproven. Early dietary, probiotic, antibiotic, and fecal microbiota transplantation studies show biological effects, yet they are not sufficient for clinical application. We propose a functional framework that prioritizes microbial enzymatic activity over taxonomy and highlight multiparametric biomarkers and selective β-glucuronidase inhibition as promising research directions for prevention and adjunct therapy in hormone-driven cancers.},
}

@article {pmid42393343,
year = {2026},
author = {Wang, S and Hu, S and Yan, Y and Wu, L and Tang, L and Hu, Y and Wang, W},
title = {Docosahexaenoic acid alleviates DSS-induced colitis by regulating the gut microbiota and restoring the gut barrier.},
journal = {International microbiology : the official journal of the Spanish Society for Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42393343},
issn = {1618-1905},
abstract = {Docosahexaenoic acid (DHA), a long-chain omega-3 polyunsaturated fatty acid, has well-recognized anti-inflammatory activity; however, the mechanisms underlying its protective effects in inflammatory bowel disease (IBD) remain incompletely understood. In this study, we investigated the effects of DHA in a dextran sulfate sodium (DSS)-induced mouse model of colitis and examined whether these effects were mediated by the gut microbiota. DHA administration markedly alleviated DSS-induced colitis, as indicated by reduced body weight loss, disease activity, mortality, colon shortening, histological injury, intestinal barrier disruption, and colonic inflammatory responses. 16 S rRNA gene sequencing showed that DHA reshaped the gut microbial community and increased the abundance of beneficial taxa, including Bifidobacterium. Antibiotic cocktail (ABX)-mediated microbiota depletion largely abolished the protective effects of DHA, whereas fecal microbiota transplantation (FMT) from DHA-treated donors transferred resistance to DSS-induced colitis to recipient mice. DHA also restored tight junction protein expression and increased the frequency of colonic regulatory T cells in a microbiota-dependent manner. These findings indicate that DHA alleviates experimental colitis by modulating the gut microbiota, restoring intestinal barrier integrity, and regulating mucosal immune homeostasis. DHA may therefore represent a promising dietary strategy for the prevention or adjunctive treatment of ulcerative colitis (UC).},
}

@article {pmid42394968,
year = {2026},
author = {Hu, Q and Jin, H and Hu, L and Li, X},
title = {The role of mitochondria in the gut-kidney axis: implications for kidney health.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1851705},
pmid = {42394968},
issn = {1663-9812},
abstract = {Mitochondria, multifunctional organelles that regulate cellular energy metabolism and signaling pathways, play a pivotal role in maintaining the physiological functions of the gut and kidneys, as well as influencing the progression of chronic kidney disease (CKD). Through the gut-kidney crosstalk, gut microbiota modulate gut and renal pathophysiology and also influence mitochondrial activity in intestinal and renal cells. This review explores the regulatory roles of mitochondria in preserving epithelial barrier integrity, regulating intestinal metabolism, and maintaining gut microbiota homeostasis. It also examines the contributions of mitochondrial biogenesis, dynamics, autophagy abnormalities, and mitochondrial DNA (mtDNA) damage to renal pathological progression. Moreover, we highlight the bidirectional interactions between intestinal and renal mitochondria via the microbiota-mitochondria-kidney axis and mechanisms involving inflammation, oxidative stress, and ferroptosis. Therefore, targeting mitochondrial regulation through non-pharmacological interventions such as dietary adjustments, probiotic supplementation and fecal microbiota transplantation (FMT) emerges as a promising therapeutic strategy for maintaining renal health by optimizing mitochondrial function. In conclusion, elucidating the mechanisms of mitochondrial involvement in the gut-kidney axis will lay the foundation for novel therapeutic approaches to CKD and other gut-kidney axis-related disorders.},
}

@article {pmid42395662,
year = {2026},
author = {Kashiv, P and Balwani, MR and Pasari, A and Saxena, K and Kute, VB},
title = {Trimethylamine N-oxide as a key microbial mediator in the progression of diabetic kidney disease.},
journal = {World journal of nephrology},
volume = {15},
number = {2},
pages = {117355},
pmid = {42395662},
issn = {2220-6124},
abstract = {In this editorial, we comment on the article by Song et al published in the recent issue of the World Journal of Nephrology, which investigates the mechanistic role of gut microbiota-derived trimethylamine N-oxide (TMAO) in accelerating diabetic kidney disease through renal fibrotic pathways. Diabetic kidney disease is increasingly recognised as a disorder influenced not only by intrinsic renal metabolic and inflammatory pathways. In the Zucker diabetic fatty model, the investigators demonstrate a reproducible pattern in which progression of renal injury is accompanied by distinct alterations in gut microbial composition and a marked rise in circulating TMAO concentrations. The incorporation of fecal microbiota transplantation further shows that the dysbiotic microbial environment characteristic of diabetic kidney disease possesses an intrinsically enhanced capacity to generate TMAO and can transfer this metabolic profile to recipient animals, establishing functional evidence that gut microbial changes can modify host metabolite production. Partial improvement in renal biochemical parameters, fibrotic protein expression, and histological abnormalities following inhibition of trimethylamine formation reinforces the mechanistic relevance of this pathway within the gut-kidney axis and supports the concept that therapeutic strategies targeting microbial metabolism may offer a promising direction for altering the clinical trajectory of diabetic kidney disease.},
}

@article {pmid42395675,
year = {2026},
author = {Almuhanna, AA and Vatte, C and Guo, Q and Elsalamouni, TS and Al-Muhanna, FA and Aboalrihy, AM and Alhabib, HA and Almomen, MF and Alali, RA and Habara, AH and Alrubaish, MA and Alfalah, KM and Cyrus, C and Abdul-Rahman, IS and Keating, BJ and Al-Ali, AK and Wang, C},
title = {Gut microbiota in a Saudi population with chronic kidney disease.},
journal = {World journal of nephrology},
volume = {15},
number = {2},
pages = {118343},
pmid = {42395675},
issn = {2220-6124},
abstract = {BACKGROUND: The gut microbiota (GM) plays an important role in chronic kidney disease (CKD) progression, and dialysis modalities can differentially impact the GM composition and function. There is also limited information on the GM in Arab populations.

AIM: To investigate the distinct microbial profiles and functional alterations associated with hemodialysis (HD) and peritoneal dialysis (PD) in a Saudi Arabian cohort.

METHODS: We performed whole-genome metagenomic sequencing on fecal samples from 189 participants (controls and CKD, HD, and PD patients).

RESULTS: We detected distinct microbial profiles across all patient groups compared with that of the controls. Microbial risk scores derived from differentially abundant taxa accurately distinguished CKD, PD, and HD patients from controls, with area under the curves exceeding 0.9. Compared with HD patients, PD patients exhibited reduced species richness, an increased abundance of opportunistic pathogens (particularly Proteobacteria), and increased virulence. Functional analysis revealed suppressed energy metabolism and activated proinflammatory pathways in PD patients. Cooccurrence network analysis demonstrated decreased microbial community resilience in PD patients, with increased Proteobacteria interactions. Conversely, the HD group showed partial recovery of microbial balance and beneficial metabolic functions, including increased short-chain fatty acid metabolism and reduced lipopolysaccharide biosynthesis.

CONCLUSION: The findings of this study highlight the potential of the microbial profile as a robust biomarker for CKD classification and underscore the differential impacts of different dialysis modalities.},
}

@article {pmid42397471,
year = {2026},
author = {Li, X and Li, H and Wang, Q and Gao, X and Gao, J and Du, M and Zhang, W and Liu, S and Liang, Y and Li, Q and Gan, Y and Tu, H},
title = {Enriched environment inhibits melanoma by reshaping gut microbiota and enriching Parabacteroides distasonis.},
journal = {Cellular oncology (Dordrecht, Netherlands)},
volume = {},
number = {},
pages = {},
doi = {10.1007/s13402-026-01249-8},
pmid = {42397471},
issn = {2211-3436},
support = {82003249//the National Natural Science Foundation of China/ ; 82203173//the National Natural Science Foundation of China/ ; 82173381//the National Natural Science Foundation of China/ ; 24ZR1465400//Natural Science Foundation of Shanghai/ ; ZZ94-2307//the State Key Laboratory of Systems Medicine for Cancer/ ; },
abstract = {PURPOSE: The role of psychological factors in the holistic regulation of cancer has garnered significant attention. Psychological eustress induced by an enriched environment (EE) inhibits various cancers including melanoma, but underlying mechanisms remain largely unknown. The brain-gut axis may play a key role in modulating psychological factors and cancer progression. This study investigates the role of gut microbiota in EE-induced anti-melanoma effects.

METHODS: C57BL/6 mice were housed in EE or standard environment (SE). Longitudinal fecal samples from EE and SE mice underwent 16S rRNA gene sequencing. SE melanoma-bearing mice received fecal microbiota transplantation (FMT) from EE or SE donors to assess the microbiota's causal role in EE's anti-tumor effects. Bacterial species upregulated by EE in tumor-bearing mice were identified;Parabacteroides distasonis (Pd) was selected for therapeutic administration. Immune cells in spleen and tumor were quantified by flow cytometry. Natural killer (NK) cell function was tested using anti-NK1.1 depletion.

