@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.},
}

@article {pmid42367597,
year = {2026},
author = {Gilroy, R and Chaloner, G and Wedley, A and Richards-Rios, P and Pottenger, S and Wigley, P},
title = {Caecal microbiome transplant inhibits transmission and intestinal colonisation of Campylobacter jejuni in broiler chickens.},
journal = {Poultry science and management},
volume = {3},
number = {1},
pages = {13},
pmid = {42367597},
issn = {3005-0715},
abstract = {Campylobacter jejuni is the most frequent cause of foodborne bacterial gastroenteritis with poultry products the most frequent source of infection. C. jejuni can colonise the intestinal tract of the chicken and in particular the large blind caeca to a high level accompanied by faecal shedding and rapid transmission in flocks. As such, reducing transmission and intestinal colonisation in poultry meat production is considered a key target to reduce human infection. Whilst vaccines and feed-based approaches including modulation of the microbiome are considered most likely to reduce numbers in the chicken caeca, neither have yet shown the capacity to lead to significant reductions. We have previously shown that administration of a caecal microbiome transplant (CMT) at hatch acts to modify the microbiome, increasing diversity and reducing Enterobacteriacae levels associated with poor gut health and increased Campylobacter susceptibility. When challenged at 21 days old with C. jejuni M1 in a seeder bird infection model, birds in groups receiving CMT showed reduced transmission and significantly lower levels of C. jejuni at post-mortem examination at 35 days of age than control birds or birds treated with a commercial microflora competitive exclusion product (Aviguard). These data show that a microbiome-based intervention has the potential to inhibit C. jejuni transmission and decrease levels in the caeca at slaughter age. This is modelled to lead to a significant reduction in human cases. CMT offers a valuable tool to determine protective taxa in the chicken gut, aiding rational development of microbial interventions as well as a low-cost platform to help understand immunological development in the chicken gut.},
}

@article {pmid42367812,
year = {2026},
author = {Wu, Y and Liu, L and You, D and Mao, T and Zheng, X and Dai, X and Xu, X and Wu, X and Zhou, H},
title = {Deoxycholic acid promotes anxiety- and depression-like behaviors in mice via modulation of the gut microbial metabolite indole-3-propionic acid.},
journal = {Frontiers in immunology},
volume = {17},
number = {},
pages = {1840574},
pmid = {42367812},
issn = {1664-3224},
mesh = {Animals ; *Depression/metabolism/chemically induced/etiology ; *Deoxycholic Acid/adverse effects ; Mice ; *Anxiety/metabolism/etiology/chemically induced ; *Gastrointestinal Microbiome/drug effects ; Male ; *Indoles/metabolism ; *Behavior, Animal/drug effects ; Disease Models, Animal ; Mice, Inbred C57BL ; Diet, High-Fat/adverse effects ; Fecal Microbiota Transplantation ; Brain-Gut Axis ; Propionates ; },
abstract = {BACKGROUND: High-fat diet (HFD)-associated anxiety- and depression-like behaviors are closely linked to disturbances in the gut-brain axis; however, the peripheral signaling mechanisms and key metabolites involved remain to be elucidated. Deoxycholic acid (DCA), a bile acid elevated by a HFD, has been reported to be associated with abnormal cognitive behaviors in mice. This study aimed to investigate whether HFD-induced anxiety- and depression-like behaviors are regulated by intestinal DCA and its underlying mechanisms.

METHODS: Four mouse models were established with different interventions: a low-fat diet (LFD), a HFD, a LFD plus DCA, and a HFD plus the bile acid binder cholestyramine. We performed behavioral phenotyping, brain tissue transcriptome sequencing, fecal 16S rRNA gene sequencing, fecal and serum metabolomics, and intestinal barrier function assessment to clarify the phenotypes and underlying mechanisms. In vitro cell experiments, ileal organoid assays, and in vivo fecal microbiota transplantation (FMT) were further used for validation.

RESULTS: DCA intervention induced HFD-like anxiety- and depression-like behaviors in the mice, accompanied by reduced levels of the key gut bacterium Clostridium_sensu_stricto_1 and its metabolite indole-3-propionic acid (IPA) in the gut and serum. IPA supplementation restored circulating IPA levels, upregulated the expression of key genes (Cyp3a11 and Abcb1a) in the cerebral pregnane X receptor (PXR) signaling, ameliorated DCA-induced emotional and behavioral abnormalities, and reversed related gut-brain axis impairments, including downregulated brain barrier-related proteins, morphological changes associated with microglial activation, intestinal barrier damage (reduced goblet cells, downregulated Claudin-1/Occludin), intestinal epithelial oxidative stress and injury, and impaired ileal organoid budding. FMT induced behavioral phenotypes, barrier impairments, reduced serum IPA, and cerebral pathological changes in recipient mice similar to those observed in DCA model mice.

CONCLUSIONS: These findings support a potential gut-brain pathway linking HFD-associated luminal DCA elevation to anxiety- and depression-like behaviors in mice. The reduction in IPA levels resulting from the remodeling of gut microbiota triggered by DCA might be the key mediating factor. Targeting abnormal bile acid metabolism or restoring IPA function is a promising intervention strategy for HFD-related emotional and behavioral abnormalities.},
}

Animals
*Depression/metabolism/chemically induced/etiology
*Deoxycholic Acid/adverse effects
Mice
*Anxiety/metabolism/etiology/chemically induced
*Gastrointestinal Microbiome/drug effects
Male
*Indoles/metabolism
*Behavior, Animal/drug effects
Disease Models, Animal
Mice, Inbred C57BL
Diet, High-Fat/adverse effects
Fecal Microbiota Transplantation
Brain-Gut Axis
Propionates

@article {pmid42368286,
year = {2026},
author = {Ruttenberg, DP},
title = {Commentary: Safety and efficacy of a novel fecal microbiota transplantation method using hydrogen nanobubble water without antibiotics or bowel cleansing in children with autism spectrum disorder.},
journal = {Frontiers in pediatrics},
volume = {14},
number = {},
pages = {1838225},
pmid = {42368286},
issn = {2296-2360},
}

@article {pmid42370690,
year = {2026},
author = {Dietz, M and Subramanian, S and Staley, C},
title = {The gut microbiome and colorectal cancer.},
journal = {Clinical microbiology reviews},
volume = {},
number = {},
pages = {e0033225},
doi = {10.1128/cmr.00332-25},
pmid = {42370690},
issn = {1098-6618},
abstract = {SUMMARYColorectal cancer (CRC) is a significant global health concern that is growing in prevalence, especially in younger populations. The gut microbiome is an increasingly recognized factor in the development and progression of numerous diseases, including CRC. This review explores the current research on the causal relationship between the microbiome and CRC, including the strengths and limitations of the current models for studying this complex interaction. We then delve into key microbial metabolites and their effects on host signaling pathways in the context of CRC and highlight specific bacterial species with direct links to CRC development and progression. Existing microbiota-targeted therapies such as pre- and pro-biotics and fecal microbiota transplantation are described, as well as innovative microbiome-focused strategies that are currently in development, like quorum quenching. Finally, we address the major challenges in the field, such as conflicting research findings and the need for a systems-level, multi-omic approach to describe the intertwined and bidirectional host-microbe interactions.},
}

@article {pmid42370841,
year = {2026},
author = {Dang, J and Lee, Y and Wills, MV and Brown, JM and Madsen, K and Mocanu, V},
title = {The Gut Microbiome in Surgical Oncology: Mechanisms, Perioperative Outcomes, and Therapeutic Opportunities.},
journal = {The British journal of surgery},
volume = {},
number = {},
pages = {},
doi = {10.1093/bjs/znag082},
pmid = {42370841},
issn = {1365-2168},
abstract = {INTRODUCTION: The gut microbiome is a fundamental determinant of gastrointestinal physiology. It is essential in maintaining host homeostasis while also implicated in cancer pathogenesis and alteration in physiological response to surgical stress. This narrative review evaluates the microbiome's mechanistic role in surgical oncology, assessing it as a biomarker for risk stratification and an emerging therapeutic target.

METHOD: The current literature was synthesized to examine microbial impacts on tumourigenesis and perioperative surgical outcomes across the lower and upper gastrointestinal tracts (including the gut-lung axis), the hepatopancreatobiliary system, and extra-abdominal malignancies (breast cancer and melanoma).

RESULTS: Dysbiotic microbial signatures, termed the oncobiome, actively drive tumour progression and immune evasion. Perioperative interventions induce acute microbial shifts linked to serious complications such as anastomotic leaks and pneumonia. Clinically, targeted modulation yields significant benefits as demonstrated by: perioperative synbiotics reducing infectious complications by 45% in colorectal surgery and 64% in major liver surgery. Furthermore, preoperative oral care reduces post-esophagectomy pneumonia by up to 50%, while Helicobacter pylori eradication halves metachronous gastric cancer risk. However, a detrimental "antibiotic paradox" exists in melanoma, where pre-treatment antibiotic exposure severely impairs immune checkpoint inhibitor efficacy. Conversely, faecal microbiota transplantation can reverse this immunotherapy resistance, achieving up to 80% response rates in trials.

CONCLUSION: The microbiome is a critical, modifiable determinant of both short-term surgical recovery and long-term oncologic survival. Future surgical oncology practice will need to integrate precision surgical microbiome-mediated biotherapeutics to optimise outcomes in multidisciplinary cancer care.},
}

@article {pmid42371176,
year = {2026},
author = {Shen, Z and Xu, D and Wang, K and Chen, Y and Dou, Q and Jin, S and Hu, B},
title = {Gut-brain axis modulation by fecal microbiota transplantation improves dual-organ injury after cerebral ischemia-reperfusion via Caspase-8 dependent inhibition of necroptosis.},
journal = {Metabolic brain disease},
volume = {41},
number = {1},
pages = {},
pmid = {42371176},
issn = {1573-7365},
support = {B20252733//Hangzhou Health Science and Technology Plan Project/ ; },
mesh = {Animals ; *Caspase 8/metabolism ; *Necroptosis/physiology ; *Reperfusion Injury/metabolism/therapy ; Male ; Rats ; *Fecal Microbiota Transplantation/methods ; *Brain Ischemia/metabolism/therapy ; Rats, Sprague-Dawley ; *Brain-Gut Axis/physiology ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism ; *Gastrointestinal Microbiome/physiology ; Intestinal Barrier Function ; Infarction, Middle Cerebral Artery/metabolism ; *Brain/metabolism ; },
abstract = {The pathological features of cerebral ischemia-reperfusion (CIR) include necroptosis activation. This study investigated how healthy fecal microbiota transplantation (H-FMT) improves CIR and intestinal barrier damage. Rats subjected to middle cerebral artery occlusion and reperfusion (MCAO/R) were treated with H-FMT and/or a Cysteine-aspartic acid protease-8 (Caspase-8) inhibitor. Survival and body weight were monitored throughout the experiment. Neurological function, tissue damage, inflammatory cytokines, and Caspase-8/Receptor-interacting protein kinase 1 (RIPK1)-Receptor-interacting protein kinase 3 (RIPK3)-Mixed lineage kinase domain-like protein (MLKL) expression were assessed. Ultrastructural changes were examined by transmission electron microscopy (TEM), p-RIPK1/p-RIPK3 expression by immunohistochemistry (IHC), and gut microbiota by 16 S sequencing. H-FMT significantly ameliorated neurological deficits and intestinal barrier disruption, reduced infarct volume and neuronal loss, and attenuated mitochondrial damage. These effects were accompanied by reduced apoptosis and inflammation, increased Caspase-8 activation, and suppressed RIPK1-RIPK3-MLKL phosphorylation. IHC confirmed reduced p-RIPK1/p-RIPK3 signals after H-FMT. 16 S sequencing revealed that H-FMT restored microbial diversity, reduced pathogenic Proteobacteria, and enriched beneficial Lactobacillus, which positively correlated with Caspase-8 activation. Our findings suggest that H-FMT alleviates CIR injury by activating Caspase-8 and suppressing necroptosis. However, due to the small sample size, these results should be considered preliminary.},
}

Animals
*Caspase 8/metabolism
*Necroptosis/physiology
*Reperfusion Injury/metabolism/therapy
Male
Rats
*Fecal Microbiota Transplantation/methods
*Brain Ischemia/metabolism/therapy
Rats, Sprague-Dawley
*Brain-Gut Axis/physiology
Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
*Gastrointestinal Microbiome/physiology
Intestinal Barrier Function
Infarction, Middle Cerebral Artery/metabolism
*Brain/metabolism

@article {pmid42371558,
year = {2026},
author = {Zhong, S and Guo, F and Chen, Q and Zhang, S},
title = {Microbiota-oriented strategies to mitigate parenteral nutrition-related complications in intestinal failure: A narrative review.},
journal = {Intestinal Failure (New York, N.Y.)},
volume = {10},
number = {},
pages = {100355},
pmid = {42371558},
issn = {2950-4562},
abstract = {BACKGROUND: Parenteral nutrition (PN) is essential for patients with intestinal failure (IF) but is associated with complications such as dysbiosis, small intestinal bacterial overgrowth, catheter-related infections, and intestinal failure-associated liver disease (IFALD). Growing evidence indicates that gut microbiota alterations contribute to the pathogenesis of these complications, supporting microbiota-oriented interventions as potential adjunctive therapies.

METHODS: Data sources: A structured literature search was conducted in PubMed, Web of Science, and Scopus from inception to December 2025.Study eligibility criteria: Clinical trials, observational studies, mechanistic studies, and relevant reviews evaluating gut microbiota features or microbiome-targeted interventions in IF or PN-dependent populations were included.Participants: Pediatric and adult patients with intestinal failure or short bowel syndrome, as well as relevant animal models.Interventions: Microbiota-oriented strategies, including probiotics, prebiotics, synbiotics, antibiotics, and fecal microbiota transplantation (FMT).Statistical analysis: Due to substantial heterogeneity in study design, interventions, and outcomes, meta-analysis was not performed; findings were synthesized qualitatively.

RESULTS: PN dependence was consistently associated with reduced microbial diversity, enrichment of Proteobacteria and Lactobacillaceae, and depletion of obligate anaerobes and short-chain fatty acid-producing taxa. Microbiota-oriented interventions demonstrated biological plausibility and microbiome modulation in selected studies; however, clinical benefits were variable and generally modest. Safety concerns, limited microbial engraftment, small sample sizes, and patient heterogeneity limited generalizability.

CONCLUSION: Gut microbiota dysbiosis plays a contributory role in PN-related complications of IF. Microbiota-oriented interventions are promising but remain unproven, underscoring the need for well-designed, stratified clinical studies to define efficacy, safety, and responsive patient subgroups.},
}

@article {pmid42372605,
year = {2026},
author = {Yuan, S and Hong, J and Zhang, H and Gao, P and Yang, P and Lei, J and He, Y and Fang, X and Lu, Y and Wang, B and Tu, P and Zhang, X and Jiang, Y},
title = {Total glycosides of Cistanche deserticola ameliorate alcohol-induced oligoasthenozoospermia via the modulation of gut microbiota-mediated spermidine metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {159},
number = {},
pages = {158483},
doi = {10.1016/j.phymed.2026.158483},
pmid = {42372605},
issn = {1618-095X},
abstract = {BACKGROUND: Oligoasthenozoospermia is a major cause of male infertility, with chronic excessive alcohol consumption being a prevalent etiology. Cistanche deserticola Ma., a traditional Chinese medicine historically employed for reproductive improvement. However, the role and mechanism in alcohol-induced reproductive dysfunction remains unexplored.

PURPOSE: This study aimed to elucidate the protective effect and underlying mechanism of total glycosides of C. deserticola (TGCD) against alcohol-induced oligoasthenozoospermia.

METHODS: The effects of TGCD were evaluated using a NIAAA mouse model. Mechanisms were elucidated through multi-omics, fecal microbiota transplantation, Lactobacillus reuteri supplementation, spermidine supplementation, and so on. Translational relevance was assessed by patients with alcohol-induced sperm abnormalities and a public single-cell transcriptome dataset.

RESULTS: TGCD administration significantly improved alcohol-impaired sperm quality, restored testosterone levels and testicular architecture. Mechanistically, TGCD selectively enriched L. reuteri, which enhanced spermidine production. Spermidine activated the Nrf2-mediated antioxidant pathway, thereby reducing ROS accumulation and reinstating the expression of key steroidogenic enzymes. Critically, these findings are corroborated by clinical data showing reduced fecal L. reuteri abundance in patients with alcohol-related sperm abnormalities, as well as human testicular single-cell transcriptomic evidence of concurrent downregulation of spermidine and Nrf2 pathways in infertile patients.

CONCLUSION: TGCD alleviates alcohol-induced oligoasthenozoospermia via a gut microbiota-dependent mechanism involving L. reuteri-enhanced spermidine production and subsequent activation of the Nrf2 antioxidant pathway. This study not only highlights the therapeutic potential of TGCD for male infertility but also underscores the gut-testis axis as a promising target. Fecal abundance of L. reuteri emerges as a potential biomarker for clinical translation in this context.},
}

@article {pmid42373460,
year = {2026},
author = {Li, Y and Yang, Z and Liu, YQ and Liu, Q and Niu, YR and Cai, W and Hu, Y},
title = {[Role of gut-derived immune cells and the gut-lung axis in acute respiratory distress syndrome].},
journal = {Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases},
volume = {49},
number = {7},
pages = {805-809},
doi = {10.3760/cma.j.cn112147-20260126-00059},
pmid = {42373460},
issn = {1001-0939},
support = {2024AFB412//Natural Science Foundation of Hubei Province/ ; 2025020701020248//Wuhan Municipal Health Commission Research Fund/ ; },
mesh = {*Respiratory Distress Syndrome/immunology/physiopathology ; Humans ; *Lung/immunology ; *Gastrointestinal Microbiome ; Animals ; Fecal Microbiota Transplantation ; },
abstract = {Acute respiratory distress syndrome (ARDS) is a critical illness with high incidence and mortality in the intensive care unit (ICU). Recent studies have demonstrated that the "gut-lung axis", a bidirectional regulatory network between the gut and the lungs, plays a pivotal role in the pathophysiology of ARDS. This review focuses on the "homing" mechanisms underlying the directed migration of gut-derived immune cells, particularly ILC2s, ILC3s, and γδ T17 cells, from the gut to the lungs. It also discusses the critical mediating role of the "gut-lymph-lung" pathway in gut-derived lung injury. Furthermore, this article summarizes interventional strategies targeting the gut-lung axis, including modulation of the gut microbiota (probiotics and fecal microbiota transplantation), supplementation with metabolites (such as short-chain fatty acids), and novel nanoparticle-based drug delivery systems. A deeper understanding of this immunoregulatory network will provide new insights and therapeutic targets for precision treatment and clinical translation of ARDS.},
}

*Respiratory Distress Syndrome/immunology/physiopathology
Humans
*Lung/immunology
*Gastrointestinal Microbiome
Animals
Fecal Microbiota Transplantation

@article {pmid42373713,
year = {2026},
author = {Liu, H and Zhi, J and Li, Z and Fan, S and Zhang, N and Liu, M and Xie, R and Wang, W and Feng, N and Wu, Y and Xu, Z and Liu, F},
title = {A nurse-led peer support intervention to enhance decision-making for fecal microbiota transplantation in recurrent UTI: a pilot study.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-58218-2},
pmid = {42373713},
issn = {2045-2322},
support = {2021BYGT-006//Open Fund of Gansu Provincial Key Laboratory of Functional Genomics and Molecular Diagnosis/ ; },
abstract = {To examine the preliminary effects and feasibility of peer support on decision-making regarding fecal microbiota transplantation (FMT) among patients with recurrent urinary tract infections (rUTIs). This was a prospective, two-arm pilot study conducted from September 2023 to April 2024 in the urology outpatient departments of two tertiary hospitals in China using convenience sampling. Patients were assigned to either a peer support group or a control group. The intervention consisted of weekly WeChat-based interactions between trained peer supporters and patients for four weeks. Decision-making was assessed using validated tools including the Decisional Conflict Scale, Preparation for Decision Making Scale, Decision Self-Efficacy Scale, Choice Predisposition Scale, and Decisional Satisfaction Scale, all derived from the Ottawa Decision Support Framework. Anxiety and depression were measured using the Self-Rating Anxiety Scale (SAS) and Self-Rating Depression Scale (SDS). A total of 24 patients were assigned to a peer support group (n = 12) and a control group (n = 12). Compared with the control group, the peer support group showed higher FMT-related knowledge, stronger choice predisposition toward FMT, higher decision-making self-efficacy, and lower decisional conflict after the intervention. No significant between-group differences were observed in preparation for decision making, decisional satisfaction, anxiety, or depression. In this small exploratory pilot study, nurse-led peer support showed preliminary potential to improve selected decision-related outcomes among women with rUTIs considering FMT. Rather than confirming efficacy, this study supports the feasibility of a structured nurse-led peer support protocol and provides a basis for future larger-scale research. Given the small sample size, convenience sampling, and single cultural context, these findings should be interpreted cautiously and require confirmation in larger studies. Future studies should also assess whether these preliminary improvements are sustained and translate into actual treatment decisions and long-term decisional satisfaction.},
}

@article {pmid42365269,
year = {2026},
author = {Fassarella, M and Smidt, H},
title = {Translational human gut microbiome research: What are the missing pieces of the puzzle?.},
journal = {Journal of translational medicine},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12967-026-08490-7},
pmid = {42365269},
issn = {1479-5876},
abstract = {BACKGROUND: Human gut microbiome research has expanded remarkably over the past two decades, revealing the fundamental role of gut microbes in human health and disease. Despite these advances, translation into evidence-based clinical practice and public health implementation remains exceptionally limited. This integrative translational perspective review evaluates human gut microbiome research across four critical aspects: translational successes, barriers to effective translation, applicability of frameworks from other medical disciplines, and strategies to enhance translational progress.

MAIN TEXT: Human gut microbiome research was evaluated through the lens of translational medical research principles, as summarised below. (1) Translational successes in human gut microbiome research are explored by analysing the developmental pathways of major microbiome-based or microbiome-targeted approaches, including faecal microbiota transplantation, probiotics, postbiotics, prebiotics, and dietary interventions, despite overall limited clinical and public health translation. (2) Established translational medical research frameworks served as a foundation to identify missing elements in current human gut microbiome research, including progression through T0-T4 phases, bidirectional knowledge flow, prioritization of unmet patient and societal health needs, patient-centric approaches, stakeholder engagement, and interdisciplinary collaboration. Integration of these principles is discussed in light of the specific characteristics, challenges, and limitations of human gut microbiome research. (3) Translational barriers in human gut microbiome research were analysed beyond limited integration of translational medical principles. These arise from the inherent complexity and high-dimensional nature of the gut microbiome, temporal and inter-individual variability, confounding factors, inconsistent methodological standardization and validation, and fragmentation across research efforts. Collectively, these barriers hinder causal inference, resulting in a low-quality evidence base and limiting effective translation. (4) A framework to advance translational human gut microbiome research is proposed based on the previous findings, including strategic priorities such as education and training in translational research principles for gut microbiome researchers.