RESULTS: EE increased the alpha diversity of the gut microbiota and alleviated the dysbiosis caused by melanoma. FMT from EE mice to SE mice inhibited melanoma growth, suggesting that the gut microbiota contributes to EE's anti-tumor effects. EE upregulated seven bacterial species in tumor-bearing mice, including Pd. Oral administration of Pd inhibited melanoma growth and increased intratumoral NK/NKT cell proportions and NK cell granzyme B expression. NK cell depletion abrogated Pd's anti-tumor effect.

CONCLUSION: This study underscores the interconnectedness of psychological eustress, gut microbiota, and cancer, providing preclinical insights into holistic cancer treatments. Leveraging the brain-gut-cancer axis, targeting psychological factors and gut microbiota could offer a potential adjunctive strategy for melanoma management.},
}

@article {pmid42398208,
year = {2026},
author = {Yi, Y and Li, D and Li, Y and Wang, H and Yang, D and Yang, S and Xing, S and Wei, S and Yang, J and Guo, H and Luo, Z},
title = {Abrus cantoniensis α-glucan-like polysaccharide alleviates influenza via gut microbial acetate to activate free fatty acid receptor 2/ mitochondrial antiviral signaling protein/interferon-beta pathway.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {159},
number = {},
pages = {158533},
doi = {10.1016/j.phymed.2026.158533},
pmid = {42398208},
issn = {1618-095X},
abstract = {BACKGROUND: The gut microbiota is critical for host defense against influenza. Polysaccharides are known for their microbiota-modulating and immunomodulatory activities; however, the anti-influenza efficacy of homogeneous Abrus cantoniensis polysaccharides (ACP) remains unexplored.

PURPOSE: The present study seeks to clarify the protective role of ACP in influenza and explore its underlying molecular mechanisms.

METHODS: Initially, crude polysaccharides were extracted via ethanol precipitation and subsequently purified by gel chromatography. Systematic structural characterization of ACP was then performed using carbohydrate chemistry techniques, including scanning electron microscopy (SEM), Fourier-transform infrared spectroscopy (FTIR), ultraviolet (UV) spectroscopy, and nuclear magnetic resonance (NMR). The therapeutic efficacy of ACP was assessed by monitoring various indicators such as body weight, survival rate, viral load, and pulmonary pathological changes in mouse models. Furthermore, to elucidate the biological mechanism underlying ACP's anti-influenza activity via regulation of pulmonary interferon-beta (IFN-β) immune networks by intestinal acetate-producing microbiota, multi-omics analyses integrating metagenomics, metabolomics, gene knockout, immunofluorescence, and Western blot were conducted. Finally, the potential anti-influenza effects of ACP via the gut-lung axis were evaluated based on in vivo and in vitro detection of protein expression of IFN-β, free fatty acid receptor 2 (FFAR2), and mitochondrial antiviral signaling protein (MAVS), as well as antiviral interferon-stimulated genes (ISGs).

RESULTS: In this study, we purified a novel polysaccharide, ACP-A1, with a backbone of→4)-α-D-Glcp-(1→,→4)-β-D-Galp-(1→, and →4,6)-α-D-Glcp-(1→ linkages and α-D-Glcp-(1→ branches at O-6. In H1N1-infected mice, oral ACP-A1 alleviated weight loss, increased survival, and reduced lung inflammation and viral load. Metagenomic and targeted metabolomic analyses showed that ACP-A1 enriched Limosilactobacillus reuteri and elevated acetate levels. Fecal microbiota transplantation, FFAR2 inhibition, and MAVS knockout experiments demonstrated that ACP-A1 enhances the FFAR2/MAVS/IFN-β antiviral pathway via microbial-derived acetate.

CONCLUSION: Collectively, our findings elucidate that ACP mitigates influenza virus-induced lung dysfunction by promoting the proliferation of acetate-producing gut microbiota, particularly Limosilactobacillus reuteri, and activating the FFAR2/MAVS/IFN-β antiviral axis in pulmonary immune cells. These findings establish ACP-A1 as a natural polysaccharide regulating IFN-β homeostasis, highlighting its potential for influenza prevention.},
}

@article {pmid42387047,
year = {2026},
author = {Qi, XY and Wang, MY and Wei, TC and Shao, FB and Liu, SH and Han, D and Cheng, JW and Zhao, YH and Shi, L and Luo, J and Cheng, T and Zhang, SX},
title = {Microbiome immune crosstalk in Sjögren's syndrome: mechanistic insights and translational perspectives.},
journal = {Immunologic research},
volume = {74},
number = {1},
pages = {},
pmid = {42387047},
issn = {1559-0755},
support = {No. 202203021221269//Natural Science Foundation of Shanxi Province/ ; No. 82001740//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Sjogren's Syndrome/immunology/microbiology/therapy/etiology ; *Dysbiosis/immunology ; Animals ; *Microbiota/immunology ; Multiomics ; Probiotics/therapeutic use ; *Gastrointestinal Microbiome/immunology ; T-Lymphocytes, Regulatory/immunology ; },
abstract = {Sjögren's syndrome (SS) is a systemic autoimmune disorder driven by interactions among genetic susceptibility, environmental factors, and alterations in mucosal microbial ecosystems. Emerging evidence from studies of the gut, oral cavity, and ocular surface indicates that microbial dysbiosis is closely associated with SS. Patients frequently exhibit reduced beneficial commensals and expansion of potentially pathogenic taxa, accompanied by epithelial barrier disruption, imbalance of T helper 17 and regulatory T cells, abnormal B-cell responses, and sustained activation of type I interferon signaling. Several mechanisms may contribute to disease development, including molecular mimicry, exosome-mediated immune communication, and alterations in microbiota-derived metabolites. Integrated multi-omics approaches, particularly high-throughput sequencing and metabolomics, have revealed SS-associated microbial signatures and metabolic pathway changes, offering insights for biomarker discovery and therapeutic targeting. Microbiota-directed strategies, such as probiotic supplementation, fecal microbiota transplantation, and investigations of drug-microbiome interactions, have shown potential to restore immune homeostasis. However, current evidence remains limited by small cohort sizes, methodological heterogeneity, and insufficient clarification of causal relationships. This review summarizes microbial alterations in SS, their roles in immune dysregulation, and the therapeutic potential of microbiome-based interventions within the framework of personalized medicine.},
}

Humans
*Sjogren's Syndrome/immunology/microbiology/therapy/etiology
*Dysbiosis/immunology
Animals
*Microbiota/immunology
Multiomics
Probiotics/therapeutic use
*Gastrointestinal Microbiome/immunology
T-Lymphocytes, Regulatory/immunology

@article {pmid42387077,
year = {2026},
author = {Chen, J and Chen, L and Cai, G and Chen, Y and Zeng, Y and Zhang, Y and Huang, J and Xia, G and Wang, C and Feng, A and Nie, X},
title = {The involvement of Anaeroplasma, caproic acid, and interleukins through the brain-gut axis may contribute to IgAV with neurological involvement.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {42387077},
issn = {1530-0447},
abstract = {BACKGROUND: Immunoglobulin A vasculitis (IgAV), the most prevalent pediatric systemic vasculitis, may involve central nervous system (CNS) manifestations with unknown mechanisms.

METHODS: To investigate gut-brain axis interactions, human gut microbiota from IgAV with or without neurological involvement and healthy children were transplanted into specific pathogen-free mice. The recipients' microbiota, fecal short-chain fatty acids (SCFAs), and serum cytokines were analyzed alongside electroencephalogram (EEG) monitoring.

RESULTS: Spike waves emerged exclusively in the EEGs of mice receiving transplants from neurologically affected IgAV children. Comparative analyses demonstrated: enrichment of Anaeroplasma in the IgAV with neurological involvement (IgAVNI) group compared to IgAV controls (P < 0.05); elevated caproic acid in IgAVNI versus controls (P < 0.05); reduced IL-1α in IgAVNI versus controls (P < 0.05); and a positive correlation between Anaeroplasma and IL-17A (r = 0.94, P = 0.004).

CONCLUSION: Gut microbiota, notably Anaeroplasma, may trigger IgAV-related CNS involvement via the gut-brain axis, co-mediated through regulation of caproic acid, IL-1α, and IL-17A.

IMPACT: First evidence that Anaeroplasma drives IgAV CNS manifestations via the gut-brain axis by regulating caproic acid, IL-1α, and IL-17A, with EEG spike waves as a specific marker. The Anaeroplasma-caproic acid-IL-17A axis fills a mechanistic gap in IgAV neurological complications, transcending current immunoinflammatory paradigms. Provides combined EEG/microbiota/metabolite biomarkers for early prediction and suggests Anaeroplasma, IL-17A, and caproic acid may represent therapeutic targets for neuroprotective interventions.},
}

@article {pmid42388391,
year = {2026},
author = {Fernandez, MF and Stricker, A and Bottero, A and Busquet, L and Waldbaum, C and Mingorance, FL and Patetta, RM and Toer, I and Juliá, A and Mangano, A},
title = {Correction: Fecal microbiota transplantation promotes gut microbiome recovery in pediatric hematopoietic stem cell transplant recipients.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1904862},
doi = {10.3389/frmbi.2026.1904862},
pmid = {42388391},
issn = {2813-4338},
abstract = {[This corrects the article DOI: 10.3389/frmbi.2026.1849762.].},
}

@article {pmid42388392,
year = {2026},
author = {Zhao, J and Fan, Y and Yang, K and Gao, H},
title = {Fecal microbiota transplantation: from empirical remedy to precision medicine.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1863308},
pmid = {42388392},
issn = {2813-4338},
abstract = {Fecal microbiota transplantation (FMT) has evolved from an empirical remedy for recurrent Clostridioides difficile infection (rCDI) into a foundational platform for precision microbiome-based therapeutics. This comprehensive review details FMT's journey, analyzing its multifaceted mechanisms of action-including restoration of colonization resistance, metabolic reprogramming via short-chain fatty acids and bile acids, and profound immunomodulation-which extend far beyond simple microbial replacement. We critically evaluate its established, high efficacy in rCDI and its expanding, albeit more variable, applications across a wide spectrum of gastrointestinal diseases (such as inflammatory bowel disease, irritable bowel syndrome, and constipation), neurological disorders (including Parkinson's and Alzheimer's disease), metabolic conditions, autoimmune diseases, and oncology (particularly in modulating response to immune checkpoint inhibitors and treating graft-versus-host disease). The review further discusses the critical challenges of donor-recipient variability, safety, and the lack of standardized protocols that have driven the field's technical evolution. This progression encompasses refined processing methods like washed microbiota transplantation (WMT), diverse delivery routes including oral capsules, and the exploration of non-bacterial components like bacteriophages through fecal filtrate transplantation (FVT). Ultimately, we highlight the field's trajectory toward next-generation, defined live biotherapeutic products (LBPs) and engineered microbial consortia, aiming to transition from the complex "black box" of whole stool to safer, more consistent, and rationally designed precision therapies that target the specific dysbiotic networks underlying diverse human diseases.},
}

@article {pmid42388393,
year = {2026},
author = {Fernandez, MF and Stricker, A and Bottero, A and Busquet, L and Waldbaum, C and Mingorance, FL and Patetta, RM and Toer, I and Juliá, A and Mangano, A},
title = {Fecal microbiota transplantation promotes gut microbiome recovery in pediatric hematopoietic stem cell transplant recipients.},
journal = {Frontiers in microbiomes},
volume = {5},
number = {},
pages = {1849762},
pmid = {42388393},
issn = {2813-4338},
abstract = {INTRODUCTION: Hematopoietic stem cell transplantation (HSCT) profoundly disrupts the gut microbiome and may contribute to adverse post-transplant outcomes. Fecal microbiota transplantation (FMT) has emerged as a strategy to restore microbial diversity; however, data in pediatric HSCT recipients remain limited.

METHODS: We conducted a longitudinal analysis of 17 pediatric HSCT recipients who received FMT. Fecal samples were collected before FMT and at days 7, 14, and 30 after treatment. Gut microbiome composition was analyzed using 16S rRNA gene sequencing.

RESULTS: Baseline samples showed reduced microbial diversity and a dysbiotic microbial profile. Following FMT, microbial diversity increased progressively, with recovery evident from day 7 and stabilization by day 30. Taxonomic analyses demonstrated depletion of dysbiosis-associated genera and enrichment of beneficial short-chain fatty acid-producing taxa, including Faecalibacterium, Blautia, Subdoligranulum, and Akkermansia. Distinct microbial configurations were observed according to gastrointestinal involvement by acute graft-versus-host disease.

CONCLUSIONS: FMT was associated with progressive restoration of gut microbiome diversity and structure in pediatric HSCT recipients, supporting its potential role as a microbiota-based strategy to promote ecological recovery after HSCT.},
}

@article {pmid42388848,
year = {2026},
author = {Yang, K and Peng, G and Zhang, X and Yang, D and Wang, Y and Chen, R},
title = {Host genotype is associated with selective colonization of human fecal microbiota in NCG and SGM3 mice: implications for microbiota-based therapies.},
journal = {Bioscience of microbiota, food and health},
volume = {45},
number = {3},
pages = {188-196},
pmid = {42388848},
issn = {2186-6953},
abstract = {Humanized mouse models are widely used to investigate host-microbiota interactions, yet the extent to which host background contributes to engraftment fidelity remains incompletely defined. In this study, we transplanted fecal microbiota from healthy human donors into NCG and SGM3 mice and characterized engraftment using 16S rRNA sequencing. Both models exhibited reduced diversity relative to donors, but their colonization trajectories diverged. NCG recipients appeared closer to donors in β-diversity space, a pattern largely associated with the expansion of a limited set of opportunistic Proteobacteria such as Escherichia-Shigella and Citrobacter. In contrast, SGM3 mice displayed modestly higher α-diversity and retained a broader set of donor-associated genera, with selective enrichment of Bacillus, yet exhibited greater predicted functional divergence, with reductions in pathways related to ABC transport and carbohydrate metabolism. Several strictly anaerobic commensals, including Faecalibacterium, failed to colonize in either genotype. Collectively, these findings suggest that host genotype is associated with selective colonization of human fecal microbiota and support the utility of integrating compositional and functional criteria when selecting experimental models for translational microbiome research.},
}

@article {pmid42389273,
year = {2026},
author = {Guo, Y and Hu, F and Zhao, AZ and Zeng, Y and Chen, H and Wang, A and Li, X and Cong, L},
title = {Omega-3 polyunsaturated fatty acids are associated with microbiota-related 18β-glycyrrhetinic acid alterations and M2 macrophage polarization in type 1 diabetes mellitus.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1871892},
pmid = {42389273},
issn = {1663-9812},
abstract = {INTRODUCTION: Omega-3 polyunsaturated fatty acids (PUFAs) have been widely reported to exert beneficial effects in type 1 diabetes mellitus (T1DM). However, the mechanisms by which Omega-3 PUFAs influence pancreatic islet function through the gut-islet axis remain incompletely understood. This study aimed to investigate whether Omega-3 PUFAs-associated alterations in gut microbiota composition and their metabolites are involved in the modulation of the pancreatic islet microenvironment in T1DM, and to explore the potential immunological mechanisms underlying these effects.

METHODS: Fecal microbiota transplantation (FMT) was performed to evaluate the effects of Omega-3 PUFAs-associated gut microbiota in non-obese diabetic (NOD) mice. Immune cell composition and inflammatory status within pancreatic islets were analyzed using transcriptomic profiling, flow cytometry, and immunohistochemistry. Metabolomics analysis was performed to investigate the association among Omega-3 PUFAs, gut microbiota, and microbiota-related metabolites. In vitro co-culture systems were further established to evaluate the effects of selected metabolites on macrophage polarization and insulin production and secretion in pancreatic β-cells.

RESULTS: Omega-3 PUFAs treatment and FMT were associated with reduced islet inflammation and a marked enrichment of the Eubacterium coprostanoligenes group (E. coprostanoligenes). Enhanced M2 macrophage polarization was observed in the islet microenvironment of FMT mice. Among gut microbiota metabolites, 18β-glycyrrhetinic acid (18β-GA) showed a strong association with E. coprostanoligenes, and in vitro experiments suggested a potential involvement of E. coprostanoligenes in the metabolic conversion process related to 18β-GA. In co-culture systems, 18β-GA promoted macrophage polarization toward an M2-like phenotype, which was accompanied by increased insulin production and secretion in pancreatic β-cells.

CONCLUSION: These findings suggest that Omega-3 PUFAs-associated alterations in gut microbiota composition and 18β-GA-related metabolic changes may contribute to the modulation of the pancreatic immune microenvironment and β-cells function in T1DM. This study provides additional insights into lipid-microbiota-immune interactions relevant to T1DM and supports further investigation of microbiota-associated immune regulation.},
}

@article {pmid42389275,
year = {2026},
author = {Zhang, P and Zhuang, YD and Lv, WW and Zhao, Y and Wang, JH and Zhang, JY and Wu, LL},
title = {Role of gut microbiota in melanosis coli: from anthraquinone biotransformation to mucosal homeostasis dysbiosis.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1791164},
pmid = {42389275},
issn = {1663-9812},
abstract = {Melanosis coli (MC) is a benign and usually reversible condition characterized by brownish-black pigmentation of the colonic mucosa and is commonly associated with chronic exposure to anthraquinone laxatives (ALs). The best-established histopathological sequence involves AL-related epithelial apoptosis, phagocytosis of apoptotic bodies by macrophages, and subsequent lipofuscin deposition. Emerging evidence suggests that the gut microbiota (GM) may contribute to this process by converting pharmacologically inactive anthraquinone glycosides into active anthrone metabolites, including rhein anthrone. This narrative review summarizes available MC-specific findings and clearly distinguishes them from mechanistic hypotheses extrapolated from constipation, intestinal barrier, and microbiome literature. We discuss microbial β-glucosidases and reductases involved in AL biotransformation, reported changes in microbial diversity and SCFA-producing taxa in MC or constipation-associated cohorts, and plausible links with barrier dysfunction, bile-acid metabolism, tryptophan-derived metabolites, and LPS-TLR4 signaling. We therefore present the "Microbiota-Apoptosis Axis" as a proposed framework rather than a validated causal pathway. Finally, we review GM-targeted strategies, including probiotics, synbiotics, and fecal microbiota transplantation, while emphasizing that direct clinical evidence in MC remains limited and that cessation of anthraquinone laxatives remains the primary management strategy.},
}