CONCLUSIONS: Human gut microbiome research remains largely confined to early translational phases, with progression toward effective translation limited by intrinsic and methodological barriers that hinder causal inference and high-level evidence generation. Integration of core translational medical research principles offers a pathway to bridge these gaps, with education and training of gut microbiome researchers emerging as a key priority for advancing translational progress.},
}

@article {pmid41580587,
year = {2026},
author = {Fiedorová, K and Obručová, H and Grombiříková, H and Vaněrková, M and Blaštíková, E and Štěpánková, S and Husová, L and Freiberger, T},
title = {Longitudinal analysis of gut bacterial and fungal dynamics after solid organ transplantation.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {132},
pmid = {41580587},
issn = {1471-2180},
support = {e-INFRA CZ (ID:90254)//the Ministry of Education, Youth and Sports of the Czech Republic/ ; IG 201802//the Centre of Cardiovascular and Transplantation Surgery (CKTCH)/ ; Programme EXCELES, ID Project No. LX22NPO5104//the European Union, Next Generation EU/ ; MUNI/A/1716/2024//Masarykova Univerzita/ ; },
mesh = {Humans ; *Bacteria/classification/genetics/isolation & purification ; *Organ Transplantation/adverse effects ; Longitudinal Studies ; *Fungi/classification/genetics/isolation & purification ; *Gastrointestinal Microbiome ; Female ; *Mycobiome ; Male ; RNA, Ribosomal, 16S/genetics ; Middle Aged ; Dysbiosis/microbiology ; Adult ; Feces/microbiology ; Aged ; },
abstract = {BACKGROUND: Solid-organ transplantation and related medical treatments can significantly alter the gut microbiome. While disruptions in bacterial communities (dysbiosis) have been associated with infections, rejection, and increased mortality in transplant recipients, research on gut fungal communities (the mycobiome) remains limited. To our knowledge, no study has yet concurrently characterized the bacterial and fungal microbiota or quantified the fungal load longitudinally in patients following solid-organ transplantation. This study aimed to describe temporal changes in these microbial communities and explore associations with clinical outcomes. RESULTS: We analysed the gut microbiota dynamics in 21 solid-organ transplant recipients and 10 healthy volunteers across six timepoints, processing 184 samples using both bacterial (16 S rRNA) and fungal (ITS) amplicon sequencing. Bacterial diversity significantly decreased shortly after transplantation but partially recovered during the later post-transplant phase. In contrast, fungal diversity was consistently lower after transplantation and showed greater temporal variability. Quantitative PCR revealed a transient increase in the fungal load at approximately two weeks post-transplant, which was negatively correlated with bacterial diversity. Patients who experienced clinical complications presented reduced microbial richness, especially during the early post-transplant period. Additionally, we identified correlations between selected fungal taxa and bacterial genera previously linked to dysbiosis, suggesting potential interkingdom interactions that may influence microbiome dynamics after transplantation. CONCLUSIONS: Our study provides a longitudinal overview of both bacterial and fungal microbiota following solid-organ transplantation. The association between fungal load and bacterial diversity indicates possible interkingdom interactions affecting microbiome recovery, but the clinical implications remain to be elucidated. These findings highlight the importance of including fungal communities alongside bacterial microbiota in future research and clinical monitoring.},
}

Humans
*Bacteria/classification/genetics/isolation & purification
*Organ Transplantation/adverse effects
Longitudinal Studies
*Fungi/classification/genetics/isolation & purification
*Gastrointestinal Microbiome
Female
*Mycobiome
Male
RNA, Ribosomal, 16S/genetics
Middle Aged
Dysbiosis/microbiology
Adult
Feces/microbiology
Aged

@article {pmid41933306,
year = {2026},
author = {Adamczak, M and Pokora, P and Kaczmarczyk, M and Gojowy, D and Wierzbicka-Woś, A and Cembrowska-Lech, D and Kolonko, A and Łoniewski, I and Więcek, A},
title = {Intestinal microbiome and acute transplanted kidney rejection - results of a single-center, case-control study.},
journal = {BMC nephrology},
volume = {27},
number = {1},
pages = {},
pmid = {41933306},
issn = {1471-2369},
mesh = {Humans ; *Kidney Transplantation/adverse effects ; *Graft Rejection/microbiology ; Female ; Male ; Case-Control Studies ; *Gastrointestinal Microbiome ; Retrospective Studies ; Adult ; Middle Aged ; Feces/microbiology ; Acute Disease ; },
abstract = {BACKGROUND: Kidney transplantation (KTx) is the preferred form of renal replacement therapy. Acute rejection of the transplanted kidney (AR) may impair long-term outcomes. The gut microbiota influences immune system activity; however, its relationship with AR remains underexplored. This study aimed to investigate the relationship between the gut microbiome and risk of AR shortly after KTx. METHODS: In this single-center, retrospective case-control study, 10 patients with consecutive biopsy-proven AR shortly after KTx (median age 43 (38, 48) years) were matched by sex and age with 20 patients without AR (median age 42 (37, 48) years) during a one-year follow-up after KTx. Stool samples were collected 4–7 days after KTx for microbiome analysis using Illumina shallow shotgun sequencing. Bioinformatics analysis included taxonomic and functional profiling, with predictive modeling performed using a random forest model (RF). Model performance was evaluated using receiver operating characteristic (ROC) curves and the area under the curve (AUC). RESULTS: No significant differences in gut microbiota diversity were observed between the groups. The differential abundance analysis did not identify any taxonomic features that remained significant after adjusting for possible covariates. The predictive RF models varied in performance, with functional KEGG pathway profiles showing the highest predictive value (AUC = 0.73). Key metabolic pathways implicated in such profiles included lipid metabolism, glycan biosynthesis and metabolism, and terpenoid and polyketide metabolism. CONCLUSION: No universal taxonomic gut microbiota markers for AR have been identified. The functional profile of the gut microbiome may be related to AR with specific metabolic pathways potentially involved in the underlying mechanisms. These findings suggest a role of immunomodulation, inflammation, and metabolic regulation in AR.},
}

Humans
*Kidney Transplantation/adverse effects
*Graft Rejection/microbiology
Female
Male
Case-Control Studies
*Gastrointestinal Microbiome
Retrospective Studies
Adult
Middle Aged
Feces/microbiology
Acute Disease

@article {pmid42362695,
year = {2026},
author = {Saensupha, T and Jirahiranpat, A and Pratumwan, N and Bubpamala, T and Jamnongkan, W and Kulthawatsiri, T and Suksawat, M and Thaiwatcharamas, K and Auiewiriyanukul, W and Attapong, M and Sritong, N and Mullish, BH and Phetcharaburanin, J},
title = {Bile reinfusion is associated with shifts in host-microbiota metabolic profiles following cholangiocarcinoma-associated microbiota transplantation.},
journal = {Scientific reports},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41598-026-58698-2},
pmid = {42362695},
issn = {2045-2322},
support = {651H114-C//Graduate School, Khon Kaen University, Thailand/ ; MR/Z504002/1//Medical Research Council Clinician Scientist Fellowship/ ; B13F670075//Program Management Unit for Human Resources & Institutional Development, Research and Innovation/ ; },
abstract = {Cholangiocarcinoma (CCA) is a heterogeneous group of malignant tumours originating along the biliary tract. Previous studies have demonstrated that CCA is characterised by altered gut microbial composition and disrupted bile acid metabolism, both of which are critical determinants of host metabolic homeostasis. Although bile reinfusion (BR) has been proposed to improve surgical outcomes in CCA patients, its systemic metabolic effects and interaction with gut microbiota remain poorly understood. Here, we employed faecal microbiota transplantation (FMT) from CCA patients, with or without BR, into Wistar rats to investigate host-microbiota metabolic interactions using integrated [1]H NMR-based metabolomics and full-length 16S rRNA gene sequencing. Rats receiving CCA-derived microbiota displayed altered systemic metabolic phenotypes, characterised by lower levels of glucose, lactate, and succinate compared to normal microbiota recipients, whilst no significant differences in faecal metabolites were observed between these groups. Notably, BR was associated with shifts in gut microbial composition, marked by enrichment of Lactobacillaceae, altered intestinal fermentation metabolites (decreased short-chain fatty acids and increased succinate), and a convergence of peripheral plasma metabolite profiles towards those observed in healthy microbiota recipients. These findings reveal associations between bile reinfusion and shifts in microbial composition and systemic metabolic phenotypes, providing a basis for investigating microbiota-bile acid-host metabolic crosstalk and potential therapeutic implications for managing CCA-associated dysbiosis.},
}

@article {pmid42364737,
year = {2026},
author = {Hajjar, C and Saint-Criq, V and Thomas, M and Butel, MJ and Bazarbachi, A and Abifadel, M},
title = {The Lung Microbiome in Hematopoietic Stem Cell Transplantation: Immune Interactions, Clinical Consequences, and Emerging Interventions.},
journal = {Respiratory medicine},
volume = {},
number = {},
pages = {109004},
doi = {10.1016/j.rmed.2026.109004},
pmid = {42364737},
issn = {1532-3064},
abstract = {Hematopoietic stem cell transplantation (HSCT) offers curative potential for hematologic malignancies and immune disorders, yet pulmonary complications remain major contributors to non-relapse morbidity and mortality. Traditionally attributed to immune suppression and graft-versus-host disease (GvHD), these complications are increasingly recognized to involve disruption of pulmonary microbial communities. A growing body of clinical and experimental evidence indicates that HSCT-associated perturbations in the lung microbiome, driven by conditioning, antimicrobials, immune injury, and infection, are associated with distinct post-transplant pulmonary phenotypes and, in some cohorts, with mortality risk. Whether these microbial shifts represent causal contributors to lung injury or contextual biomarkers of immune vulnerability remains unresolved, and this distinction carries direct implications for microbiome-targeted intervention. Dysbiotic shifts in the lung have been associated with both infectious and non-infectious complications, including idiopathic pneumonia syndrome, bronchiolitis obliterans syndrome, and fibrotic lung disease. Gut-lung microbial crosstalk may amplify or reflect systemic immune dysfunction, though the directionality of this relationship remains incompletely characterized. Multi-omics approaches, integrating metagenomics, metatranscriptomics, and metabolomics, are beginning to define the host-microbiome interaction signatures that distinguish injury subtypes and predict outcomes. This review synthesizes mechanistic insights into lung microbiome-immune interactions after HSCT, critically appraises the methodological constraints on the current evidence base, and evaluates microbiome-based interventions, including fecal microbiota transplantation, inhaled postbiotics, and precision antimicrobials, as candidate strategies for respiratory protection in transplant recipients, while acknowledging that prospective interventional evidence in this population remains limited.},
}

@article {pmid42350644,
year = {2026},
author = {Suissa, D and Fidelle, M and Reich, E and Pham, TN and Thomas, S and Björk, JR and Liu, P and Zhao, L and Kitaoka, K and Piard, E and Lebhar, I and Tian, AL and Thelemaque, C and Alves Costa Silva, C and Deutsch, E and Loriot, Y and Segata, N and Piccinno, G and Hospers, GAP and Maleki Vareki, S and Silverman, MS and Lenehan, JG and Bataille, V and Boulate, D and Kuznetsova, T and Weersma, RK and Messaoudene, M and Durand, S and van der Aalst, CM and de Koning, HJ and Schuler-Thurner, B and de Vries, IJM and Rafie, E and Saliby, RM and Machaalani, M and Haferkamp, S and Schilling, B and Porcari, S and Ciccarese, C and Iacovelli, R and Cremolini, C and Choueiri, TK and Elkrief, A and Kroemer, G and Heinzerling, L and Chamoto, K and Ianiro, G and Routy, B and Derosa, L and Paragios, N and Zitvogel, L},
title = {Metabolic determinants of cancer immunotherapy outcomes identified by plasma profiling.},
journal = {Nature medicine},
volume = {},
number = {},
pages = {},
pmid = {42350644},
issn = {1546-170X},
abstract = {Immune-checkpoint inhibitors benefit a subset of patients with advanced cancer, and the metabolic determinants of response remain unclear. Here, using targeted metabolomics and metagenomics, we profiled 4,336 plasma samples from 1,714 patients across five tumor types and 16 cohorts spanning Europe and North America, longitudinally sampled during five immune-checkpoint inhibitor-based treatment modalities, including fecal microbiota transplantation. A multimodal machine-learning framework integrating 154 metabolites with clinical variables identified five metabolites, age, body mass index and renal function as predictors of 12-month progression-free survival. The model achieved areas under the curve of 0.88 in training and 0.73 in validation cohorts of 105 and 30 patients, respectively and generalized across seven external cohorts. Histidine was a favorable prognostic feature of survival, whereas long-chain fatty acids and succinate were negatively associated with outcome. Histidine supplementation enhanced antitumor immunity in mice. Histidine-rich diets improved progression-free survival in patients lacking dysbiotic microbiome signatures associated with histidine catabolism.},
}

@article {pmid42351636,
year = {2026},
author = {Loguercio, M and Giamundo, DM and Giglio, A and Buda, E and Ambrosetti, M and Perone, F},
title = {Gut Microbiota: Cardiovascular Disease Prevention and Targeted Therapies.},
journal = {Biomedicines},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/biomedicines14061210},
pmid = {42351636},
issn = {2227-9059},
abstract = {The gut microbiota has emerged as a key regulator of cardiovascular health, influencing metabolic, inflammatory, and vascular pathways. Growing evidence indicates that gut dysbiosis, characterized by reduced microbial diversity, depletion of beneficial short-chain fatty acid-producing bacteria, and enrichment of pro-inflammatory taxa, is associated with major cardiovascular risk factors and disease progression. Microbial-derived metabolites, including trimethylamine/trimethylamine N-oxide, short-chain fatty acids, amino acids and bile acids, may play a central role in modulating lipid metabolism, endothelial function, inflammation, and thrombosis, although the underlying mechanisms remain incompletely understood. Recent multi-omics approaches have expanded this understanding by identifying personalized microbiome-metabolome signatures linked to cardiovascular risk, supporting a shift toward precision medicine. In this review, we summarize current evidence on the composition and functional role of the gut microbiota in cardiovascular disease and critically discuss emerging microbiota-targeted strategies. These include dietary interventions, prebiotics, probiotics, synbiotics, antibiotics, enzyme inhibitors, and fecal microbiota transplantation, which may contribute to both the prevention and adjunctive treatment of cardiovascular conditions. In addition, we address the challenges of integrating gut microbiota management into clinical practice and highlight the importance of tailored strategies, including exercise-based interventions, microbial enzyme inhibitors, and postbiotics. Despite promising preclinical and early clinical data, the translation of microbiome-based therapies into routine practice remains limited by heterogeneity in study design, the lack of standardized protocols, and incomplete mechanistic understanding. Overall, targeting the gut microbiota represents a novel and potentially complementary approach for cardiovascular disease prevention and management, warranting further well-designed clinical studies.},
}

@article {pmid42351694,
year = {2026},
author = {Hijová, E and Bertková, I and Benetinová, V},
title = {Gut Microbiota as an Innovative Therapeutic Target in Cardiovascular Diseases from a Metabolic and Inflammatory Perspective.},
journal = {Biomedicines},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/biomedicines14061267},
pmid = {42351694},
issn = {2227-9059},
abstract = {The gut microbiome plays a key role in the pathogenesis of cardiovascular disease through systemic inflammation, impaired lipid metabolism, and proatherogenic gut metabolites like trimethylamine N-oxide. Gut dysbiosis contributes to decreased level of microbial metabolites such as short-chain fatty acids, bile acids, coprostanol, and phenylacetylglutamine, as well as increased intestinal permeability and platelet hyper-reactivity, and exacerbating cardiovascular risk. New microbiome-focused treatments such as probiotics, prebiotics, synbiotics, and fecal microbiota transplantation are showing potential to help reduce cardiovascular diseases. However, bringing these therapies into clinical settings is difficult because they vary by strain and individual response. The gut-heart connection offers an innovative approach to preventing and treating heart condition, but additional research is needed to ensure lasting effectiveness and safety.},
}

@article {pmid42353350,
year = {2026},
author = {Trifonova, EA and Ivanov, RA and Kochetov, AV and Lashin, SA},
title = {The Microbiota in the Diagnosis and Treatment of Autism Spectrum Disorder.},
journal = {International journal of molecular sciences},
volume = {27},
number = {12},
pages = {},
doi = {10.3390/ijms27125636},
pmid = {42353350},
issn = {1422-0067},
mesh = {Humans ; *Autism Spectrum Disorder/therapy/diagnosis/microbiology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; *Gastrointestinal Microbiome ; Animals ; Signal Transduction ; Brain/metabolism ; Diet, Ketogenic ; },
abstract = {Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by impaired social interaction, communication deficits, and repetitive behaviors. Recent research highlights the role of the gut microbiota in ASD pathophysiology, particularly through the microbiota-gut-brain axis. The microbiota may influence neurodevelopment via multiple signaling pathways, including the GABAergic and serotonergic systems, as well as the mTOR signaling pathway. This analytical review examines current evidence on microbiota alterations in ASD and evaluates microbiota-targeted strategies for diagnosis and treatment, focusing on fecal microbiota transplantation (FMT), probiotics, and diet-based therapeutic approaches. The review also provides a critical appraisal of the microbiota-gut-brain axis in the context of autism spectrum disorder.},
}

Humans
*Autism Spectrum Disorder/therapy/diagnosis/microbiology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
*Gastrointestinal Microbiome
Animals
Signal Transduction
Brain/metabolism
Diet, Ketogenic

@article {pmid42353674,
year = {2026},
author = {Vashishtha, K and Borah, P and Sonowal, R},
title = {The ESKAPE Challenge: Understanding Resistance and Exploring Alternative Treatments.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {15},
number = {6},
pages = {},
doi = {10.3390/antibiotics15060550},
pmid = {42353674},
issn = {2079-6382},
abstract = {Antimicrobial resistance (AMR) constitutes a critical and escalating global public health challenge, severely limiting the potential of existing antimicrobial drugs and escalating infection-associated morbidity and mortality rates. This analysis focuses on the ESKAPE pathogens (Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species), which are prioritized by the World Health Organization (WHO) and represent a significant cause of nosocomial infections due to their extensive drug resistance. We provide an in-depth review of the global prevalence and specific antibiotic-resistant mechanisms of these pathogens. Due to the decline in the traditional antibiotic development pipeline, accelerated development of alternative therapeutic strategies is essential. The review comprehensively discusses innovative non-traditional therapies currently being explored to bypass traditional antibiotic limitations, such as phage therapy, antimicrobial peptides (AMPs), anti-virulence therapies, fecal microbiota transplantation (FMT), and targeted CRISPR-based approaches. Addressing the ESKAPE challenge requires a concerted, multi-sectoral strategy guided by the One Health principle, focusing on enhancing public awareness, improving surveillance and research, optimizing judicious antibiotic use, and cultivating sustainable investment in novel interventions.},
}

@article {pmid42354799,
year = {2026},
author = {Wu, L and Li, Z and Zhu, J and Sun, Z and Yan, L and Luo, M and Chen, H and Yin, Y},
title = {Engineering the Gut Microbiome: Emerging Genome-Editing Strategies and Therapeutic Applications.},
journal = {Microorganisms},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/microorganisms14061174},
pmid = {42354799},
issn = {2076-2607},
support = {No. 32460015//National Natural Science Foundation of China/ ; No. 2025LT0103004//Guangxi Science and Technology Department/ ; },
abstract = {The gut microbiome, often termed the human "second genome", profoundly influences host physiology through metabolic interactions, immune modulation, and gut-brain axis signaling. Dysbiosis is implicated in the pathogenesis of obesity, inflammatory bowel disease (IBD), malignancies, and neuropsychiatric disorders. However, traditional gut microbiota interventions, such as probiotic supplementation and fecal microbiota transplantation (FMT), still exhibit significant limitations in precision therapeutics. Probiotic intervention fails to achieve precise regulation at the strain or genetic level, and although FMT demonstrates definitive efficacy against recurrent Clostridioides difficile infection (rCDI), its therapeutic outcomes and safety profiles show marked interindividual variability in ulcerative colitis (UC), metabolic syndrome, and other diseases, with insufficient treatment specificity to meet the practical demands of clinical precision intervention. Recent advancements in genome editing technologies, particularly Clustered Regularly Interspaced Short Palindromic Repeats (CRISPR)-CRISPR-associated (Cas) proteins systems and base editors, have enabled targeted functional manipulation of specific gut commensals and optimization of community architectures. These engineered strategies, combined with sophisticated delivery systems, demonstrate substantial potential in disease treatment, diagnostic monitoring, and immune modulation. This review systematically examines core editing methodologies, innovative delivery platforms, and targeted design strategies, elucidating their applications in metabolic disorders, IBD, cancer immunotherapy, and neuropsychiatric conditions. We critically analyze current technical bottlenecks and biosafety concerns while prospecting future directions, including in situ editing, artificial intelligence (AI)-driven design, and personalized engineering. Collectively, these insights aim to facilitate the clinical translation of gut microbiome engineering from bench to bedside.},
}

@article {pmid42354867,
year = {2026},
author = {Zambelli, G and Masetti, M and Rasmi, S and Addati, I and Bonacorsi, L and Diona, S and Esposito, S},
title = {Restoring Microbial Balance: Clinical Applications, Challenges, and Future Directions of Fecal Microbiota Transplantation in Pediatric Disorders.},
journal = {Microorganisms},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/microorganisms14061241},
pmid = {42354867},
issn = {2076-2607},
abstract = {Fecal microbiota transplantation (FMT) has emerged as a microbiota-directed therapeutic strategy with established efficacy in recurrent Clostridioides difficile infection (rCDI) and expanding investigational applications in pediatric medicine. Given the central role of the gut microbiota in immune maturation, metabolic homeostasis, and colonization resistance-particularly during early life-restoring microbial diversity represents a biologically plausible intervention for disorders characterized by dysbiosis. This narrative review critically examines current evidence regarding the indications, efficacy, safety, and practical considerations of FMT in pediatric populations. A structured literature search was conducted across PubMed/MEDLINE, Scopus, Web of Science, and the Cochrane Library from inception through December 2025. Eligible studies included randomized controlled trials, observational studies, systematic reviews, meta-analyses, and guideline statements addressing pediatric FMT. RCDI remains the primary and best-supported indication, with reported success rates exceeding 80% after a single FMT and approaching 90% with repeat procedures. Evidence for other indications-including inflammatory bowel disease (IBD), malignancy-associated CDI, transplant recipients, multidrug-resistant organism (MDRO) decolonization, neurodevelopmental disorders, allergic colitis, and functional gastrointestinal disorders-remains limited and heterogeneous. While short-term remission rates in pediatric ulcerative colitis appear promising, data derive largely from small, non-standardized studies, and long-term efficacy and safety remain insufficiently defined. FMT usage in immunocompromised children, particularly oncology and transplant populations, is controversial due to limited pediatric-specific evidence and theoretical risks. Substantial variability in donor screening, preparation methods, dosing, and administration routes further limits standardization. Currently, FMT should be considered established therapy for pediatric rCDI, whereas other applications require well-designed, multicenter trials with long-term follow-up to clarify safety and clinical benefit.},
}