@article {pmid42389522,
year = {2026},
author = {Qian, N and Zhu, S and Song, Y and Yang, Y and Wang, H and Han, H and Xu, G and Hao, W and Jiang, H and Yang, Y and Xi, H and Ding, Y and He, W and Wei, T and Yang, W and Cheng, T},
title = {The gut-liver-kidney-brain axis in Wilson disease: copper speciation-flux and barrier-mediated organ crosstalk.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1840716},
pmid = {42389522},
issn = {1664-3224},
mesh = {*Hepatolenticular Degeneration/metabolism/therapy ; *Copper/metabolism ; Animals ; Humans ; *Liver/metabolism ; *Kidney/metabolism ; *Blood-Brain Barrier/metabolism ; *Brain/metabolism ; Intestinal Barrier Function ; Copper-Transporting ATPases/genetics ; Gastrointestinal Microbiome ; Intestinal Mucosa/metabolism ; Cuproptosis ; Mice ; },
abstract = {Wilson disease (WD) has long been framed as a hepatocentric disorder of copper accumulation. That view is now giving way to a broader model centered on the gut-liver-kidney-brain axis. In WD, copper is not simply stored in tissues as an inert burden. It circulates in dynamic, bioactive pools-particularly relative exchangeable copper (REC)-that disrupt barrier structures, including the intestinal epithelium and blood-brain barrier, and spread toxicity through measurable biochemical mediators. Major pathogenic processes include copper-induced suppression of autophagy, disruption of FXR-regulated bile acid signaling, and direct injury to the intestinal barrier. Gut dysbiosis, supported by fecal microbiota transplantation (FMT) studies in ATP7B-deficient mice, further amplifies hepatic inflammation and favors copper retention. Renal tubular dysfunction and neurotoxicity appear to reflect copper species-dependent passage across biological barriers together with secondary metabolic disturbances, including the recently described pathway of cuproptosis. In the clinic, this shift has been accompanied by greater use of copper-species biomarkers such as ceruloplasmin oxidase activity and REC, along with advanced imaging approaches such as [64]Cu-PET/CT. Treatment is also moving beyond conventional chelation alone, with increasing attention to biliary copper excretion, epithelial barrier repair, and microbiome-directed interventions. Viewed in this way, the axis model helps explain the marked phenotypic heterogeneity of WD and offers a mechanistic basis for more precise interventions aimed at breaking pathogenic feedback loops across organs.},
}

*Hepatolenticular Degeneration/metabolism/therapy
*Copper/metabolism
Animals
Humans
*Liver/metabolism
*Kidney/metabolism
*Blood-Brain Barrier/metabolism
*Brain/metabolism
Intestinal Barrier Function
Copper-Transporting ATPases/genetics
Gastrointestinal Microbiome
Intestinal Mucosa/metabolism
Cuproptosis
Mice

@article {pmid42391840,
year = {2026},
author = {Yi, X and Zhang, Y and Yang, K and Li, B and Liu, F and Tian, G and Zhang, J and Yan, T and Li, J and Li, W and Li, L and Jing, R and Zhang, Z and Qiu, X and Xiao, J and Zhang, W},
title = {6PPD-Q exposure disrupts intestinal homeostasis and impairs skeletal muscle function in mice.},
journal = {Ecotoxicology and environmental safety},
volume = {321},
number = {},
pages = {120470},
doi = {10.1016/j.ecoenv.2026.120470},
pmid = {42391840},
issn = {1090-2414},
abstract = {6PPD-Q is an emerging tire-derived contaminant, but its mammalian toxicological mechanisms and inter-organ effects remain poorly understood. Because oral exposure directly interfaces with the intestine, we investigated whether 6PPD-Q disrupts intestinal homeostasis and is associated with skeletal muscle dysfunction through a microbiota-related gut-muscle axis, and whether post-exposure sodium butyrate (NaB) intervention can alleviate these alterations. Male C57BL/6 mice were orally exposed to 6PPD-Q at 0.1, 1, or 10 μg/kg/day, and NaB intervention was evaluated after high-dose exposure. Toxic effects were mainly observed at 1 and 10 μg/kg/day. 6PPD-Q accumulated predominantly in the intestine and induced villus-crypt disruption, microvillus damage, increased permeability, inflammatory activation, and oxidative imbalance. These alterations were accompanied by reduced exercise performance, smaller myofiber cross-sectional area, and impaired myogenic differentiation. Low residual 6PPD-Q levels in perfused skeletal muscle and tissue-equivalent C2C12 exposure results suggested that intestinal dysfunction may contribute to muscle impairment. 6PPD-Q also altered gut microbial composition and fecal short-chain fatty acid profiles, with reduced butyrate emerging as a candidate metabolic alteration associated with muscle dysfunction. Fecal microbiota transplantation from 6PPD-Q-exposed donors partially transferred intestinal barrier dysfunction, inflammatory and oxidative disturbances, reduced butyrate levels, and muscle-related abnormalities to recipients, whereas microbiota from NaB-treated donors attenuated these effects. Post-exposure NaB intervention partially alleviated intestinal, microbial, metabolic, and skeletal muscle alterations without substantially reducing tissue 6PPD-Q burden.These findings suggest that oral 6PPD-Q exposure disrupts intestinal homeostasis and microbiota-SCFA profiles, which may contribute to gut-muscle axis-associated skeletal muscle dysfunction in mice.},
}

@article {pmid42391938,
year = {2026},
author = {Yi, L and Shi, W and Jia, H and Song, G and Zhang, W and Bai, G and Zhu, J and Zhao, S},
title = {From composition to function: Translating porcine gut microbiota research into strategies for improving intestinal health.},
journal = {Microbiological research},
volume = {311},
number = {},
pages = {128612},
doi = {10.1016/j.micres.2026.128612},
pmid = {42391938},
issn = {1618-0623},
abstract = {The gut microbiota plays a pivotal role in regulating host physiology, metabolism, and overall health. The diverse geographical landscape of China has contributed to the development of rich indigenous pig genetic resources, which exhibit stronger disease resistance than commercial breeds, largely attributed to the composition of their gut microbiota. Given the substantial anatomical and physiological similarities between pigs and humans concerning intestinal structure, and the fact that human-derived microorganisms can effectively colonize the porcine gut, pigs serve as excellent models for intestinal diseases. This review summarizes the geographical and spatial ecological niches of gut microbiota in Chinese indigenous pig breeds, the influences of age and environment on microbial composition, and the beneficial roles of certain microbial taxa from these local breeds in preventing intestinal disorders, including diarrhea associated with impaired intestinal barrier function, pathogen-induced diarrhea, porcine epidemic diarrhea virus infection, intestinal inflammation models, human rotavirus infection, and necrotizing enterocolitis. Their gut microbiota is characterized by the enrichment of Akkermansia, Lactobacillus, Prevotella, Bacillus, Bifidobacterium, Faecalibacterium, and Bacteroides, which have been implicated in maintaining intestinal barrier integrity and reducing inflammatory cytokine levels during pathogen-induced intestinal inflammation. In the context of gastrointestinal disease prevention and treatment, strategies have largely centered on fecal microbiota transplantation, fecal suspension transplantation, or supplementation with single bacterial strains. However, research on multi-strain combinatorial therapeutics remains limited. Future studies should expand to underexplored indigenous breeds and prioritize the development of composite microbial consortia informed by existing findings.},
}

@article {pmid41575630,
year = {2026},
author = {Weirauch, T and Yahav, D and Zahavi, I and Würstle, S and Vehreschild, MJGT},
title = {A review on antibiotic and non-antibiotic decolonization strategies of multidrug-resistant bacteria in the gastrointestinal tract.},
journal = {Infection},
volume = {54},
number = {3},
pages = {1041-1062},
pmid = {41575630},
issn = {1439-0973},
mesh = {Humans ; *Anti-Bacterial Agents/therapeutic use/pharmacology ; *Drug Resistance, Multiple, Bacterial ; *Gastrointestinal Tract/microbiology ; *Bacterial Infections/microbiology/therapy/drug therapy ; *Bacteria/drug effects ; Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome/drug effects ; Probiotics ; },
abstract = {The escalating global threat of antimicrobial resistance represents a critical challenge for contemporary medicine. Intestinal colonization by multidrug-resistant organisms (MDROs) is increasingly identified as a primary driver of hospital-acquired infections across various patient cohorts. While localized eradication via non-absorbable antibiotics was once viewed as a viable strategy, clinical evidence has failed to demonstrate its efficacy. Consequently, attention has shifted toward microbiome-modulating interventions, such as fecal microbiota transfer (FMT), probiotics, and live biotherapeutic products (LBPs), which have shown potential in preliminary studies. However, current evidence remains fragmented and lacks the support of large-scale randomized controlled trials (RCTs). This review critically assesses both traditional and novel decolonization methods and features a comprehensive summary of clinical studies to highlight existing research gaps. A notable limitation of this analysis is the absence of a formal methodological quality assessment for the included studies. Ultimately, definitive conclusions remain elusive, necessitating future large-scale, pathogen-specific RCTs to validate these emerging approaches.},
}

Humans
*Anti-Bacterial Agents/therapeutic use/pharmacology
*Drug Resistance, Multiple, Bacterial
*Gastrointestinal Tract/microbiology
*Bacterial Infections/microbiology/therapy/drug therapy
*Bacteria/drug effects
Fecal Microbiota Transplantation
*Gastrointestinal Microbiome/drug effects
Probiotics

@article {pmid42375606,
year = {2026},
author = {Fu, S and Liao, W and He, B and Wu, H and Huang, J and Jiang, W},
title = {Hylocereus undatus flower inhibits lipopolysaccharide-induced acute lung injury in mice by regulating the gut-lung axis and inflammatory response.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1803336},
pmid = {42375606},
issn = {1663-9812},
abstract = {BACKGROUND: Hylocereus undatus flower (HUF), the dried flower of H. undatus (Haw.) Britton and Rose, was first recorded in the Lingnan Record of Medicinal Herbs and is now listed in the Dictionary of Traditional Chinese Medicines. As an established traditional remedy, HUF is primarily used to treat various pulmonary conditions, including pneumonia, asthma, and tuberculosis. Acute lung injury (ALI) represents a critical and common pathological manifestation underlying severe respiratory disorders. However, the potential protective effects of HUF against ALI, and the specific mechanisms involved, remain unelucidated.

PURPOSE: To systematically evaluate the protective effects of HUF extract on ALI and the pharmacological mechanisms involved.

METHODS: Using a lipopolysaccharide-induced mouse model of ALI, we investigated the effects of HUF on the intestinal microbiota of ALI mice via microbial sequencing, metabolomics sequencing, and fecal microbiota transplantation (FMT). We explored the targets and signaling pathways of HUF intervention using transcriptomics and network pharmacology methods and then validated our results using immunological experiments and polymerase chain reaction analysis (PCR).

RESULTS: HUF reduced lung indices and wet-dry ratios associated with pulmonary edema, alleviated inflammatory responses, and mitigated the severity of pulmonary pathological damage. HUF also increased the expression of intestinal tight junction protein (ZO-1), modulated the structure and relative abundance of the gut microbiota, and elevated the levels of certain short-chain fatty acids (SCFAs). FMT experiments confirmed that the HUF-mediated remodeling of the microbiota played a significant role in alleviating ALI. Transcriptomics and network pharmacology analyses suggested that the mechanism underling the interventional effect of HUF on ALI is related to inflammatory pathways. Immunological and PCR experiments further confirmed an association with the P38 mitogen-activated protein kinase (MAPK) pathway.

CONCLUSION: HUF is associated with attenuation of ALI, correlating with modulation of the gut-lung axis and the inflammatory pathways, and HUF may be a candidate for the treatment of ALI.},
}

@article {pmid42379287,
year = {2026},
author = {Brett Moreau, G and Petri, WA},
title = {The Impact of Fecal Microbiota Transplantation on Host Immunity and Epithelial Restoration Following Clostridioides difficile Infection.},
journal = {Anaerobe},
volume = {},
number = {},
pages = {103060},
doi = {10.1016/j.anaerobe.2026.103060},
pmid = {42379287},
issn = {1095-8274},
abstract = {Fecal microbiota transplantation (FMT) has emerged as an effective therapy for the prevention of recurrent Clostridioides difficile infection (rCDI). Despite this therapeutic success, questions remain about safety and standardization of protocols, leading to calls for more defined biotherapeutics. While FMT-mediated protection is associated with restoration of the intestinal microbiota and metabolome, our understanding of its impact on host immune responses and restoration of colonic homeostasis remains incomplete. In this review, we focus on our current knowledge regarding the effects of FMT on host responses, including immune responses, colonic barrier restoration, and host metabolism. FMT is associated with restoration of immune signaling, which is depleted following antibiotic therapy. Restoration is associated with a shift towards type 2 and regulatory immune responses that limit intestinal inflammation and promote repair. FMT also modifies non-immune cells, promoting enhanced barrier integrity and significantly modifying host metabolism within the gut. FMT studies utilize a variety of experimental protocols and FMT formulations, and more mechanistic studies are required to understand how this variation impacts microbiota and host-directed changes. Better understanding of the immune and metabolic changes associated with protection against rCDI will allow for the design of more targeted therapeutics.},
}

@article {pmid42382190,
year = {2026},
author = {Duan, R and Wang, K and Duan, L},
title = {Mother-to-offspring microbial vertical transmission: timing, determinants, and impact on offspring susceptibility to gastrointestinal diseases.},
journal = {Medical review (2021)},
volume = {6},
number = {3},
pages = {243-261},
pmid = {42382190},
issn = {2749-9642},
abstract = {The establishment of the early-life microbiota is profoundly shaped by microbial vertical transmission from mother to offspring. This review synthesized the current understanding of the timing, determinants, and health implications of mother-to-offspring microbial vertical transmission. We detailed the contentious evidence regarding prenatal microbial transmission and highlighted the well-established roles of intrapartum and postnatal transmission via birth and breastfeeding, respectively. Multiple factors, including delivery mode, gestational age, feeding patterns and antibiotic exposure, are critical modulators of microbial transmission, shaping the initial microbial community. Emerging intervention strategies, such as breastfeeding, probiotic supplementation, vaginal microbiota transplantation, and fecal microbiota transplantation, offer promising avenues for restoring a healthy microbial trajectory when natural transmission is disrupted. This review underscores that vertical transmission is the cornerstone of intergenerational microbiome inheritance and a potential therapeutic target for preventing early-life dysbiosis and associated diseases.},
}

@article {pmid42382341,
year = {2026},
author = {Zhang, S and Zhang, T and Zhang, Y and Ye, C and Mu, L and He, Q and Huang, T and Wang, G and Li, Y and Xie, S and Tang, X},
title = {Correction: Akkermansia muciniphila regulates the gut microenvironment and alleviates periodontal inflammation in mice with periodontitis.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1892163},
doi = {10.3389/fmicb.2026.1892163},
pmid = {42382341},
issn = {1664-302X},
abstract = {[This corrects the article DOI: 10.3389/fmicb.2025.1643691.].},
}

@article {pmid42382646,
year = {2026},
author = {Peng, Z and Hu, Y and Wang, S and Liu, C and Zhou, Q and Xie, S and Huang, S and Liu, N and Wang, Y},
title = {Case Report: Allergic reaction following fecal microbiota transplantation in children with autism spectrum disorder: a report of two cases.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1847568},
pmid = {42382646},
issn = {2296-2360},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is increasingly used in children with autism spectrum disorder (ASD) and is generally considered to have an acceptable safety profile. However, the risk and mechanisms of severe adverse events in the high-risk subgroup of children with ASD complicated by multiple food intolerances (FI) have not been reported, and clinical strategies for risk prevention and management remain lacking.

CASE REPORT: This article reports two cases of children with ASD and multiple FIs who developed anaphylactic shock following FMT, representing the first such report in the pediatric field. Case 1 presented with early-stage shock, which was considered to be associated with IgG-mediated type III hypersensitivity. Case 2 developed classic anaphylactic shock with a biphasic course characterized by relapse after initial resolution, raising the possibility of biphasic anaphylaxis. Both children improved after standardized anti-allergy and anti-shock treatment, and one child successfully completed subsequent FMT using a low-dose regimen.

CONCLUSION: FMT carries a risk of anaphylactic shock in children with ASD and multiple FIs, who have underlying susceptibility due to impaired intestinal barrier function and immune dysregulation. Refined risk stratification, close monitoring throughout the procedure, individualized transplantation protocols, and standardized emergency procedures can effectively enhance the safety and feasibility of FMT in this high-risk subgroup.},
}

@article {pmid42382671,
year = {2026},
author = {Liu, Y and Mei, D},
title = {The gut microbiome in colorectal cancer: molecular paradigms and translational frontiers.},
journal = {Frontiers in bioengineering and biotechnology},
volume = {14},
number = {},
pages = {1864299},
pmid = {42382671},
issn = {2296-4185},
abstract = {The gut microbiome is now recognized as a causal driver of colorectal cancer (CRC) rather than a mere commensal ecosystem. This review elucidates the molecular mechanisms of keystone pathogens, specifically Fusobacterium nucleatum, pks [+] Escherichia coli, and enterotoxigenic Bacteroides fragilis, which induce DNA interstrand crosslinks, hyperactivate Wnt/β-catenin signaling, compromise the epithelial barrier, and reshape the tumor immune microenvironment. We discuss how bioengineered human organoids and microfluidic Organ-on-a-Chip platforms resolve the aerobic-anaerobic co-culture paradox, enabling patient-specific mechanistic dissection of host-microbe crosstalk. From a clinical perspective, we evaluate multi-omics signatures for noninvasive screening, intratumoral bacterial load as a prognostic indicator, and emerging therapeutic strategies including narrow-spectrum antimicrobials, bacteriophage-guided drug delivery, fecal microbiota transplantation for immunotherapy sensitization, and engineered living probiotics. By integrating mechanistic paradigms, organoid-guided validation, and translational applications, we delineate actionable trajectories for precision microbiome targeting in CRC management.},
}