@article {pmid42354994,
year = {2026},
author = {Bao, S and Xu, S and Wang, Z and Chai, S and Wang, S and Dai, D and Wang, X and Lv, J},
title = {Fecal Microbiota Transplantation Improves Biota and Hepatic Metabolism, Promoting Growth in SD Rats Under Hypobaric Hypoxia Exposure.},
journal = {Microorganisms},
volume = {14},
number = {6},
pages = {},
doi = {10.3390/microorganisms14061370},
pmid = {42354994},
issn = {2076-2607},
abstract = {Hypobaric hypoxia poses a serious threat to growth and development and can induce pronounced inflammatory responses. These effects are closely associated with the gut microbiota. However, the underlying mechanisms, particularly the role of gut microbiota in regulating hepatic metabolism under chronic hypoxic conditions, remain poorly understood. In this study, SD rats were used as recipients and assigned to three groups: a hypobaric hypoxia group (H), an antibiotic-treated group (HA), and an antibiotic-treated group receiving fecal microbiota transplantation from plateau zokors (HAM). All rats were maintained in a hypobaric hypoxia chamber simulating an altitude of 6000 m for 30 days. Subsequently, growth performance, routine hematological parameters, and multi-omics profiles were evaluated. Compared with the H group, both the HAM and HA groups showed significantly increased average daily gain (ADG) (p < 0.05), while the ADG/ADFI ratio was significantly higher in the HAM group than in the H group (p < 0.05). Monocyte count (Mon#) and monocyte percentage (Mon%) were significantly higher in the HA group than in both the H and HAM groups (p < 0.05). Microbiota analysis revealed significant enrichment of Lachnospiraceae_NK4A136_group in the HAM group, whereas Desulfovibrio was significantly enriched in the HA group (p < 0.05). Fecal metabolomics showed that ursodeoxycholic acid (UDCA) was significantly increased in the HAM group (p < 0.05). In the liver metabolome, the anti-inflammatory lipid FAHFA 18:1/20:3 was significantly elevated in the HAM group, whereas pro-inflammatory factors, including uric acid and leukotriene D4, were significantly reduced (p < 0.05). Correlation analysis further demonstrated that the abundance of Lachnospiraceae was positively correlated with FAHFA 18:1/20:3 and negatively correlated with uric acid and creatinine (p < 0.05). Collectively, these findings indicate that the gut microbiota can modulate gut-liver metabolism, alleviate inflammatory responses, and enhance the adaptation of rats to hypoxic environments. This study provides valuable insights into potential strategies for promoting sustainable animal health and adaptation under hypoxic conditions.},
}

@article {pmid42355348,
year = {2026},
author = {Piquer-Esteban, S and Pérez-Brocal, V and Domínguez-Santos, R and Latorre, A and García-Ferris, C and Moya, A},
title = {Blattella germanica Selects Microbiota Taxa from Feces and Environmental Inputs.},
journal = {Insects},
volume = {17},
number = {6},
pages = {},
doi = {10.3390/insects17060615},
pmid = {42355348},
issn = {2075-4450},
support = {Prometeo/2018/133//Conselleria d'Educació, Generalitat Valenciana (Spain)/ ; CIPROM/2021/042//Conselleria d'Educació, Generalitat Valenciana (Spain)/ ; FPU20/05756//Spanish Ministry of Universities/ ; },
abstract = {Cockroaches display a double symbiosis: an obligate intracellular one with Blattabacterium spp., and a complex extracellular non-vertically transmitted gut microbiota, that may be affected by horizontally transmitted factors. Four experiments using 16S rRNA gene amplicon sequencing were conducted to analyze the microbiota of the hindgut and feces of adult cockroaches. They aimed to understand the influence of the environment and feces on the acquisition and development of the hindgut microbiota. We observed that sample type (hindgut vs. feces), rearing conditions (environment, i.e., place and diet), coprophagy, and host influenced microbiota composition. Cockroaches initially germ-free, placed in non-sterile conditions and with blocked parental coprophagy, were unable to develop the normal microbiota of the control population, demonstrating that coprophagy is essential for acquiring a normal microbiota. This also showed that, in the absence of parental fecal input, the cockroach gut microbiota is strongly diminished. Moreover, when exploring fecal microbiota differences among three cockroach species, the greatest divergence was observed between Periplaneta americana and Blattella germanica, with Blatta orientalis occupying an intermediate position. Therefore, P. americana was selected for fecal transplantation on B. germanica. This transplantation experiment indicates that different species select different gut microbes, and that even when they receive feces from other species, only some of those bacteria are retained. Overall, these results suggest that beyond other factors, the host species had the strongest influence on shaping the cockroach gut microbiota.},
}

@article {pmid42356344,
year = {2026},
author = {Ciurea, NA and Mahdi, L and Graziani, A and Di Ciaula, A and Portincasa, P and Khalil, M},
title = {Targeting the Human Gut Microbiota-Between Conventional Therapy and Precision Genetic Engineering.},
journal = {Nutrients},
volume = {18},
number = {12},
pages = {},
doi = {10.3390/nu18121958},
pmid = {42356344},
issn = {2072-6643},
support = {CUP H93C22000950001; HORIZON-HLTH-2022-STAYHLTH-01-05; Project 101080329//PRIMA Programme (Partnership for Research and Innovation in the Mediterranean Area/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/genetics ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; *Genetic Engineering/methods ; *Precision Medicine/methods ; Prebiotics ; },
abstract = {The gut microbiota is increasingly examined as a therapeutic target because it contributes to epithelial barrier integrity, microbial metabolite production, bile acid transformation, immune regulation, and communication between the gut and distant organs. This structured narrative review synthesizes evidence on microbiota involvement in metabolic, gastrointestinal, hepatic, cancer, and neuroimmune conditions, including MASLD/MASH, inflammatory bowel disease, irritable bowel syndrome, obesity, type 2 diabetes, hypertension, colorectal cancer, Parkinson's disease, and autism spectrum disorder. Across these conditions, microbiome findings are biologically plausible but heterogeneous. Many associations are shaped by diet, geography, medication exposure, host genetics, disease stage, sampling methods, and analytical pipelines. Microbial alterations should therefore be interpreted as context-dependent signals and candidate modifiers rather than universal causal markers. Conventional microbiota targeted strategies include diet, physical activity, prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation. These approaches are clinically familiar, but their effects are often broad, host specific, strain dependent, and difficult to assign to one mechanism. Fecal microbiota transplantation has the clearest clinical role in recurrent Clostridioides difficile infection, while evidence for most other indications remains inconsistent. Engineered microbial therapeutics offer greater experimental precision through signal sensing, payload delivery, metabolic modulation, and genetic circuit design. However, most evidence remains preclinical or early translational. Progress requires stronger human trials, standardized methods, mechanistic validation, safety monitoring, ecological containment, transparent reporting, and proportionate regulation.},
}

Humans
*Gastrointestinal Microbiome/physiology/genetics
Fecal Microbiota Transplantation
Probiotics/therapeutic use
*Genetic Engineering/methods
*Precision Medicine/methods
Prebiotics

@article {pmid42356496,
year = {2026},
author = {Zhang, W and Guo, X and Zhang, J and Zhang, YW and Li, C},
title = {Microbiota-Derived SCFAs Mediate the Synergistic Antidepressant Effects of Dajianzhong Decoction and Ketamine via FFAR2-NLRP3-IL-1β Signaling.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {19},
number = {6},
pages = {},
doi = {10.3390/ph19060877},
pmid = {42356496},
issn = {1424-8247},
support = {32371304//National Natural Science Foundation of China/ ; 2023A1515110683//Guangdong Academy of Sciences/ ; 2024A1515011695//Guangdong Academy of Sciences/ ; },
abstract = {Background: Ketamine is a rapid-acting antidepressant for major depressive disorder; however, its effects are short-lasting and associated with neurotoxic side effects. Thus, identifying strategies to prolong its antidepressant effects is of critical importance. It has been shown that Dajianzhong Decoction (DJZT) prolongs the antidepressant effects of ketamine through modulation of the gut microbiota, but the underlying mechanisms remain unclear. Method: Fecal microbiota transplantation, metabolomic profiling, pharmacological interventions, and behavioral approaches were employed together with a chronic unpredictable mild stress (CUMS) mouse model to investigate how microbiota-derived signals mediate the combined effects of DJZT and ketamine. Results: Microbiota from CUMS mice induced depressive-like behaviors in recipient mice, accompanied by reduced levels of short-chain fatty acids (SCFAs), decreased FFAR2 expression in the medial prefrontal cortex, and increased neuroinflammation and synaptic deficits. These alterations were reversed by microbiota from DJZT-plus-ketamine-treated donors. Notably, acetic acid and isobutyric acid were identified as key SCFAs restored by the combined treatment and were significantly associated with behavioral outcomes. Moreover, SCFA supplementation recapitulated these effects by activating FFAR2 and suppressing NLRP3-IL-1β signaling. Importantly, pharmacological inhibition of FFAR2 using GLPG0974 abolished the antidepressant-like, anti-inflammatory, and synaptic protective effects of the microbiota from DJZT-plus-ketamine-treated donors. Conclusions: These findings demonstrate that microbiota-derived SCFAs mediate the synergistic antidepressant effects of DJZT and ketamine via a central FFAR2-dependent mechanism involving suppression of neuroinflammation. This work highlights a potential role of the SCFA-FFAR2-NLRP3- IL-1β axis in influencing ketamine efficacy and points to microbiota-modulating strategies as a possible avenue for improving antidepressant therapy.},
}

@article {pmid42357401,
year = {2026},
author = {Liu, X and Hu, J and Chen, Y and Shi, B and Shang, Z and Liang, Y},
title = {Pharmacokinetics, Excretion, and Metabolite Profiling of Leonurine in Rats: Evidence for Extensive Phase II Conjugations.},
journal = {Molecules (Basel, Switzerland)},
volume = {31},
number = {12},
pages = {},
doi = {10.3390/molecules31122002},
pmid = {42357401},
issn = {1420-3049},
mesh = {Animals ; *Gallic Acid/analogs & derivatives/pharmacokinetics/administration & dosage/chemistry/urine/metabolism ; Rats ; Male ; Administration, Oral ; Feces/chemistry ; Tandem Mass Spectrometry ; Rats, Sprague-Dawley ; Chromatography, Liquid ; Metabolome ; Biological Availability ; },
abstract = {Leonurine, a bioactive alkaloid from Leonurus japonicus, has attracted considerable pharmacological interest, yet its in vivo disposition remains insufficiently defined. In the present study, the pharmacokinetics, excretion, and metabolic profile of leonurine were systematically investigated in rats after intravenous (IV), oral (PO), and intraperitoneal (IP) administration. A validated LC-MS/MS method was used to quantify leonurine in plasma, urine, and feces, and high-resolution MS was applied for metabolite profiling. Following IV administration, leonurine exhibited rapid systemic disposition, with a half-life of 2.48 h and a clearance of 152 mL/min/kg. Oral exposure was negligible, with an absolute bioavailability of 0.14%, whereas IP administration produced markedly higher systemic exposure (66.6%). Recovery of unchanged leonurine in urine and feces remained low across all dosing routes, with total excretory recovery below 6% of doses. The results indicated that metabolic conversion, rather than parent drug excretion, was the dominant elimination pathway. A total of 30 leonurine-related components were characterized in vivo, including 24 previously unreported metabolites. The metabolic profile was dominated by phase II conjugation, comprising 12 glucuronidated and 12 sulfated metabolites, together with hydrolysis, methylation/demethylation, and other transformation products. Notably, ester bond cleavage was identified as one of the major primary biotransformation routes, and several glucuronide and sulfate conjugates were also formed on hydrolysis-derived fragments. These findings provide a more comprehensive view of leonurine disposition in rats and offer a mechanistic basis for its rapid clearance and limited systemic availability after oral administration.},
}

Animals
*Gallic Acid/analogs & derivatives/pharmacokinetics/administration & dosage/chemistry/urine/metabolism
Rats
Male
Administration, Oral
Feces/chemistry
Tandem Mass Spectrometry
Rats, Sprague-Dawley
Chromatography, Liquid
Metabolome
Biological Availability

@article {pmid42358262,
year = {2026},
author = {Ji, Y and Zhao, L and Wang, L and Wang, A and Zhang, C and Xie, Y and Luo, X},
title = {Fecal microbiota transplantation in obesity: a comprehensive overview from basic research to clinical application.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1840517},
pmid = {42358262},
issn = {1664-302X},
abstract = {BACKGROUND: Obesity involves microbiota dysbiosis, low-grade inflammation, and insulin resistance, which interacts with multiple metabolic disorders. Fecal microbiota transplantation (FMT) is an emerging therapeutic approach in obesity that enhances intestinal barrier function and regulates energy metabolism.

AIM: To provide a comprehensive overview of publication trends, research collaborations, hotspots, future directions, and the current clinical application status of FMT in obesity.

METHODS: Literature searches were conducted in the Web of Science (WoS) and PubMed databases. The primary analysis was performed using the WoS database for bibliometric analysis, while PubMed was searched to supplement the clinical research landscape, ensuring data comprehensiveness and methodological rigor.

RESULTS: A total of 517 papers were finally included, of which 116 (22.44%) were published in the top 10 academic journals. Most publications originated from China (n = 246, 47.6%) and Zhejiang University contributed the most publications (n = 18, 3.5%). Gut Microbes ranked first (21 publications, IF 10.931), followed by Frontiers in Microbiology (19, IF 4.504) and Nutrients (14, IF 4.919). Research hotspots have shifted toward "targeting the gut microbiota." "Oral supplementation" and targeted "prebiotics" may be more accessible in the future. The mini literature review of 21 clinical trials revealed that metabolic improvements following FMT are often transient and highly variable across individuals. No standardized protocol for donor selection, delivery route, or outcome measurement currently exists, and most trials had small sample sizes.

CONCLUSION: Although FMT shows promise, its clinical benefits remain transient and variable across individuals. Current evidence does not yet support routine clinical application. Targeted oral microbiota supplementation may represent a future direction, but high-quality, large-scale clinical trials are urgently needed to establish standardized protocols and evaluate long-term safety and efficacy.},
}

@article {pmid42358304,
year = {2026},
author = {Mei, X and Yang, Y and Wen, Y and Zhang, X and Li, Z and Yang, T and Li, L},
title = {Perinatal phlorizin alleviates maternal high-fat diet-induced metabolic syndrome in female mouse offspring and is associated with modulation of the gut microbiota.},
journal = {Frontiers in nutrition},
volume = {13},
number = {},
pages = {1799829},
pmid = {42358304},
issn = {2296-861X},
abstract = {INTRODUCTION: Maternal obesity induces transgenerational metabolic syndrome (MS). The role of phlorizin (PHZ) in improving MS has been confirmed; however, the transgenerational metabolic benefits of PHZ in female offspring remain unclear. This study aimed to investigate whether perinatal PHZ intake could mitigate the adverse metabolic effects of maternal high-fat diet (HFD) in female offspring and to elucidate the role of the gut microbiota in mediating these transgenerational effects.

METHODS: C57BL/6 mice with maternal HFD ± perinatal PHZ (0.8 g/kg diet) intervention were used. After weaning, Female offspring's glucolipid metabolism, gut barrier, gut microbiota, and SCFAs were analyzed. Obesogenic dietary challenge and fecal microbiota transplantation (FMT) were implemented to verify microbiota mediation.

RESULTS: Maternal HFD induces metabolic abnormalities in female offspring, characterized by disrupted glucolipid metabolism during weaning and mild obesity. In adulthood, although these offspring did not display overt obesity, they exhibited gut microbial dysbiosis (increase Firmicutes/Bacteroidetes ratio and pro-inflammatory bacteria), accompanied by insulin resistance and impaired intestinal barrier function, along with a significantly increased obesity susceptibility. Maternal PHZ co-intervention ameliorated MS and restored gut microbial balance in adulthood, increased the abundance of SCFA-producing bacteria (Akkermansia muciniphila and Blautia sp.), elevated fecal SCFAs and serum GLP1/2 levels, improved gut barrier integrity, alleviated inflammatory conditions, and reduced obesity susceptibility. To eliminate the protective effect of estrogen metabolism, antibiotic-treated (ABX) male mice were selected as the recipients for FMT. ABX male mice receiving FMT from PHZ-intervened female offspring could attenuate MS induced by receiving FMT from maternal HFD offspring via the gut microbiota-SCFA pathway.

CONCLUSION: Our findings suggested that maternal PHZ alleviates maternal HFD-induced transgenerational metabolic dysfunction in female offspring and is associated with modulation of the gut microbiota, positioning PHZ as a promising functional food component with transgenerational metabolic protective potential.},
}

@article {pmid42358596,
year = {2026},
author = {Kent, J and Chao, J and Liao, W and Singla, S},
title = {Exploring the Gut Microbiome's Association in Psoriasis and Psoriatic Arthritis: A Scoping Review.},
journal = {Journal of psoriasis and psoriatic arthritis},
volume = {},
number = {},
pages = {24755303261464171},
pmid = {42358596},
issn = {2475-5311},
abstract = {INTRODUCTION: Psoriasis (PsO) and psoriatic arthritis (PsA) are chronic inflammatory conditions treated with primarily immune-modulating medication. However, interest is growing in gut microbiome therapies. Studies have reported altered gut microbiota in PsO/PsA and explored probiotics and fecal microbiota transplantation (FMT) as potential therapies. This review synthesizes global studies on the microbiome's associations in PsO/PsA.

METHODS: We conducted a scoping literature review to understand the association between gut microbiota in PsO and PsA patients. Pubmed was used to identify 4,126 published manuscripts between 2015-2025. Thirty studies were included, encompassing 749,275 participants, with balanced gender representation and ages ranging from 18 to 76 years. These studies included 21 case-control studies, 1 case-series, 2 genome-wide analyses, 5 clinical trials, and 1 retrospective review.

RESULTS: Eighteen studies reported significant gut microbiome differences in PsO/PsA vs healthy controls. Variation in the Firmicutes/Bacteroides (F/B) ratio was of interest, with one study suggesting a low F/B ratio and five studies suggesting an elevated F/B ratio in PsO. A higher F/B ratio was linked to increased acetate production. Acetate and propionate, key short-chain fatty acids (SCFAs), were associated with modulation of the IL-23/Th17 axis in psoriasis and activation of keratinocytes. The role of therapeutics targeting the gut microbiome was explored. Ustekinumab and tofacitinib altered gut microbiome composition. Probiotic and FMT interventions showed mixed outcomes. Six of eight probiotic studies reported increased SCFA producing species and/or reduced inflammatory markers. FMT improved immune markers in mice but had no significant benefit in human trials.

CONCLUSION: Alterations in the microbiome linked to inflammation and immune response, suggest the microbiome as a potential therapeutic target for PsO/PsA.},
}

@article {pmid42359346,
year = {2026},
author = {Wu, L and Fang, J and Chen, M and Si, YC},
title = {Acupuncture modulates the microbiota-gut-brain axis to treat irritable bowel syndrome: a mechanistic exploration.},
journal = {Frontiers in neuroscience},
volume = {20},
number = {},
pages = {1820371},
pmid = {42359346},
issn = {1662-4548},
abstract = {Irritable bowel syndrome (IBS) is a common functional gastrointestinal disorder involving dysregulation of the microbiota-gut-brain (MGB) axis. Acupuncture effectively alleviates IBS symptoms, yet its underlying mechanisms remain incompletely understood. This review synthesizes current evidence to propose a mechanistic framework by which acupuncture treats IBS through MGB axis modulation. We systematically examine: (1) MGB axis dysfunction in IBS pathophysiology across neural, endocrine, and immune pathways; (2) acupuncture's modulation of gut microbiota structure (alpha/beta diversity, specific bacterial genera); (3) functional consequences including enhanced short-chain fatty acid production and tryptophan metabolism; (4) causal evidence from fecal microbiota transplantation; (5) correlations between microbiota changes and clinical improvement. Key findings reveal that acupuncture induces "convergent remodeling" of microbial structure toward a healthy profile, exerts "bidirectional regulation" on beneficial and harmful bacteria, and establishes a "niche selection" mechanism via neuro-immune pathways. These microbiota-mediated effects integrate with neural, endocrine, and immune pathways, forming a "point-to-surface" networked regulatory pattern that explains acupuncture's dual efficacy in alleviating both gastrointestinal and psychological symptoms. This review provides a novel theoretical framework for understanding acupuncture's therapeutic mechanisms and supports its clinical application in IBS management.},
}

@article {pmid42359605,
year = {2026},
author = {Feng, J and Liu, X and Zhu, H and Yang, Y and Liu, W and Jiang, X and Yang, Z},
title = {Early diabetes-like phenotypes in germ-free mice induced by gut microbiota from patients with type 2 diabetes.},
journal = {Animal models and experimental medicine},
volume = {},
number = {},
pages = {},
doi = {10.1002/ame2.70229},
pmid = {42359605},
issn = {2576-2095},
support = {2022YFF0710600//National Key Research and Development Program of China/ ; 2021-1-I2M-035//Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences/ ; 2023-PT180-01//Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences/ ; 20250333//National High-level Innovation and Entrepreneurship Talents Program for Young Backbone Talents (SpringBuds Project)/ ; },
abstract = {BACKGROUND: The contribution of gut microbiota to the early stage of type 2 diabetes (T2D) remains incompletely understood. This study established a germ-free mouse model colonized with gut microbiota from donors with T2D to determine whether diabetes-associated microbiota could induce early diabetes-like phenotypes.