@article {pmid42382782,
year = {2026},
author = {Kim, S and Lee, S and Ju, S and Bae, J and Ryu, JS and Heo, Y and Choi, WJ and Shin, KJ and Kim, SJ and Kim, N and Choi, H and Park, J and Lee, E and Yoon, CH and Kwon, S and Chung, J and Kim, MK},
title = {Gut microbiota transfer from autoimmune dry eye mice imprints stereotypic B cell receptor repertoires in the lacrimal gland and induces disease.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1827057},
pmid = {42382782},
issn = {1664-3224},
mesh = {Animals ; *Lacrimal Apparatus/immunology/metabolism ; Mice ; *Gastrointestinal Microbiome/immunology ; Disease Models, Animal ; *Sjogren's Syndrome/immunology/microbiology ; *Receptors, Antigen, B-Cell/immunology/genetics/metabolism ; Female ; Mice, Inbred NOD ; *B-Lymphocytes/immunology/metabolism ; *Autoimmune Diseases/immunology/microbiology ; Fecal Microbiota Transplantation ; *Dry Eye Syndromes/immunology/microbiology ; Mice, Inbred C57BL ; },
abstract = {Gut microbiota and humoral immunity have been suggested as key players in the pathogenesis of Sjögren disease (SjD), but their mechanisms remain unclear. In this study, we transferred the gut microbiota of SjD-like autoimmune dry eye disease model mice to B6 mice, then characterized the resulting gut microbiome composition, clinical ocular phenotype, and B cell receptor (BCR) repertoire. Notable changes were observed in the gut microbiome of NOD-FMT mice, accompanied by SjD-like clinical features, including elevated corneal fluorescein staining scores, reduced tear production, increased IL-6 mRNA levels, and decreased MUC5AC mRNA levels. Additionally, stereotypic B cell receptor (BCR) clonotypes were shared at significantly higher frequencies in NOD-FMT mice than in controls. The majority of B cell clones encoding these stereotypic clonotypes developed and expanded locally in the lacrimal gland, and some also achieved systemic presence. These results uncover a gut-ocular immune axis in which microbiota transfer induces stereotyped, systemically disseminating BCR clonotypes that contribute to the immunopathogenesis of autoimmune dry eye disease.},
}

Animals
*Lacrimal Apparatus/immunology/metabolism
Mice
*Gastrointestinal Microbiome/immunology
Disease Models, Animal
*Sjogren's Syndrome/immunology/microbiology
*Receptors, Antigen, B-Cell/immunology/genetics/metabolism
Female
Mice, Inbred NOD
*B-Lymphocytes/immunology/metabolism
*Autoimmune Diseases/immunology/microbiology
Fecal Microbiota Transplantation
*Dry Eye Syndromes/immunology/microbiology
Mice, Inbred C57BL

@article {pmid42383626,
year = {2026},
author = {Xiao, Y and Chen, B and Zhang, X and Sun, H and Wang, H and Du, P and Yang, X and Fan, G},
title = {Multiomics Integration Reveals AFB1 Causes Liver Damage Involving the Gut-Microbiota-Lipid Metabolism Axis in Piglet.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c17707},
pmid = {42383626},
issn = {1520-5118},
abstract = {Prolonged exposure to aflatoxin B1 (AFB1) poses a significant threat to livestock production. The liver is the main target, but the role of the gut-liver axis and lipid metabolism in pig hepatic toxicity is not well understood. This study evaluates the impact of AFB1 on piglet liver injury via the gut-liver axis using multiomics analysis. Chronic AFB1 exposure significantly impaired the piglet growth and induced liver injury. Meanwhile, AFB1 caused gut microbiota dysbiosis and intestinal barrier damage in the piglets. Fecal microbiota transplantation (FMT) demonstrated that AFB1-altered microbiota causally contribute to hepatic inflammation in mice. Multiomics analysis revealed systemic disruption of lipid metabolism pathways, which might be involved in the intestinal flora imbalance caused by AFB1. Abnormal lipid metabolism subsequently leads to the accumulation of inflammatory lipid mediators in the plasma, ultimately causing severe liver damage. The findings highlight the crucial roles of gut microbiota and lipid metabolism in AFB1-induced liver toxicity.},
}

@article {pmid42383946,
year = {2026},
author = {Fischer, M and Vaughn, BP and Peery, AF and Kelly, CR},
title = {AGA Clinical Practice Update on Management of Clostridioides difficile Infection in Adults: Expert Review.},
journal = {Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cgh.2026.05.007},
pmid = {42383946},
issn = {1542-7714},
abstract = {DESCRIPTION: Clostridioides difficile infection is a common cause of clinically significant diarrhea, often becomes recurrent, and can be fatal when severe or fulminant. The purpose of this America Gastroenterological Association (AGA) Clinical Practice Update Expert Review is to provide best practice advice for C difficile infection management.

METHODS: This expert review was commissioned by the AGA Institute Clinical Practice Updates Committee and the AGA Governing Board to provide timely guidance on a topic of high clinical importance to the AGA membership. The review was developed from expert opinion and a review of the published literature. Because systematic reviews were not performed, these best practice advice statements do not carry formal ratings regarding the quality of evidence or strength of the presented considerations. The review underwent internal peer review by the Practice Updates Committee and external peer review through standard procedures of Clinical Gastroenterology and Hepatology. BEST PRACTICE ADVICE STATEMENTS BEST PRACTICE ADVICE 1: Prevention of C difficile infection should include proper barrier protection and disinfection with United States Environmental Protection Agency-approved sporicidal agents in health care settings. Patients should be counseled on the importance of handwashing and to consider disinfecting areas of the home potentially contaminated with C difficile spores, to prevent reinfection. Reassurance should be provided that C difficile infection transmission to unaffected family members is uncommon. BEST PRACTICE ADVICE 2: C difficile infection is a clinical diagnosis that requires compatible symptoms (typically acute diarrhea, following antibiotics) in combination with supportive laboratory testing. Multistep testing is preferred for best diagnostic accuracy; however, patients with discordant testing who have a high clinical suspicion for C difficile infection should be treated. BEST PRACTICE ADVICE 3: Clinicians should classify hospitalized patients with C difficile infection as having nonsevere, severe, or fulminant disease at diagnosis. White blood cell count >15,000 cells/uL and/or creatinine >1.5 × baseline are indicative of severe C difficile infection and increased risk for recurrence and poor outcomes. Patients with additional findings of shock, ileus, or megacolon have fulminant C difficile infection, which can be fatal. BEST PRACTICE ADVICE 4: Fidaxomicin (200 mg twice daily oral for 10 days) is a narrower spectrum agent, and given lower recurrence rates, is favored as first-line therapy for nonfulminant C difficile infection. However, given practical considerations, vancomycin (125 mg 4 times daily oral for 10 days) is also acceptable therapy. Metronidazole should not be used outside of fulminant disease. BEST PRACTICE ADVICE 5: Cholestyramine and other bile acid-binding agents should not be used as monotherapy or concurrently with oral vancomycin or fidaxomicin. Psyllium fiber can be used to bulk stools in patients who have recovered from the infection. BEST PRACTICE ADVICE 6: Following treatment of C difficile infection, clinicians should not perform routine test of cure. Stool testing should only be performed for persistent worsening of diarrheal symptoms. BEST PRACTICE ADVICE 7: First C difficile infection recurrence (second episode) within 8 weeks of completing anti-C difficile infection therapy should be treated with either a tapering course of vancomycin or fidaxomicin. Treatment of C difficile infection should include a risk assessment for C difficile infection recurrence and consideration of microbiota restoration therapy to prevent recurrence. BEST PRACTICE ADVICE 8: Fecal microbiota-based therapies (fecal microbiota spores, live-brpk, fecal microbiota, live-jslm, or conventional fecal microbiota transplant) should be offered after treatment of a second recurrence (third C difficile infection episode). Microbiota restoration therapy may be considered after treatment of an initial infection or first recurrence in patients who are at high risk for further recurrence or in patients whose initial C difficile infection episode was particularly morbid or difficult to treat. BEST PRACTICE ADVICE 9: Prolonged, low dose, suppressive vancomycin regimen (125 mg daily) for secondary prophylaxis may be considered in patients with multiple recurrent episodes who are not candidates for fecal microbiota-based therapies due to ongoing comorbidities, limited life expectancy, or ongoing/frequent systemic antibiotics or who have failed multiple courses of fecal microbiota-based therapy. BEST PRACTICE ADVICE 10: Fulminant C difficile infection should be managed by a multidisciplinary team (gastroenterology/infectious disease, surgery, medicine/critical care) and treated with high-dose vancomycin 500 mg every 6 hours (oral or enteral), with metronidazole 500 mg intravenously every 8 hours, and if ileus is present, rectal vancomycin 500 mg every 6 hours should be added. BEST PRACTICE ADVICE 11: Multi-dose fecal microbiota transplantation (fresh-directed donors, or institutional stool banks) delivered via lower endoscopy, should be considered in individuals with fulminant C difficile infection. Fecal microbiota, live-jslm (Rebyota), and fecal microbiota spores, live-brpk (Vowst) have not been studied and are not approved for treatment of severe and/or fulminant C difficile infection. Due to high risk of C difficile infection recurrence, patients who recover from severe or fulminant C difficile infection should be maintained on a suppressive vancomycin regimen until a final fecal microbiota transplantation can be administered as an outpatient. BEST PRACTICE ADVICE 12: Use of vancomycin is not advised during systemic antibiotic administration to prevent C difficile infection. Probiotics are not advised to prevent an initial or recurrent C difficile infection. To promote restoration of healthy gut microbiota, patients should be instructed to consume a healthy diet including a variety of fruits and vegetables, rich in both soluble and insoluble fiber. BEST PRACTICE ADVICE 13: During the treatment of C difficile infection or the prevention of its recurrence, the use of proton pump inhibitors should be evaluated. If a legitimate indication exists for their use, proton pump inhibitor discontinuation is not necessary. BEST PRACTICE ADVICE 14: Individuals with a history of C difficile infection should be specifically counseled to avoid unnecessary antibiotic therapy.},
}