METHODS: Human fecal samples were collected from 18 healthy donors and 14 donors with T2D for microbiota profiling. Based on these features, samples from 12 healthy donors and 3 donors with T2D were selected, pooled within each group, and transplanted into germ-free mice, generating a healthy microbiota recipient group (HM, n = 14) and a diabetes-associated microbiota recipient group (DM, n = 13). Glucose homeostasis was assessed over 10 weeks using fasting blood glucose and intraperitoneal glucose tolerance tests. Gut microbial succession was analyzed by 16S rRNA sequencing. Fecal and plasma metabolomics were performed to identify metabolic and their associations with microbial changes.

RESULTS: DM mice developed an early diabetes-like phenotype characterized by progressive impairment of glucose tolerance, reduced insulin levels, and mild renal alterations, without sustained overt fasting hyperglycemia. Microbial divergence emerged before stable metabolic dysfunction and was accompanied by persistent dysbiosis in DM mice. Integrated metabolomic analysis identified coordinated alterations in fecal and plasma metabolites, with cholic acid and L-Dopa decreased in both compartments. L-Dopa showed consistent associations with altered genera, particularly Ruminococcus and Sellimonas.

CONCLUSIONS: Transplanting diabetes-associated human gut microbiota effectively induced early glucose dysregulation in germ-free recipient mice. This model provides a framework for studying microbiota-associated events during early T2D-related metabolic deterioration.},
}

@article {pmid42361932,
year = {2026},
author = {Ying, Y and Zheng, X and Yang, J and Ye, H and Dong, Z and Ji, Y and Li, S and Tan, X and Zhang, W},
title = {Tong-Xie-Yao-Fang Ameliorates IBS-D: Potential Role of Alistipes finegoldii-associated Gut Tryptophan Indole Metabolism.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {122061},
doi = {10.1016/j.jep.2026.122061},
pmid = {42361932},
issn = {1872-7573},
abstract = {Irritable bowel syndrome with diarrhea (IBS-D) is a prevalent chronic gastrointestinal condition characterized by visceral hypersensitivity, low-grade mucosal inflammation, and impaired epithelial barrier integrity. Current therapies remain limited, highlighting the need for more alternative strategies. Tong-Xie-Yao-Fang (TXYF), a classical Chinese herbal formula, has shown clinical efficacy in IBS-D, however, the mechanisms underlying its therapeutic effects remain unclear.

AIM OF THE STUDY: This study aimed to investigate whether and how TXYF exerts therapeutic effects by modulating colonic tryptophan metabolism, with a particular focus on the gut microbiota.

MATERIALS AND METHODS: IBS-D model was induced by combining chemical irritation and wrap restraint stress in C57BL/6J mice, and multi-omics approaches were employed to identify specific microbiota and metabolites modulated by TXYF. The multi-omics findings were further verified in vivo and in vitro.

RESULTS: TXYF treatment significantly alleviated IBS-D symptoms in our model. Non-targeted metabolomics identified the tryptophan-indole pathway as a key axis modulated by TXYF, with indole-3-acetic acid (IAA) emerging as a prominent differential metabolite in colonic tissue. Western blot analysis showed that TXYF activated the aryl hydrocarbon receptor (AhR) in the colon. Integrative metagenomic and metabolomic analyses revealed a strong association between Alistipes finegoldii and colonic indole and IAA levels. Consistent with these findings, transplantation of A. finegoldii combined with tryptophan supplementation, or administration of IAA alone, recapitulated the therapeutic effects of TXYF against IBS-D. In vitro, both IAA and faecal supernatant from TXYF-treated mice protected against tumour necrosis factor-induced epithelial barrier disruption in an AhR-dependent manner.

CONCLUSION: Collectively, the present study suggests that the therapeutic efficiency of TXYF against IBS-D is closely associated with its ability to modify microbiota-derived colonic IAA production, with gut microbiota member Alistipes finegoldii playing a key role in this effect.},
}

@article {pmid42361952,
year = {2026},
author = {Guo, Y and Liu, A and Hao, X and Cao, X and Li, Y and Liu, X},
title = {The gut microbiota, neurodevelopment and autism spectrum disorder: A close connection.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111811},
doi = {10.1016/j.pnpbp.2026.111811},
pmid = {42361952},
issn = {1878-4216},
abstract = {The gut microbiota plays a crucial role in early neurodevelopment, particularly during the highly adaptable prenatal and postnatal stages. Dysbiosis in these periods can disrupt the microbiota-gut-brain axis, hinder neural development, and increase the risk of autism spectrum disorder (ASD). This review examines how maternal and infant gut microbiota dysbiosis affects neurodevelopment, explores microbial differences in ASD children and their neurotypical siblings, and analyzes the link between microbial patterns and ASD severity. It also summarizes current microbiota-targeted therapies for ASD and their mechanisms. Overall, the review aims to connect maternal-infant gut microbiota, neurodevelopment, and ASD, providing insights for microbiota-based prevention and intervention strategies for ASD.},
}

@article {pmid42362557,
year = {2026},
author = {Shuai, Y and Xing, J and Liu, X and Song, Z and Lin, S and Lu, C and Zeng, W and Wang, G},
title = {Atractylodes macrocephala polysaccharide orchestrates anti-tumor immunity via a dual-network mechanism targeting the gut microbiota and spleen.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {42362557},
issn = {2055-5008},
support = {81873225//National Natural Science Foundation of China/ ; },
abstract = {Colorectal cancer (CRC) is a common global malignancy, and its advanced stage is closely linked to a gut microbiota-metabolism-immunity vicious cycle requiring early intervention. In this study, anti-CRC effects of PAMK in CT26 tumor-bearing mice were explored. Results showed that PAMK significantly inhibited tumor growth and improved the quality of life of tumor-bearing mice by enhancing antitumor immunity, including increased NK cell infiltration and NKG2D expression, elevated CD4[+]:CD8[+] ratios, and higher serum IFN-γ levels. However, therapeutic effects of PAMK were not observed in antibiotic‑induced microbiota depletion (AIMD) mice. Notably, following fecal microbiota transplantation (FMT), therapeutic effects of PAMK were largely restored. PAMK alleviated tumor-induced gut microbiota dysbiosis characterized by enriched g_Alistipes, and remodeled fatty acid and steroid metabolism, which was closely associated with enhanced antitumor immunity and a potential microbiota-metabolism-immunity axis. Meanwhile, PAMK modulated multiple metabolic, circadian and immune pathways in the spleen as verified by transcriptomics and qPCR. Integrative multi-omics analysis indicated that the gut microbiota-metabolite-spleen gene axis may act synergistically to mediate anti-CRC effects of PAMK in tumor-bearing mice. This study highlights the potential of PAMK in CRC tumor immune adjuvants, providing experimental and theoretical support for its clinical translation and novel tumor immunotherapies.},
}

@article {pmid41729343,
year = {2026},
author = {Bénard, MV and Zonneveld, R and Haaften, PB and Wentink-Bonnema, EMS and Matamoros, S and Ponsioen, CY},
title = {Lower prevalence of Blastocystis spp. and Dientamoeba fragilis in ulcerative colitis and association with disease activity.},
journal = {European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology},
volume = {},
number = {},
pages = {},
pmid = {41729343},
issn = {1435-4373},
abstract = {AIM: To evaluate the prevalence of intestinal protozoan parasites Blastocystis spp. and Dientamoeba fragilis in ulcerative colitis (UC) patients and healthy controls, and to assess their association with UC disease activity. METHODS: Fecal samples were collected from 103 UC patients and 95 healthy volunteers during the screening of the TURN2 trial, a randomized controlled trial on the efficacy of anoxic-prepared fecal microbiota transplantation (FMT) in active UC. The presence and load of protozoa were assessed by microscopy and PCR. Disease activity was assessed using the Simple Clinical Colitis Activity Index (SCCAI), Partial Mayo Score and fecal calprotectin (FCP). RESULTS: The prevalence of Blastocystis spp. was significantly higher in healthy controls (33% by microscopy and 34% by PCR, respectively) compared to UC patients (6% by both methods, p < 0.001). Similarly, D. fragilis was more common in healthy controls (34% by microscopy and 37% by PCR) than UC patients (9% and 12% respectively, both p < 0.001). Microscopic detection of D. fragilis was significantly associated with lower disease activity, as measured by the Simple Clinical Colitis Activity Index (median [IQR]: 4 [4] vs. 6 [4], p = 0.023) and the Partial Mayo Score (median [IQR]: 4 [2] vs. 6 [2], p = 0.009). Amongst the D. fragilis positive samples, higher D. fragilis loads, as assessed by either microscopy or PCR, were significantly associated with lower FCP levels (p = 0.010 and p = 0.040). PCR detection of D. fragilis showed similar but non-significant associations with disease activity scores. No associations were found between Blastocystis spp. and disease activity. CONCLUSION: Our findings show a higher prevalence of Blastocystis spp. and D. fragilis in healthy individuals compared to UC patients, challenging their pathogenicity in the context of UC and in general. The reported association between D. fragilis presence and load and lower UC disease activity warrants further investigation in larger cohorts.},
}

@article {pmid41739244,
year = {2026},
author = {Long Depaquit, T and Michel, F and Madec, FX and Peyrottes, A and Chiron, P and Mohammad, S and Bruyere, F and Savoie, PH and Karsenty, G},
title = {Comparison of rectourethral fistula repairs: york mason vs. transperineal repair with gracilis flap interposition.},
journal = {World journal of urology},
volume = {44},
number = {1},
pages = {},
pmid = {41739244},
issn = {1433-8726},
abstract = {INTRODUCTION: Rectourethral fistulas (RUFs) are rare but severe complications of prostate or rectal cancer treatment. The York Mason (YM) procedure and transperineal repair with gracilis muscle flap interposition (TPGF) are the two most frequently used approaches, but direct comparative data are limited. METHODS: We conducted a multicenter retrospective cohort study including all patients who underwent RUF repair with either YM or TPGF at four French tertiary referral centers between 2011 and 2024. Fistulas were classified using the Rivera and Mundy–Andrich systems. The primary endpoint was reintervention-free survival (RFS), assessed by Kaplan–Meier analysis and Cox regression. Secondary endpoints were first-attempt and overall closure rates, perioperative complications, and postoperative urinary and fecal continence. RESULTS: Fifty-seven patients were included (YM = 27, TPGF = 30). Median follow-up was 39 months (YM 27 vs. TPGF 53). Kaplan–Meier analysis showed superior RFS after TPGF (12-month estimates: 94.7% vs. 68.2%; log-rank p = 0.038). First-attempt success was higher with TPGF (77% vs. 44%; p = 0.013), as was overall success at last follow-up (94% vs. 70%; p = 0.046). Operating time and hospital stay were longer after TPGF, but complication rates were comparable (50% vs. 37%; p = 0.12). Stress urinary incontinence occurred in 53% of TPGF and 41% of YM patients (p = 0.34). No de novo fecal incontinence was observed. On Cox regression, complex fistula morphology predicted YM failure (HR 6.5, 95% CI 1.15–36.8), whereas no predictive factor for failure was identified in the TPGF group. CONCLUSION: In this multicenter cohort, TPGF achieved higher RFS than YM without increased morbidity. TPGF appears particularly suitable for complex or irradiated RUFs, while YM may remain appropriate for selected simple, nonirradiated cases.},
}

@article {pmid41774360,
year = {2026},
author = {Fawzy, MN and Fathy, MK},
title = {Targeting the Gut-Brain-Ferroptosis Axis: Molecular Mechanisms and Therapeutic Potential in Alzheimer's Disease and Epilepsy.},
journal = {Journal of molecular neuroscience : MN},
volume = {76},
number = {1},
pages = {},
pmid = {41774360},
issn = {1559-1166},
abstract = {Alzheimer’s disease (AD) and epilepsy share underlying mechanisms of oxidative stress and neuroinflammation, yet effective targeted therapies remain limited. This review presents a novel integrative model linking gut microbiota dysbiosis to ferroptosis, an iron-dependent form of regulated cell death. We propose a vicious cycle in which dysbiosis promotes systemic inflammation and disrupts cerebral iron homeostasis, impairing the glutathione/GPX4 antioxidant system and sensitizing neurons to lipid peroxidation and ferroptotic death. This neuronal damage further fuels neuroinflammation and may exacerbate gut barrier dysfunction. Evidence from both conditions reveals altered gut microbiota alongside ferroptosis markers such as iron accumulation, reduced GPX4, and elevated lipid peroxides. Therapeutically, we examine two complementary approaches: central inhibition of ferroptosis using specific inhibitors and iron chelators, and peripheral modulation of the gut-brain axis via probiotics, prebiotics, or fecal transplantation. Preclinical studies indicate that targeting either pathway can reduce pathology and improve outcomes. We conclude that the most promising strategy involves combined therapies that simultaneously inhibit ferroptosis and restore gut microbial balance, offering a novel, multi-target approach to disrupt the pathogenic cycle in AD and epilepsy.},
}

@article {pmid41838338,
year = {2026},
author = {Hu, M and Xiao, Y and Zhang, X and Guo, J and Shen, T and Wang, Y and Deng, J and Liu, D},
title = {The role of gut microbiota in the development, diagnosis, and treatment of gastric cancer.},
journal = {Folia microbiologica},
volume = {},
number = {},
pages = {},
pmid = {41838338},
issn = {1874-9356},
support = {AD23026316//Guangxi Science and Technology Base and Talent Special Project/ ; 2021KY0106//Guangxi Young and Middle-aged University Teachers' Scientific Research Ability Enhancement Project/ ; },
abstract = {Gastric cancer (GC) remains a significant global health challenge, and the relationship between the gut microbiota and GC has garnered increasing attention. A growing body of research has demonstrated that the gut microbiota plays a key role in the development and progression of GC through a complex network of mechanisms. This review analyzes key factors such as microbial dysbiosis, urease-assisted colonization, and the formation of nitrosamines and other carcinogenic metabolites, highlighting their influence on GC. Additionally, we emphasize the roles of chronic inflammation and immune dysregulation, which are driven by microbial activities, in gastric carcinogenesis. The recent advances in microbiota-based biomarkers for GC are summarized. The clinical value of microbial-related therapies, including probiotics, antibiotic therapy, and fecal microbiota transplantation is also explored. This review discusses the complex and close relationship between the gut microbiota and GC, along with its clinical implications. It aims to provide deeper insights into dysbiosis-related GC research, the development of microbiota-based diagnostic biomarkers, and the advancement of treatment strategies.},
}

@article {pmid41963684,
year = {2026},
author = {Mc Closkey, C and El-Hakeem, AA and Gafar, ME and Slattery, E},
title = {Trends in Clostridioides Difficile Hospitalisations in Ireland (2009-2022).},
journal = {Irish journal of medical science},
volume = {},
number = {},
pages = {},
pmid = {41963684},
issn = {1863-4362},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) is a leading cause of hospital-acquired infection associated with significant morbidity, mortality and healthcare costs. Comparisons of disease burden between countries are complicated by heterogeneity in diagnostic testing and surveillance practices. AIMS: To quantify CDI-related hospitalisations in Ireland between 2009 and 2022 and to examine temporal trends in patient demographics, length of stay (LOS), admission type, and in-hospital mortality. METHODS: We conducted a retrospective analysis of the national Hospital Inpatient Enquiry (HIPE) database, including all discharges from Irish public hospitals coded with CDI (ICD-10-AM A04.7) between 2009 and 2022. Temporal trends were examined, and multivariable logistic regression was conducted using SPSS (v30) to identify factors independently associated with in-hospital mortality. RESULTS: Between 2009 and 2022, 20,956 CDI-related hospitalisations were recorded, accounting for approximately 0.2% of all hospitalisations in Ireland. Annual CDI-related hospitalisations increased by 66%, from 1,301 in 2009 to 1,962 in 2022. Over the same period, in-hospital mortality declined from 21.0% to 11.8%, and mean LOS decreased from 44.0 to 31.5 days. Logistic regression adjusting for age, sex, LOS, admission type, and year of hospitalisation, found the odds of in-hospital mortality were approximately 45% lower in 2022 versus 2009. Increasing age was the strongest independent predictor of mortality; patients aged ≥ 85 years had 72-fold higher odds of mortality compared with the youngest age group. CDI was recorded as the primary diagnosis in 28% of hospitalisations and was associated with lower mortality (adjusted OR 0.36, p < 0.001). Male sex (adjusted OR 1.26, p < 0.001) and elective admission (adjusted OR 1.31, p < 0.001) were independently associated with higher mortality. CONCLUSIONS: CDI-related hospitalisations in Ireland increased substantially between 2009 and 2022, while in-hospital mortality rates and LOS declined. Despite these improvements, CDI is still associated with significant mortality among the elderly. Further research should examine the impact of acute hospital bed availability, faecal microbial transplant (FMT) access, and recurrent infections on CDI case rates.},
}

@article {pmid42343035,
year = {2026},
author = {Lan, M and Ding, H and Cao, Y and Liu, J and Tu, L and Fu, S and Guo, W},
title = {Gut microbiota and aging: current understanding and future perspectives.},
journal = {Molecular biomedicine},
volume = {7},
number = {1},
pages = {},
pmid = {42343035},
issn = {2662-8651},
support = {202503AP140024//Yunnan International Joint Laboratory for Exploration and Utilization of Aromatic Chinese Medicinal Materials in Agriculture/ ; 32272955//Innovative Research Group Project of the National Natural Science Foundation of China/ ; 32372961//National Natural Science Foundation of China/ ; 32472984//National Natural Science Foundation of China/ ; 32372959//National Natural Science Foundation of China/ ; 45124031D101//Jilin University Outstanding (Excellent) Young Talent Development Program/ ; },
mesh = {Humans ; *Aging/physiology ; *Gastrointestinal Microbiome/physiology ; Animals ; Dysbiosis/microbiology ; Probiotics ; },
abstract = {Aging is a complex biological process characterized by progressive functional decline at molecular, cellular, and systemic levels, accompanied by increased susceptibility to chronic diseases. Accumulating evidence indicates that the gut microbiota plays a critical role in shaping aging trajectories and age-related health outcomes. This review systematically summarizes current research progress on the relationship between gut microbiota and aging. We first describe the characteristic alterations of the gut microbiota during aging, including reduced microbial diversity, shifts in core bacterial taxa, and profound changes in microbial metabolite profiles such as short-chain fatty acids, bile acid derivatives, and tryptophan metabolites. We then discuss the mechanistic links between gut microbiota dysbiosis and age-related functional decline, focusing on immunosenescence and inflammaging, gut barrier dysfunction, metabolic disorders and oxidative stress, as well as endocrine and neuroendocrine regulation through gut-organ axes. In addition, major internal and external factors influencing gut microbiota composition in the elderly, including diet, medication use, lifestyle, host immunity, and living environment, are reviewed. Finally, we summarize current and emerging gut microbiota-targeted anti-aging intervention strategies, such as dietary modulation, probiotics, prebiotics, postbiotics, fecal microbiota transplantation, and natural product-based approaches, and discuss future research directions and clinical translation challenges. Overall, this review highlights the gut microbiota as a key modifiable factor in aging biology and underscores its potential as a promising target for promoting healthy aging.},
}

Humans
*Aging/physiology
*Gastrointestinal Microbiome/physiology
Animals
Dysbiosis/microbiology
Probiotics

@article {pmid42343158,
year = {2026},
author = {Aryal, S and Mell, B and Tummala, R and Manandhar, I and Kumariya, S and Kondapalli, N and Yeoh, BS and Ahlidja, W and Mautin Akinola, O and Pachhain, S and Bardhan, P and Saha, P and Zeydabadinejad, S and Osman, I and Thodeti, C and Yang, T and Vijay-Kumar, M and Reddivari, L and Joe, B},
title = {Gut microbiome drives glycodeoxycholic acid-mediated attenuation of hypertension.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2691346},
doi = {10.1080/19490976.2026.2691346},
pmid = {42343158},
issn = {1949-0984},
mesh = {Animals ; *Hypertension/microbiology/metabolism/physiopathology/drug therapy ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Gastrointestinal Microbiome ; Rats, Inbred Dahl ; Blood Pressure/drug effects ; Rats ; Male ; *Glycodeoxycholic Acid/metabolism ; Bile Acids and Salts/metabolism ; Cecum/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {Gut microbiota and bile acids are increasingly recognized to regulate blood pressure, but the mechanisms remain unclear. Takeda G-protein coupled receptor 5 (TGR5) is a major receptor for secondary bile acids. We hypothesized that loss of TGR5 function remodels gut microbiota and influences blood pressure. Using CRISPR/Cas9, TGR5 knockout (Tgr5KO) rats on the Dahl Salt-Sensitive (S) background were generated and characterized. Compared to the control S rats, Tgr5KO rats demonstrated significantly lower blood pressure, a distinct shift in gut microbiota composition, and an increase in the secondary bile acid, particularly, glycodeoxycholic acid. Supplementation of glycodeoxycholic acid to the control S rats produced a similar gut microbial shift and lowered blood pressure. Furthermore, cecal microbiota transplantation from Tgr5KO to control S rats lowered blood pressure in the recipient rats. This first loss-of-function study demonstrates that deletion of TGR5 remodels gut microbiota, increases glycodeoxycholic acid, and lowers blood pressure regardless of TGR5 signaling status, identifying a promising gut-liver axis target for lowering hypertension.},
}

Animals
*Hypertension/microbiology/metabolism/physiopathology/drug therapy
Receptors, G-Protein-Coupled/genetics/metabolism
*Gastrointestinal Microbiome
Rats, Inbred Dahl
Blood Pressure/drug effects
Rats
Male
*Glycodeoxycholic Acid/metabolism
Bile Acids and Salts/metabolism
Cecum/microbiology
Fecal Microbiota Transplantation

@article {pmid42343653,
year = {2026},
author = {Bruggeman, A and Vandenbroucke, RE and Santens, P},
title = {Rationale and current status of fecal microbiota transplantations for Parkinson's disease.},
journal = {Journal of Parkinson's disease},
volume = {},
number = {},
pages = {1877718X261455608},
doi = {10.1177/1877718X261455608},
pmid = {42343653},
issn = {1877-718X},
abstract = {Treating a neurological disorder through the gut may seem counterintuitive, yet multiple lines of evidence highlight the gut's important role in Parkinson's disease (PD). Prodromal gastrointestinal symptoms, the presence of aggregated α-synuclein in enteric neurons, increased intestinal inflammation, and impaired epithelial barrier integrity all point to gut-level involvement in PD pathophysiology. The gut microbiome, markedly altered in individuals with PD, may be a key driver of these changes. Fecal microbiota transplantation (FMT) is currently the most effective strategy for achieving broad and durable modifications of gut microbiota composition. However, FMT is a complex, multi-step procedure requiring stringent methodological control. Modulating gut bacteria has demonstrated therapeutic potential in preclinical models of PD, and recent clinical trials have begun evaluating FMT in patients, although outcomes have been variable. In this review, we examine potential explanations for these divergent results, with a particular focus on methodological differences across trials. We also outline future directions for optimizing FMT study design in PD and discuss how these insights may guide the development of next-generation microbiota-targeted therapies.},
}

@article {pmid42344668,
year = {2026},
author = {Huang, F and Zhang, Z and Zhao, Y and Ye, S and Gan, M and Li, X and Zhang, Y and Chen, L and Zhang, Y and Chen, L and Wang, T and Huang, J and Zhang, X},
title = {Altitude-Associated Divergence of the Gut Microbiome in Endangered Forest Musk Deer: Evidence From Integrated Metagenomics, Metabolomics, and Culturomics.},
journal = {Evolutionary applications},
volume = {19},
number = {6},
pages = {e70285},
pmid = {42344668},
issn = {1752-4571},
abstract = {High-altitude environments expose mammals and their gut symbionts to multifaceted stressors-hypoxia, cold, and intense UV radiation. Whether gut microbial communities undergo compositional restructuring in response to these stressors, and whether such restructuring carries translational value for captive conservation, remain unresolved questions. Here, we integrated deep shotgun metagenomics (≥ 15 Gb per sample), untargeted fecal metabolomics, and culturomics in 75 captive forest musk deer (Moschus berezovskii Flerov, 1929) housed at high altitude (~3900 m) and low altitude (~1450 m) facilities under uniform husbandry. Neutral community modeling showed a greater contribution of deterministic processes at high altitude (only 34.3% of species conformed to neutral expectations vs. 89.3% at low altitude), consistent with stronger environmental filtering. At high altitude, we observed enrichment of a functionally coherent guild of short-chain fatty acid (SCFA)-producing bacteria-centered on Flavonifractor plautii, Intestinimonas butyriciproducens, and Enterococcus faecium-that formed antagonistic co-occurrence networks with opportunistic pathogens including Clostridioides difficile and Campylobacter species, mirroring SCFA enrichment in phylogenetically diverse high-altitude mammals. Fecal metabolomics revealed coordinated shifts in urolithin biosynthesis, branch-specific regulation of the tryptophan-kynurenine pathway, and energy metabolism remodeling, all robustly predicted by microbiome composition via neural network modeling. Culturomics yielded seven safety-validated isolates with confirmed gastrointestinal stress tolerance and broad-spectrum pathogen-antagonistic activity in vitro. These findings provide an actionable framework for altitude-informed facility siting, fecal microbiota transplantation (FMT) donor selection, host-derived probiotic development, and non-invasive health surveillance in captive endangered species, and are broadly transferable to other taxa facing microbiome-associated disease pressure in captivity.},
}

@article {pmid42344729,
year = {2026},
author = {Qian, X and Wu, Y and Wang, W and Shao, H and Xu, Z},
title = {The selection of matching donors for patients in fecal microbiota transplantation.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1859411},
pmid = {42344729},
issn = {1664-302X},
abstract = {Fecal microbiota transplantation (FMT) is an emerging therapeutic strategy with potential applications in the treatment of various diseases, particularly those associated with gut microbiome dysbiosis. However, clinical trials have demonstrated considerable variability in FMT efficacy-even among patients with the same disease. The heterogeneity of gut microbiota from donors is considered a key factor influencing patient outcomes. Consequently, the development of donor-recipient matching models has emerged as an advanced approach to enhance the effectiveness of FMT. As a practical clinical intervention, the therapeutic impact of FMT on specific diseases requires further investigation. This article reviews the development of donors and the matching patterns between donors and recipients, and summarizes the key factors influencing the transfer of the microbiota. It provides new insights for exploring novel and effective donor-recipient matching patterns.},
}

@article {pmid42344797,
year = {2026},
author = {Zhang, M and Lu, Y and Yuan, X},
title = {The tumor microenvironment: a dynamic ecosystem and therapeutic nexus in modern oncology.},
journal = {Frontiers in pharmacology},
volume = {17},
number = {},
pages = {1836055},
pmid = {42344797},
issn = {1663-9812},
abstract = {The tumor microenvironment (TME) has emerged as a central orchestrator of carcinogenesis, therapeutic resistance, and immune evasion, fundamentally reshaping the understanding of cancer as an ecosystem disease rather than a cell-autonomous genetic disorder. This review synthesizes contemporary advances in deconstructing the cellular and acellular architecture of the TME, encompassing cancer-associated fibroblasts, tumor-associated macrophages, aberrant vasculature, and a dynamically remodeled extracellular matrix. The molecular underpinnings of TME-mediated pathogenesis are critically evaluated, including metabolic reprogramming, epigenetic dysregulation, and systemic microbiome crosstalk, which collectively enforce immunosuppression and drive adaptive resistance. Building on this mechanistic framework, a new generation of therapeutic strategies designed to reprogram this malignant niche is highlighted: precision nanotechnologies for targeted and stimuli-responsive delivery; next-generation immunotherapies such as logic-gated CAR-T cells, bispecific engagers, and oncolytic viruses; metabolic and epigenetic modulators; stromal and vascular normalization approaches; and microbiome-based interventions, for instance fecal microbiota transplantation and defined bacterial consortia. Transformative tools, including patient-derived organoids, tumor-on-a-chip systems, 3D bioprinting, and artificial intelligence-powered multi-omics, are now enabling predictive modeling and personalized therapeutic forecasting. Despite persistent challenges posed by intratumoral heterogeneity, cellular plasticity, and the complexity of combination trial design, the convergence of these multidisciplinary approaches provides an unprecedented toolkit to durably reprogram the TME. Mastering this dynamic ecosystem is paramount to overcoming therapeutic roadblocks, and the strategic integration of these advances heralds a definitive paradigm shift toward TME-centric, adaptive, and personalized cancer therapy.},
}

@article {pmid42345020,
year = {2026},
author = {Ismaiel, A and Almonajjed, MB and Wardeh, M and Abdelghafar, A and Popa, SL and Sabo, C and Dumitrascu, DL},
title = {From dysbiosis to malignancy: decoding gut-driven pathways to clinical management in hepatocellular carcinoma.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1852380},
pmid = {42345020},
issn = {2235-2988},
mesh = {Humans ; *Dysbiosis/complications ; *Liver Neoplasms/therapy/etiology/pathology/microbiology ; *Carcinoma, Hepatocellular/therapy/etiology/pathology/microbiology ; *Gastrointestinal Microbiome ; Animals ; },
abstract = {Hepatocellular carcinoma (HCC) is undergoing a profound global epidemiological shift, transitioning from viral-driven etiologies to metabolic dysfunction-associated steatotic liver disease (MASLD). This transition challenges traditional cirrhosis-centric surveillance, as a significant proportion of MASLD-HCC develops in non-cirrhotic livers. Parallel to these metabolic shifts, the gut-liver axis has emerged as a central orchestrator of hepatocarcinogenesis. This review decodes the complex gut-driven pathways fueling HCC, highlighting the oncogenic consequences of structural and functional dysbiosis. Dietary patterns and etiology-specific microbial shifts compromise the intestinal and gut-vascular barriers, precipitating a structural "leaky gut". This disruption facilitates the robust translocation of pathogen-associated molecular patterns (PAMPs), particularly lipopolysaccharide (LPS), and toxic microbial metabolites like secondary bile acids, specifically deoxycholic acid, into the portal circulation. Consequently, hepatic innate immunity is chronically activated via Toll-like receptor 4 (TLR4) signaling on Kupffer and hepatic stellate cells, fostering metainflammation, cellular senescence, genomic instability, and a highly immunosuppressive, pro-tumorigenic microenvironment. Furthermore, the depletion of keystone commensals diminishes the protective reservoir of short-chain fatty acids (SCFAs), exacerbating oncogene activation. Translating these mechanistic insights into the clinic, we explore the utility of distinct microbial signatures and metabolomic profiles as non-invasive diagnostic biomarkers. Such tools are urgently needed to bridge the early-detection gap in the expanding MASLD demographic. Finally, we discuss the pivotal role of the microbiome in modulating responses to immune checkpoint inhibitors (ICIs), notably through immune-stimulating taxa like Akkermansia muciniphila, and outline emerging gut-targeted therapies, including next-generation probiotics and fecal microbiota transplantation, aimed at restoring host-microbiome homeostasis to prevent and manage HCC. By decoding these gut-driven pathways, this review provides a comprehensive framework for integrating the microbiome-onco axis into precision oncology, offering novel avenues to combat the rising global burden of hepatocellular carcinoma.},
}

Humans
*Dysbiosis/complications
*Liver Neoplasms/therapy/etiology/pathology/microbiology
*Carcinoma, Hepatocellular/therapy/etiology/pathology/microbiology
*Gastrointestinal Microbiome
Animals

@article {pmid42345401,
year = {2026},
author = {Wang, R and Zheng, B and Guo, M and Xu, K and Wang, Z and Guo, X and Li, J and Wang, J and Li, Y and Sohail, A and Wang, D},
title = {Effects of Heat-Moisture Treatment on the Physicochemical Properties, Structural Characteristics, and Anti-Ulcerative Colitis Activity of Yam Starch.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.6c04224},
pmid = {42345401},
issn = {1520-5118},
abstract = {Yam starch (YS) alleviates ulcerative colitis (UC), but whether heat-moisture treatment (HMT) enhances this effect remains unclear. This study examined the impact of HMT on the structural features of yam starch and yam flour (YF) and their UC-mitigating capacity. The results showed that HMT increased the resistant starch (RS) content in YF by forming starch-lipid complexes and, in YS, it enhanced the RS content through recrystallization. Animal experiments demonstrated that YF, HMT-modified YF, YS, and HMT-modified YS all alleviate UC symptoms, with HMTYS being the most effective. Specifically, HMTYS corrected DSS-induced intestinal flora imbalances by promoting beneficial bacteria (Lachnospiraceae_NK4A136_group, bacteroides, and akkermansia). Short-chain fatty acids produced from RS fermentation by these bacteria repaired the intestinal barrier and inhibited inflammation, creating a cycle that alleviated the colitis. Fecal microbiota transplantation (FMT) experiments confirmed that HMTYS alleviates UC by modulating the gut microbiota and increasing the level of SCFA production.},
}

@article {pmid42346015,
year = {2026},
author = {Habtemariam, S},
title = {The Gut Microbiome Dependency Continuum in Drug Discovery: A Unified Pharmacology Framework Linking Clinical Drugs, Natural Products, and Engineered Microbial Therapeutics.},
journal = {Biotech (Basel (Switzerland))},
volume = {15},
number = {2},
pages = {},
pmid = {42346015},
issn = {2673-6284},
abstract = {Highlighting its pivotal role in modern pharmacology, the gut microbiome is emerging as a key determinant of drug efficacy, toxicity, and bioavailability. This review proposes the Gut Microbiome Dependency Continuum, a four-layer framework describing progressively deeper levels of microbiome involvement in drug discovery and therapeutic function. The first layer, intact functional microbiome-dependent therapeutics and includes interventions such as faecal microbiota transplantation and defined microbial consortia. The second layer, microbiome-modulated approved drugs include widely used therapeutics whose pharmacokinetics or pharmacodynamics are strongly influenced by microbial metabolism. Examples include metformin, irinotecan, levodopa, and digoxin, where gut microbial interactions influence efficacy, toxicity, and inter-individual variability in treatment outcomes. The third layer, microbiota-transformable natural products, encompasses dietary and plant-derived compounds such as polyphenols, ginsenosides, alkaloids, fibres, isoflavones, lignans, and glucosinolates. Their biological activity depends on microbial biotransformation into bioactive metabolites. The fourth layer, engineered microbiome therapeutics, includes synthetic biology approaches such as programmable microbial systems, engineered probiotics, CRISPR-based microbiome editing, and microbiome-responsive drug delivery systems. It also includes synthetic microbial consortia, enabling targeted sensing, therapeutic delivery, and ecological reprogramming of gut microbial communities. Altogether, these layers define a continuum in which the gut microbiome evolves from a passive modulator to an essential metabolic organ and ultimately a programmable therapeutic platform. The article provides an integrated framework for microbiome-informed drug discovery. It also supports the development of precision, ecology-aware, and engineered microbial therapeutics.},
}

@article {pmid42346347,
year = {2026},
author = {He, J and Qin, L and Sun, X},
title = {Bile Acids and the Gut-X Axis: TCM-Mediated Systemic Protection and Therapeutic Opportunities for Multi-Organ Diseases.},
journal = {Metabolites},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/metabo16060366},
pmid = {42346347},
issn = {2218-1989},
support = {82405310//National Natural Science Foundation of China/ ; 1020241792//Natural Science Foundation of the Jiangsu Higher Education Institutions of China/ ; },
abstract = {The gut microbiota regulates host physiology and drives extraintestinal diseases through the gut-X axis. Bile acids (BAs) function as key mediators of this interorgan crosstalk by activating nuclear and membrane receptors (FXR, TGR5, PXR, VDR). Traditional Chinese Medicine (TCM) demonstrates efficacy across multiple organ systems through multi-component formulations. This narrative review synthesizes evidence from preclinical and clinical studies supporting that TCM exerts systemic protection via strategic modulation of the microbiota-BA-host receptor axis, which functions as a core regulatory circuit within a larger network of microbial metabolites. Mechanistically, representative TCM formulas remodel gut microbial ecology and reinforce intestinal barrier integrity, leading to optimized BA profiles. These favorable BA signatures engage tissue-specific receptor signaling to resolve inflammation, mitigate fibrosis, and restore metabolic homeostasis across the gut-heart, gut-kidney, gut-liver, gut-bone, and gut-endocrine axes. Support for this causal relationship is provided by microbiota depletion, fecal transplantation, and multi-omics studies, collectively suggesting that TCM's benefits are microbiota-dependent and at least partially BA-mediated. Moreover, context-dependent modulation of BA receptors, such as differential regulation of FXR, enables TCM to achieve pathology-specific outcomes. Current evidence is derived predominantly from preclinical models, and clinical data remain lacking. Nonetheless, the microbiota-BA-organ axis thus provides a potential framework for understanding TCM's systemic actions and establishes a molecular basis for developing microbiome-informed precision therapeutics. Future directions include patient stratification and precision intervention design inspired by TCM's ecological modulation strategies.},
}

@article {pmid42346411,
year = {2026},
author = {Vankayala, USA and Sohail, A and George, B and Singh, M and Khayat, O and Kreidieh, M and Hasham, A and Quiel, L},
title = {The Gut Microbiome in Heart Failure: Pathways to Inflammation and Therapeutic Targets.},
journal = {Metabolites},
volume = {16},
number = {6},
pages = {},
doi = {10.3390/metabo16060431},
pmid = {42346411},
issn = {2218-1989},
abstract = {Heart failure (HF) continues to be a major global health burden, with persistent morbidity and mortality despite guideline-directed and device-based therapies. Evidence suggests the gut-heart axis is a critical and underrecognized contributor to HF progression. Alterations in cardiac output and systemic venous congestion in HF lead to intestinal hypoperfusion, mucosal edema, and loss of barrier integrity, increasing intestinal permeability, gut dysbiosis, and translocation of microbial products. This systemic translocation is associated with chronic low-grade inflammation that activates innate immune pathways that correlate with endothelial dysfunction, oxidative stress, fibroblast activation, and adverse cardiac remodeling. Gut-derived metabolites derived by microbial metabolism modulate cardiovascular health by altering the metabolic profiles. Dysbiosis results in loss of protective short-chain fatty acid (SCFA)-producing bacteria and enriches pro-inflammatory taxa such as trimethylamine N-oxide (TMAO)-producing bacteria. Elevated TMAO is associated with increased mortality and hospitalization in HF, whereas SCFAs enhance barrier integrity and immune tolerance. Secondary bile acids and uremic toxins such as indoxyl sulfate and p-cresyl sulfate further link dysbiosis to fibrosis and vascular stiffness. Circulating markers such as TMAO, lipopolysaccharide-binding protein (LBP), and soluble CD14 carry prognostic value beyond traditional cardiac biomarkers. This review highlights current experimental, translational, and clinical evidence describing gut dysbiosis and its molecular links to HF progression. Targeting the gut-heart axis represents a novel therapeutic approach in HF. Dietary modulation, probiotics/prebiotics, fecal microbiota transplantation, and inhibitors of microbial metabolic pathways show promise. Future research should emphasize microbiota-based interventions in HF management.},
}

@article {pmid42346775,
year = {2026},
author = {He, Z and Nie, Y and Li, C and Sun, G and Zheng, W and Liu, H and Geng, M and Tian, J and Zhang, Y},
title = {GV-971 Ameliorates Chronic Restraint Stress-Induced Depression-like Phenotypes Accompanied by Reshaping of the Microbiota-Gut-Brain Axis.},
journal = {Marine drugs},
volume = {24},
number = {6},
pages = {},
pmid = {42346775},
issn = {1660-3397},
support = {2024CXPT029, 2025CXPT011//Key R&D Program of Shandong Province, China/ ; ZR2024QH615//Shandong Provincial Natural Science Foundation/ ; SYS202205//Shandong Laboratory Program/ ; },
mesh = {Animals ; *Depression/drug therapy/etiology ; *Gastrointestinal Microbiome/drug effects ; Male ; Mice ; *Stress, Psychological/drug therapy ; *Brain-Gut Axis/drug effects ; *Oligosaccharides/pharmacology ; Restraint, Physical ; Disease Models, Animal ; *Antidepressive Agents/pharmacology ; Mice, Inbred C57BL ; Brain/drug effects/metabolism ; Phenotype ; Hippocampus/drug effects/metabolism ; Intestinal Barrier Function ; },
abstract = {Depression is increasingly linked to microbiota-gut-brain axis dysfunction, yet current monoaminergic antidepressants show limited efficacy. This study investigated the therapeutic potential and underlying mechanisms of GV-971, a marine-derived oligosaccharide, in a chronic restraint stress (CRS) mouse model. We first established that 8 h of daily restraint for 4-8 weeks induces a stable depression-like phenotype characterized by behavioral despair and significant reduction in peripheral monoamine neurotransmitters (5-HT and norepinephrine). GV-971 treatment robustly attenuated CRS-induced depression- and anxiety-like behaviors, restored hippocampal serotonin levels, reduced elevated plasma corticosterone concentrations, and ameliorated CRS-induced adrenal cortical hyperplasia. Mechanistically, GV-971 significantly suppressed neuroinflammation by inhibiting microglial hyperactivation in the prefrontal cortex and hippocampus. Concurrently, it repaired intestinal barrier dysfunction, evidenced by reduced permeability, restored mucosal integrity, and recovered goblet cell numbers. Crucially, integrated shot-gun metagenomics and plasma metabolomics revealed that GV-971 not only reshaped microbial taxonomy but also functionally recalibrated the gut ecosystem. It enriched beneficial taxa (e.g., Bifidobacterium pseudolongum, Bacteroides uniformis) and specific metabolic pathways, leading to increased short-chain fatty acids (valeric and caproic acids) and a significant reduction in plasma levels of tryptophan-kynurenine pathway metabolites, specifically the neurotoxic compounds kynurenine and quinolinic acid. Fecal microbiota transplantation (FMT) from GV-971-treated donors partially recapitulated the antidepressant and gut-protective effects in CRS recipients, confirming a causal role for the remodeled microbiota. Collectively, GV-971 exerts antidepressant effects by coordinately remodeling the gut microbiota, normalizing tryptophan and SCFA metabolism, restoring gut barrier integrity, and dampening central neuroinflammation, supporting its potential as a novel gut-brain axis-targeted therapy for depression.},
}

Animals
*Depression/drug therapy/etiology
*Gastrointestinal Microbiome/drug effects
Male
Mice
*Stress, Psychological/drug therapy
*Brain-Gut Axis/drug effects
*Oligosaccharides/pharmacology
Restraint, Physical
Disease Models, Animal
*Antidepressive Agents/pharmacology
Mice, Inbred C57BL
Brain/drug effects/metabolism
Phenotype
Hippocampus/drug effects/metabolism
Intestinal Barrier Function

@article {pmid42347926,
year = {2026},
author = {Voigt, RM and Keshavarzian, A and Hall, DA},
title = {Fecal Microbiota Transplant in Parkinson's Disease: Insights into the Gut-Brain Axis and the Challenge of Sustained Response.},
journal = {Annals of neurology},
volume = {},
number = {},
pages = {},
doi = {10.1002/ana.78259},
pmid = {42347926},
issn = {1531-8249},
}

@article {pmid42350167,
year = {2026},
author = {Yao, Y and Liu, Y and Li, Y and Lu, B and Lyu, D and Cui, X and Pan, X},
title = {Re: Fecal Microbiota Transplantation plus Immunotherapy in Metastatic Renal Cell Carcinoma: The Phase 1 PERFORM Trial.},
journal = {European urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.eururo.2026.05.015},
pmid = {42350167},
issn = {1873-7560},
}

@article {pmid42337290,
year = {2026},
author = {Roubalová, R and Luthar, J and Procházková, P and Zadáková, K and Coufalová, K and Kreisinger, J and Semerád, J and Nehasilová, A and Mácha, H and Luptáková, D and Tlaskalová-Hogenová, H and Holanová, P and Lambertová, A and Papežová, H},
title = {Gut microbiota contributions to anorexia nervosa pathogenesis: insights from the activity-based anorexia model.},
journal = {NPJ biofilms and microbiomes},
volume = {},
number = {},
pages = {},
doi = {10.1038/s41522-026-01055-y},
pmid = {42337290},
issn = {2055-5008},
support = {NU23-04-00381//Ministerstvo Zdravotnictví Ceské Republiky/ ; NU22-04-00010//Ministerstvo Zdravotnictví Ceské Republiky/ ; Talking microbes - understanding microbial interactions within One Health framework (CZ.02.01.01/00/22_008/0004597)//Ministry of Education, Youth, and Sports of the Czech Republic/ ; Cooperatio Program 207038//Univerzita Karlova v Praze/ ; },
abstract = {Anorexia nervosa (AN) is a severe eating disorder that profoundly affects quality of life. Despite increasing understanding of the neurobiological basis of the disease, many patients develop a chronic course of illness accompanied by a variety of physical and psychiatric comorbidities. To investigate the contribution of the gut microbiome to disease progression, we employed the activity-based anorexia (ABA) mouse model of AN. We performed fecal microbiota transplantation using samples from three donor groups: healthy controls, patients with acute AN, and patients with severe and enduring AN (SEAN). We continuously assessed changes in the gut microbiota and fecal metabolites (e.g., short-chain fatty acids, serotonin, and GABA) throughout the experiment, along with behavioral traits across the three groups of mice. Mice colonized with microbiota from acute AN patients exhibited reduced hunger signaling (via NPY, AgRP, MCH, and orexin), accompanied by decreased food intake. In contrast, mice transplanted with microbiota from SEAN patients showed appetite signaling and food consumption comparable to those colonized with microbiota from healthy controls but displayed significantly higher running activity relative to the other groups. However, the distinct microbiota did not affect the development of the ABA phenotype. Overall, our findings suggest that changes in the gut microbiome during disease development contribute to disease progression. Our results also indicate that restoration of a healthy gut microbiome is essential for complete recovery.},
}

@article {pmid42337655,
year = {2026},
author = {Scott, JS and Munir, S and Lynn, MA and Duggan, JA and Castro, J and Harrington, AM and Brierley, SM and Schober, G and Cash, K and Gutschmidt, B and Hutchinson, MR and Yong, A and Costello, SP and Sikdar, S and Tangseefa, P and Hewett, DR and Cross, CB and Park, SB and Ryan, FJ and Zannettino, ACW and Lynn, DJ and Vandyke, K and Wardill, HR and Mrozik, KM},
title = {Bortezomib-induced gastrointestinal dysfunction, peripheral neuropathy and neuroimmune signalling are influenced by the gut microbiota in mice.},
journal = {Journal of neuroinflammation},
volume = {},
number = {},
pages = {},
doi = {10.1186/s12974-026-03909-w},
pmid = {42337655},
issn = {1742-2094},
support = {1163245//Priority-driven Collaborative Cancer Research Scheme and co-funded by Cancer Australia, Cure Cancer, and Leukaemia Foundation of Australia/ ; },
abstract = {BACKGROUND: Peripheral neuropathy and gastrointestinal dysfunction are frequent, debilitating side effects of the neurotoxic myeloma drug bortezomib that reduce quality of life and adherence to optimal therapy. Therapeutic strategies to manage these complications are limited. Here, we have developed a mouse model of bortezomib side effects to investigate the role of the gut microbiota in their development.