@article {pmid42384640,
year = {2026},
author = {Zhang, X and Fu, Y and Chen, J and Shen, H and Du, Y and Wu, J and Lai, H and Liu, Y and Chen, J and Hou, X and Chang, W and Hu, X},
title = {An exercise-associated gut microbiota signature enhances endurance performance: A study combining a human cohort and a mice FMT model.},
journal = {PloS one},
volume = {21},
number = {7},
pages = {e0351316},
doi = {10.1371/journal.pone.0351316},
pmid = {42384640},
issn = {1932-6203},
mesh = {Animals ; Humans ; *Gastrointestinal Microbiome/physiology ; Mice ; *Fecal Microbiota Transplantation ; Male ; Young Adult ; *Physical Endurance/physiology ; RNA, Ribosomal, 16S/genetics ; Adult ; Female ; *Exercise/physiology ; Feces/microbiology ; Cohort Studies ; },
abstract = {BACKGROUND: The gut microbiota is closely related to exercise, but the interrelationship between the two remains elusive. In this study, we aimed to explore differences in the gut microbiota between young adults with exercise and sedentary lifestyles. In addition, we evaluated the effects of gut microbiota from these different lifestyle populations on endurance exercise capacity.

METHODS: The exercise status and nutritional characteristics of young adults were evaluated by PARS-3 and food frequency questionnaires. The gut microbiota of young adults from exercise and sedentary lifestyle groups was analyzed by 16S rRNA analysis. Subsequently, we performed fecal bacteria transplantation (FMT) from the human donors into mice and evaluated the effects on their endurance exercise capacity.

RESULTS: The exercise group exhibited significantly higher gut microbiota diversity compared to the sedentary group. Several beneficial bacteria, including Veillonella, Faecalibacterium, and Bacteroides, were enriched in the exercise group. The FMT experiment confirmed that mice receiving microbiota from the exercise group showed significantly improved endurance exercise capacity.

CONCLUSION: Young people who exercise regularly possess a more diverse gut microbiota enriched with beneficial bacteria. This exercise-associated microbiota has the potential to directly improve exercise capacity.},
}

Animals
Humans
*Gastrointestinal Microbiome/physiology
Mice
*Fecal Microbiota Transplantation
Male
Young Adult
*Physical Endurance/physiology
RNA, Ribosomal, 16S/genetics
Adult
Female
*Exercise/physiology
Feces/microbiology
Cohort Studies

@article {pmid41919665,
year = {2026},
author = {Kataria, S and Singla, A and Mamoria, VP and Sharma, I},
title = {The burden of cyclosporiasis in immuno-compromised patients: A growing public health issue lessons from case studies.},
journal = {Tropical doctor},
volume = {56},
number = {3},
pages = {514-520},
doi = {10.1177/00494755261437456},
pmid = {41919665},
issn = {1758-1133},
mesh = {Humans ; *Cyclosporiasis/epidemiology/parasitology/diagnosis ; *Cyclospora/isolation & purification ; Male ; *Immunocompromised Host ; Middle Aged ; Female ; Feces/parasitology ; Oocysts ; Animals ; Risk Factors ; Public Health ; Diarrhea/parasitology ; },
abstract = {Cyclospora cayetanensis is an emerging notifiable food-and-water-borne coccidian parasite causing gastro-intestinal-disease in humans. Detailed information about its biology-associated risk-factors and routes of transmission remain poorly understood; the lack-of-comprehensive epidemiological data underlines a critical need for targeted research into effective prevention and control. Acid variable (pink to brilliant red colour) oocysts of Cyclospora spp. were observed in 16/162 samples, predominantly in 51-60 years males in October. Most cases were among transplant recipients presenting with diarrhoea, therapeutic options among whom remains limited.},
}

Humans
*Cyclosporiasis/epidemiology/parasitology/diagnosis
*Cyclospora/isolation & purification
Male
*Immunocompromised Host
Middle Aged
Female
Feces/parasitology
Oocysts
Animals
Risk Factors
Public Health
Diarrhea/parasitology

@article {pmid42373816,
year = {2026},
author = {Yang, J and Ling, Z and Zhou, M and Tao, M and Mao, J and Guo, H and Wang, J and Qu, X and Wang, Y and Zhu, Y and Zhang, K and Yan, X},
title = {Ketogenic diet alleviates acute radiation-induced intestinal injury through JAK2/STAT3/RORγt/IL-17A signaling pathway via gut microbiome.},
journal = {Communications biology},
volume = {},
number = {},
pages = {},
doi = {10.1038/s42003-026-10546-9},
pmid = {42373816},
issn = {2399-3642},
support = {81902422//National Natural Science Foundation of China (National Science Foundation of China)/ ; BK20250559//Natural Science Foundation of Jiangsu Province (Jiangsu Provincial Natural Science Foundation)/ ; },
abstract = {Emerging evidence suggests dietary interventions regulate inflammatory signaling through gut microbiome modulation, yet their therapeutic potential in radiation-induced intestinal injury (RIII) remains underexplored. This study demonstrates that ketogenic diet (KD), a high-fat and low-carbohydrate dietary regimen, exerts protective effects against RIII through dual mechanisms involving microbial regulation and inflammatory pathway inhibition. Using high-salt diet (HSD) as a dietary control, KD significantly attenuated intestinal inflammation by downregulating pro-inflammatory cytokines while enhancing barrier integrity through tight junction protein upregulation in radiation-exposed murine model. 16S rDNA sequencing showed KD enriched Akkermansia and reduced Enterobacteriaceae, whereas HSD exhibited inverse patterns. Mechanistically, RNA sequencing revealed that KD uniquely suppressed the JAK2/STAT3 pathway in RIII mice. In vitro studies demonstrated that β-hydroxybutyrate, a key ketone metabolite, effectively suppressed RORγt expression and subsequent downregulation of IL-17A gene transcription via the inhibition of JAK2/STAT3 pathway, thus mitigate inflammatory damage. Fecal microbiota transplantation validated that KD-modified microbiome directly inhibited JAK2/STAT3 signaling activation, as well as the downregulation of RORγt and IL-17A. These findings establish KD as a promising dietary strategy mitigate acute RIII through synergistic modulation of gut microbiota and inflammatory signaling, providing novel insights into nutritional approaches targeting microbial-host crosstalk in radiation injury.},
}

@article {pmid42375360,
year = {2026},
author = {Zhou, K and Lu, P and Xu, H and Wang, L and Liang, X},
title = {Molecular studies on the impact of microbiome on anticancer drug resistance.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1848345},
pmid = {42375360},
issn = {1664-3224},
mesh = {Humans ; *Drug Resistance, Neoplasm/immunology ; Animals ; *Antineoplastic Agents/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/immunology/drug effects ; *Neoplasms/drug therapy/microbiology/immunology ; Tumor Microenvironment/immunology ; Probiotics ; Prebiotics ; Fecal Microbiota Transplantation ; },
abstract = {Cancer remains a leading global health challenge, with drug resistance posing a critical barrier to the durable efficacy of anticancer therapies, including chemotherapy, immunotherapy, and targeted treatments. Growing evidence highlights the gut microbiome as a key modulator in this resistance process. The gut microbiome-a dynamic and diverse microbial ecosystem-can influence drug efficacy through multiple mechanisms, including the biotransformation of chemotherapeutics, modulation of immune responses, alteration of host drug-metabolizing enzymes, and reshaping of the tumor microenvironment. Notably, specific bacterial taxa can enzymatically inactivate chemotherapeutic drugs, while microbial metabolites and signaling pathways further promote resistance by rewiring cellular survival and immune-regulatory programs. In this review, we synthesize recent molecular insights into microbiome-driven anticancer drug resistance and discuss emerging microbiome-targeted strategies, such as dietary intervention, probiotics and prebiotics, fecal microbiota transplantation, and advanced drug delivery systems. A deeper understanding of host-microbiome-drug interactions may provide new opportunities to overcome therapeutic resistance and advance precision oncology.},
}

Humans
*Drug Resistance, Neoplasm/immunology
Animals
*Antineoplastic Agents/therapeutic use/pharmacology
*Gastrointestinal Microbiome/immunology/drug effects
*Neoplasms/drug therapy/microbiology/immunology
Tumor Microenvironment/immunology
Probiotics
Prebiotics
Fecal Microbiota Transplantation