METHODS: C57BL/6 specific pathogen-free (SPF), germ-free (GF) and ex-GF mice (colonised with healthy gut microbiota via faecal microbiota transplantation [FMT]) were treated with bortezomib (1 mg/kg) twice-weekly for two weeks. Neurotoxicity and neuroimmune signalling were assessed by serum neurofilament light chain (NfL) quantitation and real-time qPCR analysis of inflammatory markers in sensory and autonomic nerve ganglia, respectively. Faecal microbiota composition was characterised using 16S rRNA gene sequencing. Bortezomib side effects were assessed using behavioural phenotyping, von Frey mechanical sensitivity and rotarod testing, and FITC-dextran gut permeability and Evans Blue dye transit assays.

RESULTS: Bortezomib-treated SPF mice displayed altered spontaneous behaviour and developed acute gastric retention, altered gastrointestinal motility and increased intestinal permeability, in the absence of intestinal micro-architecture changes. Concurrently, bortezomib induced sensory loss in, and increased grooming of, paws, and reduced motor performance, indicative of peripheral neuropathy. Bortezomib neurotoxicity was evidenced by elevated serum NfL levels and neuroimmune signalling in sciatic nerve dorsal root and vagal nerve nodose ganglia. In SPF mice, bortezomib altered gut microbiota composition with an acute decrease in microbial diversity and expansion of Lactobacillus gasseri. Notably, GF mice developed a milder symptom profile following bortezomib treatment compared with SPF mice, while FMT mice did not develop overt bortezomib side effects despite displaying evidence of nerve damage.

CONCLUSIONS: This is the first study to model gastrointestinal side effects of bortezomib in rodents, implicating neuroimmune dysregulation of the vagus nerve. Our data show that the gut microbiota is not a primary driver of bortezomib side effects. However, the absence of a symptom profile in FMT mice suggests that, in GF mice, the gut microbiota beneficially modulates the host to protect against bortezomib side effects. Further studies are required to determine whether this can be harnessed to mitigate clinical complications of bortezomib.},
}

@article {pmid42338488,
year = {2026},
author = {Chen, B and Chen, J and Feng, Z and Lv, H and Lin, Q and Jiang, G},
title = {Gut microbiota reconstruction after liver transplantation and its association with early postoperative infections in patients with liver failure.},
journal = {Frontiers in cellular and infection microbiology},
volume = {16},
number = {},
pages = {1845273},
pmid = {42338488},
issn = {2235-2988},
mesh = {Humans ; *Liver Transplantation/adverse effects ; Female ; *Gastrointestinal Microbiome ; Retrospective Studies ; *Postoperative Complications/microbiology ; Dysbiosis/microbiology ; Male ; *Liver Failure/surgery/complications ; Probiotics/administration & dosage/therapeutic use ; Middle Aged ; Metagenomics ; Feces/microbiology ; Adult ; *Bacterial Infections/microbiology/epidemiology ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {BACKGROUND: Postoperative infection remains a major cause of morbidity after liver transplantation (LT) in patients with liver failure. Increasing evidence suggests that gut microbiota dysbiosis may contribute to infection risk, but its dynamic changes after LT are not fully understood.

METHODS: This retrospective study included 60 patients with liver failure who underwent LT and developed postoperative infection-related risk. Patients were divided into a probiotic group and a non-probiotic group. Fecal samples were collected before transplantation and on postoperative days 7, 14, 21, and 28. Metagenomic sequencing was performed to analyze gut microbial composition, diversity, and antibiotic resistance genes.

RESULTS: The probiotic group showed a significantly lower rate of postoperative bacterial infection, especially intra-abdominal infection. After LT, gut microbiota gradually recovered in both groups, but restoration was faster in the probiotic group. The non-probiotic group showed persistent dysbiosis, characterized by enrichment of opportunistic pathogens such as Enterococcus and Klebsiella, whereas beneficial genera including Bifidobacterium and Lactobacillus were more abundant in the probiotic group. Antibiotic resistance genes were also more enriched in the non-probiotic group.

CONCLUSION: Early postoperative gut microbiota reconstruction is closely associated with infectious complications after LT, and modulation of gut microbiota may help improve postoperative outcomes.},
}

Humans
*Liver Transplantation/adverse effects
Female
*Gastrointestinal Microbiome
Retrospective Studies
*Postoperative Complications/microbiology
Dysbiosis/microbiology
Male
*Liver Failure/surgery/complications
Probiotics/administration & dosage/therapeutic use
Middle Aged
Metagenomics
Feces/microbiology
Adult
*Bacterial Infections/microbiology/epidemiology
Bacteria/classification/genetics/isolation & purification

@article {pmid42338743,
year = {2026},
author = {Zhao, H and Ao, L and Hao, L and Wei, Y and Yin, HZ and Lee, XQ and Guo, C and Wang, Z and Yang, J and Yang, R and Zhou, GL},
title = {Integrative mechanisms and intervention targets of the microbiota-gut-brain axis in depressive disorders: advances across immune, endocrine, and central nervous system pathways.},
journal = {Frontiers in psychiatry},
volume = {17},
number = {},
pages = {1848918},
pmid = {42338743},
issn = {1664-0640},
abstract = {Depressive disorders are highly heterogeneous syndromes characterized not only by depressed mood but also by cognitive impairment, sleep-circadian rhythm disturbances, altered appetite, somatic discomfort, and metabolic or gastrointestinal comorbidities. In recent years, the microbiota-gut-brain axis (MGBA) has been increasingly recognized as an integrative biological framework linking abnormalities in mood regulation, immune responses, endocrine function, metabolism, and neuroplasticity. This review provides a systematic synthesis of gut microbial ecology and host phenotypic features associated with depressive disorders, with particular emphasis on the depletion of short-chain fatty acid-producing commensals, the enrichment of potentially pro-inflammatory taxa, and the functional remodeling of key metabolic pathways, including the tryptophan-kynurenine pathway, short-chain fatty acids, bile acids, and trimethylamine N-oxide. We further discuss how bidirectional gut-to-brain and brain-to-gut communication may contribute to the onset and progression of depressive disorders through intestinal barrier disruption, low-grade systemic inflammation, hypothalamic-pituitary-adrenal axis activation, vagal signaling, and dysregulation of neurotransmitter and neurotrophic pathways. Current interventional evidence suggests that dietary and lifestyle modification, psychobiotics, and fecal microbiota transplantation may exert antidepressant potential in selected populations; however, the overall effect sizes remain limited and between-study heterogeneity is substantial. Patients with prominent gastrointestinal symptoms, metabolic abnormalities, or low-grade inflammatory states may represent priority candidates for MGBA-targeted interventions; nevertheless, a putative microbiota-responsive phenotype should not be simply equated with high stress exposure alone, and its definition requires prospective validation integrating stress burden, host responses, and microbial/metabolic readouts. Overall, MGBA research is gradually moving beyond descriptive profiling of microbial composition toward functional integration and clinical translation; however, causal inference, multi-omics standardization, and the identification of stratification biomarkers remain major challenges. Future studies should incorporate phenotype-based stratification, strengthened functional readouts, and precision intervention designs to determine which patients are most likely to benefit from microbiota-targeted therapies.},
}

@article {pmid42340049,
year = {2026},
author = {Mao, H and Wang, X and Pang, Y and Lu, Y and Wang, H and Li, H and Ni, Y and Jia, W},
title = {The Gut Microbiome-Endocrine Axis in Obesity: Mechanisms and Therapeutics.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70511},
pmid = {42340049},
issn = {1440-1746},
support = {C2406002//Shenzhen Medical Research Fund/ ; 92357305//Major Research Plan of National Natural Science Fund of China (NSFC)/ ; 24HAA01325//Excellent Young Scientists Fund of the National Natural Science Foundation of China (Overseas)/ ; },
abstract = {Obesity, a major global health challenge and a key risk factor for metabolic diseases, represents a state of dysregulated energy homeostasis. The gut microbiome has emerged as a critical mediator of obesity pathogenesis, yet the precise endocrine mechanisms linking microbial signals to metabolic dysfunction remain incompletely understood. Therefore, at the perspectives of gut microbiome-endocrine axis encompassing gut-brain, gut-adipose, and gut-pancreas axes, this review elucidates how gut microbiota and their metabolites influence systemic endocrine homeostasis through energy intake, fat storage, and hormonal secretion. Mechanistic studies highlight the roles of short-chain fatty acids, bile acids, and microbial peptides in modulating obesity control and related metabolic health. We further summarize the current therapeutics targeting gut microbiome in the gut-endocrine axis, including prebiotics, probiotics, synbiotics, postbiotics, fecal microbiota transplantation, and lifestyle approaches and highlight their mechanistic and translational relevance. The major challenges of gut microbiome studies are discussed, including obscure phenotyping, insufficient cross-organ integration, and limited causal inference. Overcoming these limitations by precise obesity measurement, integrated cross-organ models, and AI-driven causal modeling could advance the pathophysiological insight and management of obesity.},
}

@article {pmid42341529,
year = {2026},
author = {Wu, C and Zheng, T and Huang, S and Meng, C and Wang, W and Li, M and Cheng, H and Ju, Z and Wang, Y and Mao, W and Zhou, X},
title = {Lithospermic acid-induced gut microbiota remodeling alleviates intraplaque inflammation.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {159},
number = {},
pages = {158462},
doi = {10.1016/j.phymed.2026.158462},
pmid = {42341529},
issn = {1618-095X},
abstract = {BACKGROUND: Atherosclerosis is a leading cause of mortality worldwide. The gut microbiota (GM) plays a significant role in the initiation and progression of atherosclerosis, making its modulation a promising therapeutic strategy for atherosclerotic cardiovascular disease. Salvia miltiorrhiza, a traditional Chinese medicine renowned for its therapeutic effects in treating cardiovascular diseases, contains lithospermic acid (LA) as one of its key active constituents.

PURPOSE: To elucidate whether LA can alleviate atherosclerosis and its mechanism.

STUDY DESIGN AND METHODS: Atherosclerosis was induced in Apolipoprotein E knockout mice through a Western diet, followed by a 12-week treatment with LA. In a separate model, low-density lipoprotein receptor knockout mice were fed a Western diet for 8 weeks prior to receiving LA for an additional 12 weeks. The role of GM in LA-mediated alleviation of atherosclerosis was assessed using fecal microbiota transplantation (FMT) models coupled with 16S rRNA gene sequencing. Furthermore, serum metabolomics was employed to elucidate the mechanism by which LA modulates serum metabolites via GM to attenuate atherosclerosis.

RESULTS: LA administration significantly attenuated the development of atherosclerosis in both models. FMT experiments further indicated that the GM contributes to the anti-atherosclerotic effects of LA. 16S rRNA gene sequencing revealed that LA modified the composition of the GM. Metabolomic analysis demonstrated that LA reduced serum levels of lysophosphatidylcholine (LysoPC), a metabolite critical for macrophage function.

CONCLUSION: Collectively, these findings highlight the therapeutic potential of LA in the treatment of atherosclerosis.},
}

@article {pmid42342152,
year = {2026},
author = {Gray, SM and Wood, MC and Mulkeen, SC and Ahmed, S and Thaker, SD and Chen, B and Sander, WR and Bibeva, V and Zhang, X and Yang, J and Herzog, JW and Moss, AD and Zhang, S and Dogan, B and Simpson, KW and Sartor, RB and Montrose, DC},
title = {Dietary protein source mediates colitis pathogenesis through bacterial modulation of bile acids.},
journal = {Cellular and molecular gastroenterology and hepatology},
volume = {},
number = {},
pages = {101825},
doi = {10.1016/j.jcmgh.2026.101825},
pmid = {42342152},
issn = {2352-345X},
abstract = {BACKGROUND AND AIMS: Evidence-based dietary recommendations for individuals with inflammatory bowel diseases (IBD) are limited. Red meat consumption is associated with increased IBD incidence and relapse in patients, suggesting that switching to a plant-based diet may limit gut inflammation. However, the components and mechanisms underlying the differential effects of these diets remain poorly understood. This study investigated the differential impact of dietary protein source on experimental colitis and related mechanisms.

METHODS: Isocaloric synthetic diets containing protein isolates from beef (BP), egg whites (EP), casein (CP), soy (SP) or pea (PP) were tested in acute (dextran sodium sulfate-induced) and chronic (Il10-deficient) murine colitis models. Gut resident microbes were quantified with 16S-sequencing and their role evaluated by antibiotic depletion, germ-free, selectively colonized gnotobiotic, and fecal microbiota transplant mouse studies.

RESULTS: Mice fed a BP diet exhibited the most severe colitis, while mice fed PP developed mild inflammation. The colitis-promoting effects of BP were microbially-mediated. In the absence of colitis, BP-feeding reduced abundance of Lactobacillus johnsonii and Turicibacter sanguinis and expanded Akkermansia muciniphila, which localized to the mucus in association with decreased mucus thickness and quality. BP-fed mice had elevated primary and conjugated fecal bile acids (BAs), and taurocholic acid administration to PP-fed mice worsened colitis. Dietary psyllium protected against BP-mediated inflammation, restored BA-modulating commensals and normalized BA ratios.

CONCLUSIONS: These data suggest that the protein component of red meat may be responsible, in part, for the colitis-promoting effects of this food source and provide insight into dietary factors that may influence IBD severity.},
}

@article {pmid42342194,
year = {2026},
author = {He, H and Liu, LZ and Duan, HF and Fan, LL and Feng, YC and Liang, XJ and Peng, ZW},
title = {Gut Microbiota from GAD patients with divergent early pharmacological responses transmits anxiety-like behaviors and distinct metabolic profiles in recipient mice.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111803},
doi = {10.1016/j.pnpbp.2026.111803},
pmid = {42342194},
issn = {1878-4216},
abstract = {The gut microbiota is implicated in the pathogenesis of generalized anxiety disorder (GAD), but whether microbial differences between GAD patients with remission (R-GAD) and those with poor early treatment response (P-GAD) causally contribute to variable therapeutic outcomes remains unclear. Here, we transplanted feces from R-GAD and P-GAD patients into antibiotic-pretreated male C57BL/6 mice. P-GAD recipients showed heightened anxiety-like behaviors (reduced central zone time in open field test and shorter open-arm duration in elevated plus-maze), lower gut microbial α-diversity, and distinct β-diversity. Linear discriminant analysis effect size (LEfSe) detected 155 differentially abundant taxa. Genera enriched in R-GAD mice included Blautia, Roseburia, and Lachnospiraceae_NK4A136_group, whereas P-GAD mice were characterized by higher abundances of Bacteroides, Ileibacterium, and Allobaculum. Metabolomic analysis revealed that P-GAD mice had higher levels of neurotoxic tryptophan metabolite indoxyl-β-D-glucuronide (Indoxyl-GlcA) and lower levels of neuroprotective metabolites (indole-3-lactic acid, ILA; L-kynurenine, L-Kyn). Among 34 fatty acids, only C22:5 N3 (docosapentaenoic acid, DPA) was significantly lower in P-GAD mice. Correlation analyses further revealed that genera enriched in P-GAD mice were positively associated with pro-anxiety behaviors and neurotoxic metabolites, whereas those enriched in R-GAD mice showed the opposite trends. These findings suggest that gut microbiota from GAD patients with poor early treatment response may transmit anxiety-like phenotypes and metabolic disturbances in mice, providing a rationale for microbiota-targeted interventions in GAD.},
}

@article {pmid42332289,
year = {2026},
author = {Porcari, S and Ferrari, M and Melekhova, A and Severino, A and Fusco, W and Carlà, AS and De Maio, F and Tilg, H and Gasbarrini, A and Elinav, E and Ianiro, G},
title = {Klebsiella genus as driver of human disease: from infections to non-communicable disorders.},
journal = {Nature reviews. Microbiology},
volume = {},
number = {},
pages = {},
pmid = {42332289},
issn = {1740-1534},
abstract = {Klebsiella spp. are pathobionts associated with acute infections, including pneumonia and infections in the urinary tract and bloodstream, often acquired in health-care settings. They represent a global threat owing to the prevalence of multidrug-resistant strains. Moreover, Klebsiella spp., similarly to other members of the human gut microbiota, can contribute to the pathogenesis of non-communicable disorders. In this Review, we describe the taxonomical and molecular characteristics of the Klebsiella genus, as well as its epidemiology and impact as an infectious agent. We also review current evidence that associates Klebsiella spp. with different non-communicable disorders, including chronic inflammatory and metabolic disorders and cancer. We discuss different approaches to target Klebsiella spp., including tailored antibiotics, faecal microbiota transplantation, live biotherapeutic products and bacteriophages. Finally, we discuss the importance of preventative measures, such as epidemiological surveillance, infection control practices and lifestyle interventions, to reduce the spread of Klebsiella spp. in health-care settings and the broader community.},
}

@article {pmid42334201,
year = {2026},
author = {Moutsoglou, D and Staley, C and Kabage, AJ and Khoruts, A and Vaughn, BP},
title = {Colonoscopic and oral microbiota transplant therapy yield similar stool and neoterminal ileal engraftment profiles in a single-blind pilot randomized trial.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izag096},
pmid = {42334201},
issn = {1536-4844},
support = {T32 HL144472//National Institutes of Health/ ; //Achieving Cures Together (a nonprofit)/ ; //Crohn's and Colitis Litwin Pioneer Award/ ; },
abstract = {BACKGROUND: The intestinal microbiota play a key role in Crohn's disease (CD) and postoperative recurrence following ileocecal resection. Microbiota transplant therapy (MTT) could impact postoperative CD recurrence. This study aimed to compare donor engraftment kinetics in the stool and neoterminal ileum in CD participants with a history of ileocecal resection given either liquid MTT administered via colonoscopy or encapsulated, lyophilized, oral MTT.

METHODS: We performed a single-blind (participant), pilot, randomized trial evaluating ileal and stool engraftment kinetics in participants given MTT either via colonoscopy or oral capsules. Participants with a history of ileocecal resection underwent baseline colonoscopy and were randomized (1:1) to a single administration of liquid MTT at the time of colonoscopy or 5 days of MTT capsules. All underwent ileocolonoscopy with biopsies at week 8. Clinical assessments were obtained over 16 weeks.

RESULTS: Alpha and beta diversity were significantly different between baseline neoterminal ileum and stool samples. Stool and mucosal-adherent ileal engraftment levels were not significantly different from each other based on the delivery method at week 8, and stool and ileal engraftments were significantly correlated to each other. Following MTT, there was a significant reduction in CD symptoms measured by the Harvey-Bradshaw Index; however, no differences were noted by the MTT administration route. Donor engraftment did not correlate to clinical outcomes.

CONCLUSIONS: In this pilot study of MTT in postoperative CD, oral and colonoscopy administration had similar donor engraftment. Oral MTT was well tolerated, supporting further evaluation of oral administration earlier in the postoperative disease course.NCT05248191, FMT for Postop Crohn's Disease, https://clinicaltrials.gov/study/NCT05248191.},
}

@article {pmid42335639,
year = {2026},
author = {Yu, D and Jia, B and Zu, F and Zhang, W and Guo, D},
title = {Ciwujianoside B alleviates cholestatic liver injury by regulating TMAO synthesis via remodeling of the gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {159},
number = {},
pages = {158426},
doi = {10.1016/j.phymed.2026.158426},
pmid = {42335639},
issn = {1618-095X},
abstract = {BACKGROUND: Cholestatic liver injury (CLI) is mainly driven by intrahepatic cholestasis, a pathological condition characterized by systemic and intrahepatic accumulation of bile acids. Ciwujianoside B (CWB), the active constituent of Eleutherococcus senticosus, has demonstrated protective effects in various hepatic pathologies, but its functional role in CLI has not yet been investigated.

PURPOSE: This study aims to evaluate the therapeutic potential of CWB against CLI and investigate its mechanism.

METHODS: CLI was induced via bile duct ligation, and the protective effects of CWB were assessed through H&E, Sirius red, and immunohistochemical staining. Inflammatory cytokines in serum were measured by ELISA. Integrated analysis of 16S rDNA sequencing, serum metabolomics, and fecal microbiota transplantation was performed to investigate the interactions between gut microbiota and host metabolism. Trimethylamine oxide (TMAO) was supplemented to evaluate its impact on the hepatoprotective effects of CWB. In AML-12 cells, flavin-containing monooxygenase 3 (FMO3) was knockdown or overexpressed to assess TMAO levels, apoptosis, reactive oxygen species (ROS) content, and endoplasmic reticulum (ER) stress. The interaction between CWB and FMO3 was evaluated with molecular docking and molecular dynamics simulations.

RESULTS: CWB alleviated hepatocellular damage and apoptosis, which was accompanied by reduced serum levels of ALT, AST, ALP, and inflammatory cytokines. Mechanistic analyses revealed that CWB remodeled the gut microbiota, suppressed Cut C and Cut D levels in feces, thereby reducing systemic TMAO accumulation. Exogenous TMAO supplementation reversed the protective effect of CWB. Antibiotic treatment partially abrogated the hepatic protective effects of CWB. CWB significantly suppressed FMO3 expression. Knockdown of FMO3 in AML-12 cells led to a reduction in intracellular TMAO levels, apoptosis rate, ROS content and ER stress activation. Molecular docking revealed a stable binding interaction between CWB and FMO3.

CONCLUSIONS: Our results suggest that CWB alleviates CLI by suppressing TMAO biosynthesis, primarily through reducing trimethylamine-producing bacteria and directly inhibiting hepatic FMO3 expression.},
}

@article {pmid42335643,
year = {2026},
author = {Kong, Y and Feng, J and Xu, H and Chen, X and Huo, W and Pan, S and Wang, Q and Chen, J and Liu, Y and Li, J and Lu, Y},
title = {Psoralen ameliorates sepsis-induced acute lung injury by regulating microbiota-dependent tryptophan metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {159},
number = {},
pages = {158396},
doi = {10.1016/j.phymed.2026.158396},
pmid = {42335643},
issn = {1618-095X},
abstract = {BACKGROUND: Sepsis frequently leads to acute lung injury (ALI). Despite the documented anti-inflammatory effects of Psoralen (PSO), the exact mechanism by which it confers protection against septic ALI remains poorly understood.

PURPOSE: This research explored the protective efficacy and mechanistic aspects of PSO in sepsis-induced ALI.

METHODS: Lipopolysaccharide (LPS) was employed to create a murine ALI model. Pathological and inflammatory responses were evaluated. The dependency on gut microbiota was assessed through intestinal flora ablation and fecal microbiota transplantation. The aryl hydrocarbon receptor (AhR) engagement was demonstrated by its agonist FICZ and antagonist CH-223191.

RESULTS: In a septic ALI model, PSO ameliorated the histopathological damage and attenuated the inflammatory response. Evidence for this included a lower lung neutrophil percentage and decreased amounts of the proinflammatory mediators tumor necrosis factor-α, interleukin-6, interleukin-1β, as well as MPO-DNA complexes. Additionally, PSO downregulated the abundance of key markers in pulmonary tissue, including peptidylarginine deiminase 4, colony-stimulating factor 2, citrullinated histone H3, and MPO, thereby suppressing neutrophil extracellular trap formation. Furthermore, PSO altered gut microbial diversity, an effect that relied on tryptophan metabolism originating from the gut microbiota. The treatment raised the relative abundance of indole-3-propionic acid (IPA) in serum, which subsequently triggered the AhR/CYP1A1 pathway and thereby alleviated ALI. Moreover, PSO enhanced intestinal tight junction protein expression. Nonetheless, these protective effects were abolished by the AhR inhibitor CH-223191.},
}

@article {pmid42336338,
year = {2026},
author = {Su, Z and Huang, Z and Huang, Y and Guo, J and Wang, Q and Xu, S and Kang, Y and Wang, Z and Shi, Y and Jia, B},
title = {Context-Dependent Short-Chain Fatty Acids in Inflammatory Skin Diseases: Immunometabolic Mechanisms, Evidence Boundaries, and Translational Perspectives.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {108318},
doi = {10.1016/j.phrs.2026.108318},
pmid = {42336338},
issn = {1096-1186},
abstract = {Inflammatory skin diseases(ISDs) arise from dynamic interactions among epithelial barrier dysfunction, immune dysregulation, microbial imbalance and metabolic cues. Within gut-skin and skin-microbiome axes, short-chain fatty acids (SCFAs) have attracted attention as microbial metabolites with anti-inflammatory and barrier-regulatory potential. However, treating SCFAs as uniformly beneficial obscures major biological and translational uncertainties. This narrative review synthesizes evidence from mechanistic, preclinical and clinical studies to define how acetate, propionate and butyrate regulate cutaneous immunity and barrier function. SCFAs act through free fatty acid receptors(FFARs), hydroxycarboxylic acid receptor 2(HCAR2), histone deacetylase inhibition(HDAC) and metabolic-substrate effects, but their outcomes depend on species, source, dose, tissue bioavailability, pH, receptor expression, target-cell identity and disease stage. Gut-derived SCFAs are more likely to support systemic immunometabolic regulation and barrier maturation, whereas locally produced cutaneous SCFAs can either maintain microbial and lipid homeostasis or amplify Toll-like receptor-driven inflammation in pilosebaceous niches. We discuss these mechanisms across immune cells, keratinocytes, sebocytes, fibroblasts, adipocytes and endothelial cells, and interpret their relevance to atopic dermatitis, psoriasis, acne vulgaris, rosacea, hidradenitis suppurativa, chronic spontaneous urticaria and contact dermatitis. We further evaluate dietary, prebiotic/probiotic, topical, fecal microbiota transplantation, engineered probiotic, prodrug and delivery-based strategies, distinguishing SCFA-specific causality from broader microbiome remodeling. A context-resolved framework is needed to translate SCFA biology into rational immunometabolic interventions for ISDs.},
}

@article {pmid42326403,
year = {2026},
author = {Ryazanov, V and Vershinina, I and Inchagova, K and Bukareva, E and Kolpakov, V and Ruchay, A and Kosyan, D and Marinchev, M and Zdorov, A},
title = {Fecal microbiota and microbial community transplantation: a review of current research.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1814047},
pmid = {42326403},
issn = {1664-302X},
abstract = {Homeostasis across diverse ecosystems, ranging from human hosts to environmental matrices, is profoundly governed by microbial communities. Dysbiosis, the disruption of this microbial equilibrium, leads to significant adverse outcomes in medicine, agriculture, aquaculture, and environmental health. This review synthesizes current knowledge on microbial transfusions, defined as the deliberate transfer of microbial communities or their components to restore, reconstitute, or enhance functional capacities across these systems. We explore the historical context and cutting-edge applications, including Fecal Microbiota Transplantation (FMT) for Clostridioides difficile infection, metabolic and neurological disorders, alongside advancements in vaginal microbiota transplantation. In agriculture, we summarize the engineering of soil microbiomes for enhanced plant health, stress adaptation, and bioremediation, as well as transplantation practices in livestock and wild species. Furthermore, we discuss the role of microbiota transplantation in aquaculture for improving fish health and disease resistance, highlighting both natural and synthetic consortia. The application of microbial communities in bioremediation and ecological restoration is explored, addressing challenges such as stability, cost, and ecological impacts. Ultimately, this review integrates these diverse applications within a "One Health" framework, emphasizing the systemic links among human, animal, and environmental microbiomes. We underscore the potential of microbiota transplantation as a sustainable strategy for restoring ecological balance while identifying critical research gaps and future directions regarding standardized methodologies and the long-term functionality of transplanted microbiomes.},
}

@article {pmid42326424,
year = {2026},
author = {Liang, L and Min, L and Liu, J and Liu, Y and Cheng, W},
title = {Gut microbiota dysbiosis in endometriosis: mechanistic insights and gut microbiota-targeted therapeutic strategies.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1776574},
pmid = {42326424},
issn = {1664-302X},
abstract = {Endometriosis (EMs) is a prevalent, estrogen-dependent gynecological disorder characterized by the ectopic implantation and proliferation of endometrial-like tissue outside the uterine cavity, affecting approximately 10% of reproductive-aged women globally. Despite its high incidence, the exact pathogenesis of EMs remains incompletely elucidated, and current clinical treatments are often limited by suboptimal efficacy and adverse effects. Accumulating evidence over the past decade has revealed a strong observational association between gut microbiota dysbiosis and EMs development, suggesting that the gut microbiota may serve as a novel potential target for understanding and managing this disease. This review systematically summarizes the potential mechanistic links underlying the interplay between gut microbiota dysbiosis and EMs progression, focusing on three core pathways: intestinal barrier dysfunction and microbial translocation, immune dysregulation and ectopic lesion immune escape, and estrogen metabolism disorder mediated by microbial enzymes and metabolites. In addition, this review stratifies gut microbiome profiles by EMs clinical subtypes (peritoneal, ovarian, deep infiltrating), clarifies anatomical correlations of the gut-lesion axis, and discusses confounding factors and causal inference methodologies. Beyond mechanistic insights, this review also discusses emerging gut microbiota-targeted therapeutic strategies for EMs, including probiotic supplementation, prebiotic intervention, fecal microbiota transplantation (FMT), and dietary modulation, with supplementary ethical considerations for FMT. Collectively, this review provides a comprehensive overview of the gut microbiota-EMs axis, highlighting current evidence levels and offering perspectives for the development of innovative, effective, and safe therapeutic approaches for EMs patients.},
}

@article {pmid42326427,
year = {2026},
author = {Chen, L and Wu, W and Kong, Q},
title = {Gut microbiota alters cardiac metabolism and immune system composition in viral myocarditis mice.},
journal = {Frontiers in microbiology},
volume = {17},
number = {},
pages = {1828423},
pmid = {42326427},
issn = {1664-302X},
abstract = {BACKGROUND: The effects of the gut microbiota on the regulation of host physiology have recently garnered considerable attention, particularly in metabolism and the immune system. However, the role of the gut microbiota in viral myocarditis (VMC) remains to be fully elucidated.

METHODS: Balb/c mice were injected with CVB3 to induce VMC. VMC mice were treated with fecal microbiota transplantation (FMT) or antibiotics (ABX) to evaluate the therapeutic effects of these interventions. Echocardiography, HE, and Masson's staining of the heart were used to assess cardiac function and pathological changes. 16S rDNA sequencing was conducted to explore alterations in gut microbial composition. UPLC-MS/MS-based metabolomics was used to detect disturbances of cardiac metabolic profiles. Flow cytometry was applied to analyze the dynamics of immune cell subsets, including M1, M2, Th1, Th2, Th17, and Treg cells. RT-PCR was performed to quantify cytokine expression levels in the heart.

RESULTS: FMT reduced cardiac inflammation and fibrosis, enhanced heart function, remodeled the structure of gut microbiota in VMC, and increased bacterial diversity, with an enrichment of p-Proteobacteria, the reduction of g-Pseudomonas, g-Streptococcus, and g-Ralstonia. Meanwhile, FMT induced alterations in cardiac metabolites in VMC, with enrichment of the steroid hormone biosynthesis pathway. A significant negative correlation was found between desoxycortone, corticosterone, 21-deoxycortisol, and cortodoxone with p_Spirochaetota and p_Kapabacteria. Furthermore, FMT reduced the proportions of M1 macrophages, Th1, and Th17 cells, as well as the cytokines TNF-a, IL-6, and IL-1β, and increased M2 macrophages and Treg cells. Regarding the role of antibiotics in VMC, our findings indicated that antibiotics altered the gut microbiota, myocardial metabolism, and immune response. Compared with antibiotics, FMT exerted a better effect on the alleviation of cardiac inflammation and fibrosis.

CONCLUSION: In VMC mice, the gut microbiota, which mediates disturbances in cardiac metabolites and the host immune response, may contribute significantly to the development of cardiac inflammation and fibrosis. Furthermore, FMT may represent a promising therapeutic approach for VMC.},
}

@article {pmid42327212,
year = {2026},
author = {Damiani, F and Ashtiani, KC and Tognozzi, A and Abdelkarim, S and Cornuti, S and Caldarelli, M and Baldi, P and Tognini, P},
title = {The Critical Period Microbiota Shape Brain Plasticity.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.64898/2026.06.08.730811},
pmid = {42327212},
issn = {2692-8205},
abstract = {The gut microbiota is increasingly recognized as a regulator of brain function, yet its role in experience-dependent plasticity during postnatal development remains largely unknown. Here, we show that disrupting the gut microbiota with antibiotics during critical periods of visual cortex development impairs ocular dominance plasticity (ODP) in juvenile mice. Antibiotic treatment induces marked changes in microbial community composition and is accompanied by extensive transcriptional remodeling of the visual cortex, including pathways involved in extracellular matrix organization, blood-brain barrier function, and myelination. Remarkably, fecal transplantation of the juvenile microbiota into adult recipients restores ODP. These findings identify the gut microbiota as a previously unrecognized regulator of neurodevelopmental plasticity and support the existence of microbiota-dependent critical periods of brain development. More broadly, our results suggest that early-life microbial perturbations may have lasting consequences for lifelong brain function and reveal that juvenile microbiota-derived signals could be exploited to promote plasticity in the adult brain.},
}

@article {pmid42327683,
year = {2026},
author = {Knudsen, MJS and Rubin, IMC and Mirsepasi-Lauridsen, HC and Tomiak, J and Halkjær, SI and Petersen, AM and Helms, M},
title = {Decolonisation of a multi-drug-resistant Escherichia coli and a vancomycin-resistant Enterococcus faecium after intervention with faecal microbiota transplantation.},
journal = {Infection prevention in practice},
volume = {8},
number = {3},
pages = {100554},
pmid = {42327683},
issn = {2590-0889},
abstract = {In this study, we report a case of decolonisation of a multi-drug-resistant extended spectrum beta-lactamase-producing Escherichia coli, and a vancomycin-resistant Enterococcus faecium after intervention with capsulated faecal microbiota transplantation (FMT). Following eradication, our patient acquired an extended-spectrum beta-lactamase-producing Klebsiella pneumoniae, which was subsequently eliminated after a second round of FMT capsules. Additionally, we report the detection of six distinct carbapenemase-producing organisms in this patient, who was evacuated from the war in Ukraine.},
}

@article {pmid42328867,
year = {2026},
author = {Wang, Y and Sheng, P and Wang, S and Zhong, X and Cao, H and Li, D and Yan, J and Yang, J and Wang, Y and Peng, J and Sun, F and Wang, S and Feng, Y and Sun, J and Zhang, F},
title = {Gut microbiota translocation contributes to early islet apoptosis in streptozotocin-induced diabetes.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0017226},
doi = {10.1128/msystems.00172-26},
pmid = {42328867},
issn = {2379-5077},
abstract = {Dysbiosis of the gut microbiota and impaired intestinal barrier are associated with diabetes development. The translocation of gut microbiota induced by streptozotocin (STZ) has been confirmed to damage pancreatic islets. However, it remains uncertain whether dysregulated gut microbiota plays an essential role in the translocation leading to pancreatic injury. In specific pathogen-free (SPF) and germ-free (GF) mice treated with STZ, we measured glucose metabolism levels, pancreatic islet damage, intestinal barrier integrity, and bacterial content in the pancreas to investigate the role of gut microbiota translocation in diabetes development. Shotgun metagenomic sequencing was used to analyze the impact of STZ on gut microbiota structure and function. Fecal microbiota transplantation was performed to explore if gut microbiota translocation depends on STZ-induced structural dysregulation. STZ induced intestinal damage in SPF mice, resulting in gut microbiota translocation to the pancreas, pancreatic apoptosis, and dysregulated glucose metabolism. Despite inherent intestinal barrier damage, absence of pancreatic apoptosis in GF mice further indicates that gut microbiota translocation is an essential prerequisite for STZ-induced pancreatic islet apoptosis. STZ significantly altered mouse gut microbiota composition and function. Transplantation of fecal microbiota from STZ-treated or saline-treated mice into STZ-induced GF mice also resulted in microbial translocation and pancreas apoptosis. Apoptosis of β cells in STZ-treated mice results from gut microbiota translocating to the pancreas through impaired intestinal barrier caused by STZ treatment independent of alterations in the gut microbial community.IMPORTANCEIn our study, the apoptosis of β cells in STZ-treated mice is the result of the translocation of gut microbiota to the pancreas through the impaired intestinal barrier induced by STZ, independent of alterations in the gut microbiota. These findings proposed the potential role of compounds in impairing the intestinal barrier integrity, promoting microbiota migration and finally damaging pancreatic islets.},
}

@article {pmid42332220,
year = {2026},
author = {Piñero-Pérez, C and Velasco-Guardado, A and Pérez-López, E and Cortés-Rodríguez, M and Cabrero-Calvo, M and Martín-López, AA and Sánchez-Guijo, F and López-Corral, L},
title = {Fecal calprotectin as a biomarker for the diagnosis of gastrointestinal graft-versus-host disease following allogeneic hematopoietic stem cell transplantation.},
journal = {Bone marrow transplantation},
volume = {},
number = {},
pages = {},
pmid = {42332220},
issn = {1476-5365},
abstract = {Gastrointestinal graft-versus-host disease (GI-GVHD) is a major complication after allogeneic hematopoietic stem cell transplantation (allo-HSCT), often requiring invasive endoscopy for diagnosis. Fecal calprotectin (FC) offers a non-invasive marker of intestinal inflammation, but its utility in GI-GVHD needs clarification. In this prospective observational study of 165 adult allo-HSCT recipients, FC was measured on days +7, +14, and +21 post-transplant, at GI-GVHD onset, and 7 days post-treatment, alongside clinical, endoscopic, and histological data. GI-GVHD developed in 52.7% of patients, with histological confirmation in 90.3% of cases. FC lacked predictive value on day +7 (AUC = 0.50) but showed moderate-to-high accuracy on days +14 (AUC = 0.69) and +21 (AUC = 0.77), with an optimal day +21 cutoff of 52.5 µg/g (sensitivity 75%, specificity 87%). At diagnosis, median FC was 120 µg/g, correlating with endoscopic severity (r = 0.31; p = 0.02) but not clinical or histological grades. FC declined significantly post-treatment (120 to 51.5 µg/g; p = 0.04), though concurrent infections elevated levels without compromising discriminative ability. FC serves as a dynamic biomarker for predicting, diagnosing, and monitoring GI-GVHD, but requires integrated clinical interpretation due to limited specificity amid other inflammations.},
}

@article {pmid41612728,
year = {2026},
author = {Li, S and Che, C and Zhou, Y and Fan, D and Bai, X and Lu, Y and Zhao, X},
title = {Gut microecology empowers cancer immunotherapy: commensal microbiota-mediated mechanisms and translational prospects of PD-1/PD-L1 therapy.},
journal = {Cancer biology & medicine},
volume = {23},
number = {1},
pages = {60-77},
pmid = {41612728},
issn = {2095-3941},
support = {82222058//National Natural Science Foundation of China/ ; 82425046//National Natural Science Foundation of China/ ; 82273142//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Neoplasms/therapy/immunology/drug therapy/microbiology ; *Immunotherapy/methods ; *Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Animals ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *B7-H1 Antigen/antagonists & inhibitors ; Fecal Microbiota Transplantation ; Tumor Microenvironment/immunology ; },
abstract = {Anti-programmed cell death protein 1 (PD-1) or its ligand (PD-L1) are immune checkpoint inhibitors (ICIs) that have revolutionized cancer therapy. However, the efficacy of anti-PD-1 and anti-PD-L1 is limited by resistance and inter-individual variability. In recent years increasing evidence has highlighted the pivotal role of the gut microbiota in modulating the response to PD-1/PD-L1 immunotherapy. Extensive preclinical studies have demonstrated that commensal microbes can increase the efficacy of PD-1/PD-L1 blockade through multiple mechanisms, including the production of metabolites, such as short-chain fatty acids (SCFAs), tryptophan derivatives, and extracellular polysaccharides that remodel the tumor microenvironment, as well as the activation of immune pathways involving dendritic cells, CD8[+] T cells, and M1 macrophages to increase antitumor immunity. Moreover, clinical studies have shown that fecal microbiota transplantation (FMT) and targeted probiotic interventions show promise for improving the response to PD-1/PD-L1 therapy, while reducing the risk of immune-related adverse events (irAEs). This review systematically explores the multifaceted regulatory roles of the commensal microbiota in PD-1/PD-L1 therapy and examines the preclinical prospects of microbiota-based personalized immunotherapeutic strategies. The integration of multiomics technologies, synthetic biology, and precise microbiota interventions may further optimize PD-1/PD-L1 immunotherapy and offer novel insights into antitumor immune modulation.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Neoplasms/therapy/immunology/drug therapy/microbiology
*Immunotherapy/methods
*Programmed Cell Death 1 Receptor/antagonists & inhibitors
Animals
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*B7-H1 Antigen/antagonists & inhibitors
Fecal Microbiota Transplantation
Tumor Microenvironment/immunology

@article {pmid41613006,
year = {2025},
author = {Wang, ZQ and Zheng, HD and Li, LJ and Cao, LL and Shen, L and Qiao, Y and Chen, YY and Wu, LY and Li, GN and Wu, HG},
title = {Electroacupuncture alleviates Parkinson's disease by targeting HDAC/SIRT-mediated deacetylation of 14-3-3.},
journal = {Frontiers in aging neuroscience},
volume = {17},
number = {},
pages = {1719326},
pmid = {41613006},
issn = {1663-4365},
abstract = {INTRODUCTION: Parkinson's disease (PD) is a neurodegenerative disorder characterized by the loss of dopaminergic neurons and the accumulation of pathological α-synuclein. Although current treatments can alleviate symptoms, they do not modify disease progression. Growing evidence implicates gut microbiota dysbiosis and aberrant protein acetylation in PD pathogenesis. Electroacupuncture (EA) has shown therapeutic potential in PD; however, its effects on protein acetylation remain unclear.

METHODS: A PD mouse model was established through MPTP induction and fecal microbiota transplantation (FMT) from PD patients. Mice received EA stimulation at Baihui (GV20) and Yanglingquan (GB34) acupoints for 14 days. Behavioral tests, immunohistochemistry, Western blot, qPCR, and 4D label-free acetyl proteomics were employed to assess motor function, neuronal integrity, protein expression, and acetylation profiles.

RESULTS: EA significantly improved motor coordination, enhanced sensorimotor function in the adhesive removal test, and increased open-field activity in PD mice. It attenuated the loss of tyrosine hydroxylase-positive neurons and decreased α-synuclein accumulation in the substantia nigra. Proteomic analysis revealed hyperacetylation of Ywhaq (14-3-3) in PD mice, which was reversed by EA. Mechanistically, EA upregulated the expression of deacetylases HDAC1/2/3 and SIRT1/2 at both protein and mRNA levels, restoring acetylation homeostasis.