@article {pmid42365572,
year = {2026},
author = {Abebaw, D and Adugna, A and Tegegne, BA and Teffera, ZH and Selabat, B and Kindie, Y and Tilahun, M and Belew, H and Baylie, T and Mengistu, G and Jemal, M and Atnaf, A},
title = {Harnessing the gut microbiome for improved immune checkpoint inhibition in colorectal cancer immunotherapy: a narrative Review.},
journal = {Clinical and experimental medicine},
volume = {},
number = {},
pages = {},
doi = {10.1007/s10238-026-02222-3},
pmid = {42365572},
issn = {1591-9528},
abstract = {Colorectal cancer (CRC) remains among the most prevalent and deadliest malignancies worldwide, with limited survival outcomes, particularly in patients with metastatic disease. Despite advances in immunotherapy, immune checkpoint inhibitors (ICIs) have shown efficacy mainly in mismatch repair-deficient (dMMR) CRC, while responses in mismatch repair-proficient (pMMR) microsatellite-stable (MSS) cases remain limited. Emerging evidence highlights the gut microbiome as a critical factor influencing CRC development, progression, and therapeutic response. In particular, the gut microbiota has been shown to affect the efficacy of ICIs, with dysbiosis contributing to treatment resistance and specific microbial taxa enhancing antitumor immune responses. Preclinical and clinical studies have demonstrated that microbiome-based interventions, including probiotics, fecal microbiota transplantation (FMT), dietary modulation, and traditional medicines, can restore immune function by modulating immune cell populations and producing immunoregulatory metabolites. These effects may enhance responsiveness to ICIs and contribute to the suppression of tumor growth. However, we also address key limitations in this field, including inconsistent findings and safety concerns, such as infection risks, to guide future translational efforts. Overall, while microbiome-based interventions represent a promising adjunct to CRC immunotherapy, rigorous clinical trials and mechanistic validation are required before their routine clinical implementation.},
}

@article {pmid42366511,
year = {2026},
author = {Yin, Y and Gao, J and Zhang, K and Meng, F and Feng, T},
title = {Novel treatments for Parkinson's disease.},
journal = {Chinese medical journal},
volume = {},
number = {},
pages = {},
pmid = {42366511},
issn = {2542-5641},
abstract = {Parkinson's disease (PD) is a progressive neurodegenerative disorder associated with a rapidly rising global disease burden and a substantial decline in patients' quality of life. Although currently approved therapies offer symptomatic relief, their clinical efficacy inevitably wanes over time. This review provides a comprehensive summary of recent advancements in both symptomatic treatments and experimental therapies focused on neuroprotection and disease modification. These novel treatments for PD include continuous dopaminergic stimulation, adaptive deep brain stimulation, transcranial temporal interference stimulation, anti-α-synuclein immunotherapies, oral anti-α-synuclein therapies, non-receptor tyrosine kinase inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, iron chelators, fecal microbiota transplantation, glucosylceramide synthase inhibitors, as well as stem cell therapies and gene therapies. However, the majority of these novel treatments are still in the investigational phase and necessitate additional validation via randomized controlled trials. Future research should also focus on optimizing trial methodologies, including the timing of intervention, stratification of PD subjects, and selection of treatment endpoints.},
}

@article {pmid42366893,
year = {2026},
author = {Chen, J and Su, S and Zhang, X and Xiong, F and Zheng, H and Zhang, W and Shen, Y and Lin, P and Gao, H and Li, Y},
title = {Vancomycin Protects Against Lung Injury and Promotes Butyrate Metabolism.},
journal = {FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
volume = {40},
number = {13},
pages = {e72084},
pmid = {42366893},
issn = {1530-6860},
support = {81970066//National Natural Science Foundation of China (NSFC)/ ; },
mesh = {Animals ; *Vancomycin/pharmacology ; Mice ; *Butyrates/metabolism ; Mice, Inbred C57BL ; Humans ; *Acute Lung Injury/metabolism/microbiology/drug therapy/prevention & control ; Male ; *Gastrointestinal Microbiome/drug effects ; Anti-Bacterial Agents/pharmacology ; Lung/metabolism/drug effects ; *Lung Injury/metabolism/prevention & control ; },
abstract = {Lung injury is one of the most common clinical respiratory diseases, caused by the exposure of lung tissue to various stimuli (including hypoxia, ischemia-reperfusion, and foreign substances). Among them, chronic lung injury is characterized by continuous inflammation in the lungs, which damages the endothelial and epithelial cell barriers within the lungs. Clinically, it presents as severe hypoxia and diffuse functional impairment, and on imaging, it shows diffuse alveolar damage, accompanied by varying degrees of inflammation and airway obstruction. Several studies have highlighted the role of gut microbiota in modulating immune responses and pathological features of respiratory diseases through the gut-lung axis. However, the precise metabolic mechanism remains unknown. A lung injury model was generated by transplanting microbiota from acute lung injury (ALI) patients into healthy C57BL/6J mice. The changes in the gut microbiota and metabolic phenotypes of the feces samples from ALI patients and lung-injured mice were analyzed using 16S rRNA sequencing technology and metabolomics based on [1]H-nuclear magnetic resonance ([1]H-NMR), respectively. The effect of gut microbiota on lung injury was also explored after giving an oral vancomycin treatment to lung-injury mice. The data presented here show that Firmicutes formed the vital species of microbiota that was different in lung-injury mice. Moreover, butyrate (produced by Firmicutes) was the most crucial metabolite in the feces samples of ALI patients and lung-injury mice. ELISA and Hematoxylin-Eosin results showed aggravated functional disturbances in the intestinal barrier of ALI patients and lung inflammation in the lung-injured mice. These phenomena were significantly alleviated after the oral administration of vancomycin. Besides, the utilization of butyrate in the colon of mice was increased considerably. Thus, vancomycin can affect the metabolism of butyrate in the colon by influencing the intestinal microbiota, and it can help in the treatment of lung injury.},
}

Animals
*Vancomycin/pharmacology
Mice
*Butyrates/metabolism
Mice, Inbred C57BL
Humans
*Acute Lung Injury/metabolism/microbiology/drug therapy/prevention & control
Male
*Gastrointestinal Microbiome/drug effects
Anti-Bacterial Agents/pharmacology
Lung/metabolism/drug effects
*Lung Injury/metabolism/prevention & control

@article {pmid42367132,
year = {2026},
author = {Qu, J and Fu, J and Wang, Y and Jiang, X and Ma, Y and Yi, J and Wu, J and Liu, Y and Huang, K and Wang, J and Yuan, Z and Wen, L and Liu, S},
title = {Chronic Exposure to NaAsO2 Induces Renal Fibrosis by Modulating Gut Microbiota-Mediated AhR/NLRP3 Inflammasome Signaling Pathway.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c05585},
pmid = {42367132},
issn = {1520-5118},
abstract = {Arsenic is an environmental contaminant with potent renal toxicity. Accumulating evidence has indicated that gut microbiota dysbiosis plays an important role in kidney disease. However, the role of gut microbiota in arsenic-exposure-induced renal injury remains unclear. In our study, chronic exposure to NaAsO2 and fecal microbiota transplantation (FMT) from NaAsO2-exposed mice increased intestinal permeability and elevated renal indoxyl sulfate (IS), a key metabolite of gut microbiota, which promoted renal fibrosis and activated the AhR/NLRP3 inflammasome signaling pathway. Moreover, AST-120, a non-specific adsorbent, alleviated chronic NaAsO2 exposure-induced renal fibrosis by reducing the IS level in mice. In HK-2 cells, IS mediated NaAsO2-induced fibrosis via the AhR/NLRP3 inflammasome signaling pathway. Collectively, we confirmed that chronic exposure to NaAsO2 caused renal fibrosis and intestinal barrier dysfunction. Meanwhile, the gut-kidney axis plays a significant role in the mechanism of NaAsO2-induced renal fibrosis, providing a new therapeutic target for the prevention and treatment of arseniasis.},
}

@article {pmid42367194,
year = {2026},
author = {Abaakil, K and Liu, Z and Wang, M and Kuznecova, E and Sung, MSC and Marchesi, JR and Mausz, MA and Li, JV},
title = {Antibiotic course frequency and recovery strategies alter gut microbial composition and metabolism.},
journal = {ISME communications},
volume = {6},
number = {1},
pages = {ycag145},
pmid = {42367194},
issn = {2730-6151},
abstract = {Antibiotics profoundly alter the gut microbiome, but how exposure frequencies shape microbial recovery remains unclear. The effectiveness of post-antibiotic interventions, e.g. probiotics or autologous fecal microbiota transplantation, (aFMT) requires further exploration. This study investigated how antibiotic course timing and recovery strategies influence gut microbiome and metabolism in male Wistar rats. A single oral dose of vancomycin-ciprofloxacin (VC) caused rapid urinary and fecal metabolic shifts within 8-12 h and reduced bacterial α-diversity in cecal and colonic contents. When three VC courses were administered at regular (every 3 weeks; VCr) or irregular (1-3 weeks; VCi) intervals, VCr showed greater suppression of fecal α-diversity and stronger disruption of amino acid and host-microbial co-metabolism than VCi. Over the 3-week recovery period, VCr exhibited slower fecal α-diversity restoration; at week 3, β-diversity remained significantly different between groups, and cecal butyrate levels were persistently reduced in VCr. Both groups showed elevated levels of 5-aminovalerate in feces and colon compared with controls, whereas only VCi showed reductions in jejunal and ileal amino acids. Probiotics or aFMT had limited influence on small intestinal alterations, though aFMT accelerated fecal α-diversity recovery, and both interventions promoted partial normalization of fecal amino acids and 5-aminovalerate, without achieving complete restoration. Overall, shorter antibiotic intervals exerted stronger effects on the small intestinal luminal chemical environment, whereas longer intervals led to greater suppression of colonic and fecal microbial metabolism. Probiotics and aFMT supported selective metabolic recovery without fully reversing antibiotics-induced disturbances, highlighting the need for more targeted restoration strategies across gastrointestinal regions.},
}