CONCLUSION: Electroacupuncture ameliorates behavioral and neuropathological phenotypes in a PD mouse model by restoring deacetylase expression and normalizing protein acetylation, particularly of 14-3-3. Our results underscore the therapeutic potential of EA and highlight acetylation modulation as a promising strategy for PD treatment.},
}

@article {pmid41613143,
year = {2025},
author = {Liu, L and Zhang, X and Wang, C and Zhou, K and Bao, J and Cheng, Z and Sun, H and Zhu, C and Yu, G and Xiao, W and Wan, R},
title = {Dysregulation of the microbiota-gut-brain axis induced by chronic pancreatitis mediates anxiety- and depression-like behaviors in mice.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1753424},
pmid = {41613143},
issn = {1664-3224},
mesh = {Animals ; *Depression/etiology/microbiology ; *Anxiety/etiology/microbiology ; *Gastrointestinal Microbiome ; Mice ; *Pancreatitis, Chronic/psychology/microbiology/complications/chemically induced ; Male ; Disease Models, Animal ; Mice, Inbred C57BL ; Behavior, Animal ; *Brain-Gut Axis ; Dysbiosis ; Fecal Microbiota Transplantation ; *Brain/metabolism ; RNA, Ribosomal, 16S/genetics ; },
abstract = {BACKGROUND: Anxiety and depression are common psychological complications in patients with chronic pancreatitis (CP). This study aims to investigate the dysregulation of microbiota-gut-brain axis induced by CP in driving anxiety- and depression-like behaviors in mice.

METHODS: C57BL/6J mice injected with caerulein (Cae) were used to establish an experimental CP model. Behavioral tests were performed to assess anxiety- and depression-like behaviors. The gut microbiota composition and serum metabolites were analyzed via 16S rRNA sequencing and liquid chromatography-mass spectrometry, respectively. Antibiotic cocktail (ABX) and fecal microbiota transplantation (FMT) models were employed to validate the direct role of the gut microbiota, while mixed probiotic gavage was used for intervention evaluation.

RESULTS: Cae-injected mice presented typical CP symptoms and significant anxiety- and depression-like behaviors. 16S rRNA sequencing revealed altered gut microbiota composition in CP mice, with a reduced abundance of Lactobacillus and enrichment of Helicobacter. ABX and FMT experiments confirmed that the CP-derived gut microbiota can independently induce anxiety/depression-like behaviors. In CP mice, Serum corticosterone and its metabolite levels were significantly increased in CP mice. CP-induced microbiota dysbiosis can induce the downregulation of intestinal barrier and blood-brain barrier functions, increase inflammatory levels, and extensively dysregulate neurotransmitter transmission in the brain. Treatment with mixed probiotics improved anxiety- and depression-like behaviors in CP mice.

CONCLUSIONS: CP promotes anxiety- and depression-like behaviors in mice by inducing gut microbiota dysbiosis. This study provides experimental evidence for the use of microbiota-targeted interventions for treating the psychological complications of CP.},
}

Animals
*Depression/etiology/microbiology
*Anxiety/etiology/microbiology
*Gastrointestinal Microbiome
Mice
*Pancreatitis, Chronic/psychology/microbiology/complications/chemically induced
Male
Disease Models, Animal
Mice, Inbred C57BL
Behavior, Animal
*Brain-Gut Axis
Dysbiosis
Fecal Microbiota Transplantation
*Brain/metabolism
RNA, Ribosomal, 16S/genetics

@article {pmid41613791,
year = {2026},
author = {Mozga, K and Synowiecka, O and Rydzyk, I and Marek, A and Wieczorek, E and Petniak, A and Gil-Kulik, P},
title = {The Frontier of Melanoma Treatment: Defeating Immunotherapy Resistance-A Systematic Review.},
journal = {Oncology research},
volume = {34},
number = {2},
pages = {4},
pmid = {41613791},
issn = {1555-3906},
mesh = {Humans ; *Melanoma/immunology/therapy/drug therapy ; *Immunotherapy/methods ; *Drug Resistance, Neoplasm/immunology ; Animals ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; },
abstract = {OBJECTIVES: Immunotherapy based on immune checkpoint blockade (ICB) has become a key treatment for melanoma. However, the increasing number of cases of melanoma resistant to immunotherapy highlights the need to develop methods to overcome this resistance. This study aims to collect the most recent information on melanoma immunotherapy, discuss potential strategies to overcome resistance to immunotherapy, and identify areas that require further analysis.

METHODS: To achieve this goal, scientific publications from 2021-2024 available in PubMed and Google Scholar databases were analyzed. The databases were searched using the following terms: "melanoma", "immunotherapy", "Immune Checkpoint Blockade", and "immunoresistance".

RESULTS: The results of preclinical and early-stage clinical research indicate the potential application of tank-binding kinase 1 (TBK-1), fecal microbiota transplant (FMT), Toll-like Receptor 9 (TLR9), lipid nanoparticles (LNPs) containing a stimulator of an interferon gene agonist (STING), BRAF inhibitors, Lymphocyte Activation Gene (LAG-3), T-Cell Immunoglobulin and ITIM Domain (TIGIT), and oncolytic viruses (OVs) as potential methods to enhance melanoma sensitivity to ICB.

DISCUSSION: To optimize immunotherapy, further research is needed to determine the detailed mechanisms of action, safety profiles, tolerability, and precise patient selection criteria for methods capable of overcoming melanoma's immunoresistance.},
}

Humans
*Melanoma/immunology/therapy/drug therapy
*Immunotherapy/methods
*Drug Resistance, Neoplasm/immunology
Animals
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology

@article {pmid41614677,
year = {2026},
author = {Pettersson, M and La Sala, G and Gunnarsson, A and Vildhede, A and Sparklin, B and Holm, B and Petrović, D and Lasky, G and Turick, S and Szydlowska, M and Gopalakrishnan, V and Bake, T and Petersen, J and Brånalt, J and Westerlund, K and Taillefer, M and Henricsson, M and Ek, M and Warrener, P and Roth, R and Cohen, T and Sjögren, T and Fahlander, U and Jurva, U and Morias, Y and Liddle, J},
title = {Discovery of a Highly Potent and Selective Small-Molecule Inhibitor of In Vivo Anaerobic Choline Metabolism by Human Gut Bacteria.},
journal = {Journal of medicinal chemistry},
volume = {69},
number = {3},
pages = {2115-2129},
doi = {10.1021/acs.jmedchem.5c01451},
pmid = {41614677},
issn = {1520-4804},
mesh = {Humans ; Animals ; Methylamines/metabolism ; Rats ; *Choline/metabolism ; Mice ; *Enzyme Inhibitors/pharmacology/chemistry ; *Gastrointestinal Microbiome/drug effects ; *Small Molecule Libraries/pharmacology/chemistry ; Anaerobiosis ; *Drug Discovery ; Structure-Activity Relationship ; *Lyases/antagonists & inhibitors/metabolism ; Male ; },
abstract = {Trimethylamine (TMA) Lyase is an enzyme expressed in human gut bacteria that plays a pivotal role in the formation of trimethylamine oxide (TMAO), a metabolite implicated in the development of heart failure. Here, we describe a strategy to design covalent inhibitors targeting the active site thiyl radical involved in the catalytic cycle of the enzyme under anaerobic conditions. This strategy led to the discovery of 7, a previously unreported highly potent and selective inhibitor of TMA Lyase. When dosed orally to rats, 7 shows a significant reduction of circulating TMAO levels and, importantly, demonstrates inhibition of TMAO generated from a human microbiome when profiled in a human fecal mouse transplant model.},
}

Humans
Animals
Methylamines/metabolism
Rats
*Choline/metabolism
Mice
*Enzyme Inhibitors/pharmacology/chemistry
*Gastrointestinal Microbiome/drug effects
*Small Molecule Libraries/pharmacology/chemistry
Anaerobiosis
*Drug Discovery
Structure-Activity Relationship
*Lyases/antagonists & inhibitors/metabolism
Male

@article {pmid41614846,
year = {2025},
author = {Montoya Montoya, J and Gómez, EC and Tabares Guevara, JH and Arango Rincón, JC and Naranjo Preciado, TW},
title = {Effect of Gut Microbiota Alteration on Colorectal Cancer Progression in an In Vivo Model: Histopathological and Immunological Evaluation.},
journal = {Current issues in molecular biology},
volume = {48},
number = {1},
pages = {},
pmid = {41614846},
issn = {1467-3045},
support = {646-2021//Ministerio de Ciencia, Tecnología e Innovación/ ; },
abstract = {Background/Objectives: Colorectal cancer (CRC) is one of the leading causes of cancer-related mortality worldwide, with its development influenced by diet, obesity, and gut microbiota (GM) alterations. This study aimed to evaluate the impact of human fecal microbiota transplantation (FMT) on the progression of CRC in a murine model. Methods: CRC was chemically induced in BALB/c mice using azoxymethane/dextran sulfate sodium (AOM/DSS). Mice were transferred with GM via FMT and divided into two experimental groups according to the microbiota source (healthy donors or CRC patients). A positive control group (AOM/DSS without FMT) and a negative control group (no CRC induction or FMT) were included. Clinical parameters, histopathological analyses, and cytokine profiling were performed. Results: Mice receiving FMT, particularly from CRC patients, exhibited increased mitotic activity, dysplasia, neoplastic proliferation, structural alterations in the colon, and more pronounced GALT hyperplasia. At the immunological level, both FMT groups (healthy and CRC-derived) showed modulation of IL-1β, IL-4, IL-6, IL-10, IL-17A, and TNF-α compared to the positive control. Conclusions: Human GM transplantation modulated the colonic microenvironment through histopathological and immunological changes, influencing CRC progression in this murine model. These findings highlight the role of GM in shaping CRC development and suggest that human-derived microbiota may significantly impact tumor dynamics.},
}

@article {pmid41614917,
year = {2026},
author = {Zhan, M and Chen, H and Fu, X and Tang, S and Song, X and Li, H and Zhu, L and Wang, B},
title = {TUDCA Ameliorates Cognitive Impairment in APP/PS1 Mice by Modulating the Microbiota-Gut-Brain Axis.},
journal = {Current issues in molecular biology},
volume = {48},
number = {1},
pages = {},
pmid = {41614917},
issn = {1467-3045},
support = {2020ZY013802//Chongqing Municipal Health Commission and Chongqing Science and Technology Bureau/ ; },
abstract = {Tauroursodeoxycholic acid (TUDCA), a bile acid conjugate, has been suggested to improve cognition in models of Alzheimer's disease (AD), although its underlying mechanisms remain unclear. This study aimed to evaluate the effects of TUDCA and its potential pathways in APP/PS1 mice. Behavioral tests, assessments of amyloid-β (Aβ) deposition, neuroinflammation, peripheral inflammatory responses, intestinal barrier integrity, and gut microbiota composition were performed, along with pseudo-sterile mouse experiments and fecal microbiota transplantation (FMT). The expression of genes related to the TLR4/NF-κB/NLRP3 pathway was also examined. TUDCA significantly ameliorated cognitive impairments, reduced Aβ accumulation, and suppressed inflammatory responses in both the central nervous system and peripheral tissues. It improved intestinal barrier function and reshaped gut microbial composition by reducing pro-inflammatory taxa. FMT demonstrated that TUDCA-modulated microbiota contributed to improved learning and memory in AD mice, whereas antibiotic-induced pseudo-sterility indicated that TUDCA also exerted cognitive benefits independent of gut flora. Moreover, TUDCA inhibited the activation of the TLR4/NF-κB/NLRP3 pathway. In conclusion, TUDCA alleviates AD-related cognitive deficits partly through modulation of the microbiota-gut-brain axis while also acting via microbiota-independent mechanisms, supporting its potential as a promising therapeutic strategy for AD.},
}

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

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

@article {pmid41616125,
year = {2026},
author = {Zhu, S and Bian, S and Lu, J and Wang, Y and Iqbal, M and Kiani, FA and Dong, H and Zhang, X and Yuan, Z and Liu, F and Li, A},
title = {Pathogenesis of Bovine Mastitis and Influence of the Gut Microbiota: A Review.},
journal = {Journal of agricultural and food chemistry},
volume = {74},
number = {5},
pages = {4222-4234},
doi = {10.1021/acs.jafc.5c13667},
pmid = {41616125},
issn = {1520-5118},
mesh = {Animals ; Cattle ; Female ; *Mastitis, Bovine/microbiology/immunology/therapy/metabolism ; *Gastrointestinal Microbiome ; Bacteria/genetics/isolation & purification/classification ; Intestinal Barrier Function ; Toll-Like Receptors/genetics/immunology ; },
abstract = {Bovine mastitis (BM) is a highly prevalent bacterial infection that causes significant economic losses in the dairy industry. Its pathogenesis involves the recognition of pathogen-associated molecular patterns by Toll-like receptors (TLRs, primarily TLR2 and TLR4) and the subsequent activation of the NF-κB signaling pathway. Emerging evidence highlights the critical role of the gut microbiota in regulating BM through the "gut-mammary axis." Gut dysbiosis reduces microbial diversity, impairs the intestinal barrier, and promotes endotoxemia or translocation of metabolites, such as LPS (lipopolysaccharide) and short-chain fatty acids (SCFAs), which modulate mammary inflammation. Traditional antibiotic therapy is increasingly limited by resistance and residues, necessitating alternative approaches: targeting the gut microbiota through probiotics, fecal microbiota transplantation (FMT), or plant-derived active components offers promising strategies to restore microbial balance, enhance intestinal barrier function, and suppress excessive inflammation, thereby providing novel avenues for the prevention and treatment of BM.},
}

Animals
Cattle
Female
*Mastitis, Bovine/microbiology/immunology/therapy/metabolism
*Gastrointestinal Microbiome
Bacteria/genetics/isolation & purification/classification
Intestinal Barrier Function
Toll-Like Receptors/genetics/immunology

@article {pmid41617211,
year = {2026},
author = {Sang, X and Zheng, Q and Qin, M and Chen, M and Wan, X and Hao, M and Yang, Q and Cao, G},
title = {Pentagalloylglucose, a limited oral bioavailability polyphenol, improves allergic asthma through regulating gut microbiota and modulating enteritis.},
journal = {British journal of pharmacology},
volume = {183},
number = {10},
pages = {2556-2577},
doi = {10.1111/bph.70345},
pmid = {41617211},
issn = {1476-5381},
support = {82274101//National Natural Science Foundation of China/ ; 82374123//National Natural Science Foundation of China/ ; LY24H280002//Natural Science Foundation of Zhejiang Province/ ; LQ23H280004//Natural Science Foundation of Zhejiang Province/ ; 2025JKZKTS23//Research Project of Zhejiang Chinese Medical University/ ; 2024R410A033//Students Science and Technology Innovation Activity Plan of Zhejiang Province/ ; },
mesh = {Animals ; *Asthma/drug therapy/microbiology/immunology ; *Hydrolyzable Tannins/pharmacology/administration & dosage/pharmacokinetics/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; Mice ; Biological Availability ; Administration, Oral ; Fecal Microbiota Transplantation ; Mice, Inbred BALB C ; Female ; *Anti-Asthmatic Agents/pharmacology/pharmacokinetics/administration & dosage ; Male ; *Polyphenols/administration & dosage/pharmacology/pharmacokinetics ; Colitis/drug therapy/microbiology ; },
abstract = {BACKGROUND AND PURPOSE: Pentagalloylglucose (PGG), a natural hydrolysable gall tannin, has limited bioavailability, and its biological activities are concentrated in the digestive system. However, our study discovered that this nonabsorbable compound can improve allergic asthma. This study focuses on elucidating the mechanisms underlying PGG's anti-allergic asthma effects.

METHODS: PGG serum metabolites were analyzed by UPLC/Q-TOF MS. To further explore its mechanisms, 16S rRNA sequencing, qPCR, and UPLC/Q-TOF MS were used to assess gut microbiota and metabolites. Fecal microbiota transplantation from PGG-treated mice into antibiotic-treated asthmatic mice evaluated its microbiota-dependent effects. Flow cytometry analyzed PGG's modulation of pulmonary ILC2s in a murine asthma‑colitis comorbid model.

KEY RESULTS: PGG's serum metabolites were below the quantification limit. PGG administration improved colonic injury and modulated L. reuteri; notably, exogenous L. reuteri alleviated asthma via increasing I3A from Trp metabolism. However, fecal microbiota transplantation from PGG-treated mice did not alleviate asthma, and PGG remained effective in microbiota-depleted mice, suggesting its action is microbiota-independent. Furthermore, PGG alleviated intestinal inflammation in both normal and antibiotic-treated asthmatic mice. In a comorbid colitis-asthma model, PGG counteracted colitis-aggravated asthma symptoms by modulating lung ILC2s.

CONCLUSION AND IMPLICATIONS: Although PGG modulates the gut microbiota and related metabolites, its anti-asthmatic effect is not primarily dependent on this pathway. Notably, it can ameliorate lung ILC2 dysregulation by alleviating enteritis.},
}

Animals
*Asthma/drug therapy/microbiology/immunology
*Hydrolyzable Tannins/pharmacology/administration & dosage/pharmacokinetics/therapeutic use
*Gastrointestinal Microbiome/drug effects
Mice
Biological Availability
Administration, Oral
Fecal Microbiota Transplantation
Mice, Inbred BALB C
Female
*Anti-Asthmatic Agents/pharmacology/pharmacokinetics/administration & dosage
Male
*Polyphenols/administration & dosage/pharmacology/pharmacokinetics
Colitis/drug therapy/microbiology

@article {pmid41617714,
year = {2026},
author = {Du, Q and Li, Q and Ullah, H and Wei, Y and Liao, G and Xiao, X and Yao, J and Li, K},
title = {Harnessing gut microbiota for brain health: protective role of Hungatella hathewayi for post-mTBI cognitive impairment.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {41617714},
issn = {2055-5008},
support = {2024NSFSC0592//Sichuan Province Science and Technology Support Program/ ; U22A20334//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; Rats ; Male ; *Cognitive Dysfunction/etiology/prevention & control/microbiology/therapy ; Humans ; *Brain ; *Eubacteriales/physiology ; Microglia ; Fecal Microbiota Transplantation ; Butyrates/metabolism ; Fatty Acids, Volatile/metabolism ; *Brain Concussion/complications/microbiology ; Disease Models, Animal ; Feces/microbiology/chemistry ; },
abstract = {Cognitive impairment (CI) following mild traumatic brain injury (mTBI) poses a clinical challenge, with emerging evidence implicating gut microbiota. This study found that mTBI patients who developed CI exhibited decreased Hungatella hathewayi, while those without CI showed an increase. Microbiota transplantation in mTBI rats revealed that higher Hungatella hathewayi levels enriched beneficial, short-chain fatty acid (SCFA) -producing bacteria and reduced harmful ones. Elevated Hungatella hathewayi improved performance in the Morris water maze and novel object recognition tests, indicating enhanced spatial learning and memory. It also reduced gut and brain inflammation, shown by lower TNF-α and IL-6 mRNA expression, and promoted M2 microglia polarization in the peri-lesional cortex. Metabolomics identified increased fecal and serum butyrate, a SCFA with anti-neuroinflammatory properties. Thus, Hungatella hathewayi may mitigate Post-mTBI CI by boosting butyrate production, which alleviates intestinal inflammation, shifts microglia toward the protective M2 phenotype, reduces neuroinflammation, and supports neuroprotection, ultimately lowering CI risk after mTBI. This study was registered with the Chinese Clinical Trial Registry (ChiCTR) on May 31, 2023 (Registration number: ChiCTR2300072000, URL: https://www.chictr.org.cn/showproj.html?proj=197867).},
}

Animals
*Gastrointestinal Microbiome
Rats
Male
*Cognitive Dysfunction/etiology/prevention & control/microbiology/therapy
Humans
*Brain
*Eubacteriales/physiology
Microglia
Fecal Microbiota Transplantation
Butyrates/metabolism
Fatty Acids, Volatile/metabolism
*Brain Concussion/complications/microbiology
Disease Models, Animal
Feces/microbiology/chemistry

@article {pmid41618079,
year = {2026},
author = {Cheng, C and Li, Y and Lv, W and Zhao, J and Zhang, Y and Lu, H},
title = {A dual pathway intervention of tES and FMT enhances emotion regulation in stressed military personnel.},
journal = {Discover mental health},
volume = {6},
number = {1},
pages = {},
pmid = {41618079},
issn = {2731-4383},
support = {LHJJ24XL08//The Project of Psychological Interdisciplinary Integration/ ; },
abstract = {This review explores novel strategies for enhancing emotion regulation in military personal under stress, based on the interaction mechanisms of the microbiota-brain-gut axis. Military stress often triggers emotional fluctuations, cognitive decline, and physiological dysregulation, significantly impairing both mental health and combat performance. Existing research has primarily focused on psychological remediation, with insufficient attention paid to physiological mechanisms-particularly brain-gut interactions in emotion regulation. This paper proposes a dual-mode intervention strategy combining "top-down" and "bottom-up" approaches. On one hand, non-invasive neuromodulation techniques such as transcranial electrical stimulation (tES) are used to precisely regulate emotion-related brain regions, enabling immediate mitigation of negative emotions. On the other hand, fecal microbiota transplantation (FMT) is employed to restore gut microbial balance, thereby modulating neurotransmitter production and central nervous function via the gut-brain axis to enhance long-term emotional stability. Ultimately, we propose an integrated intervention combining tES and FMT, which addresses both acute emotional control and sustained regulation. This approach offers a promising theoretical and practical framework for enhancing emotion regulation, safeguarding psychological health, and maintaining combat effectiveness in high-stress military environments.},
}

@article {pmid41618133,
year = {2026},
author = {Wang, S and Fan, X and Zheng, Z and Gu, Q and Xu, S and Zhu, Y and Zhang, F and Diao, M and Hu, W},
title = {Multi-omics characterized the effects of Akkermansia muciniphila and fecal microbiota transplant on the microglial activation after traumatic brain injury.},
journal = {BMC microbiology},
volume = {26},
number = {1},
pages = {117},
pmid = {41618133},
issn = {1471-2180},
support = {2024ZL718//Science and Technology Program of Traditional Chinese Medicine in Zhejiang Province/ ; 2025KY1055//The medical and healthresearch project of Zhejiang province/ ; 2025KY1091//The medical and healthresearch project of Zhejiang province/ ; A20250077//Hangzhou Health Science and Technology Program/ ; 20220919Y006//Hangzhou Science and Technology guide project/ ; 2025HZZD04//The Construction Fund of Key Medical Disciplines of Hangzhou/ ; },
abstract = {BACKGROUND: The microbiota-gut-brain axis plays a pivotal role in numerous neurological disorders, including traumatic brain injury (TBI). TBI induces neuroinflammation accompanied by alterations in the gut microbiota. However, the contribution of gut microbiota dysbiosis to post-TBI neuroinflammation and its underlying mechanisms remain poorly understood.

RESULTS: Here, we found that TBI mice treated with Akkermansia(Akk) exhibited increased Akkermansia abundance at 28 days post-TBI, whereas those receiving fecal microbiota transplantation (FMT) showed elevated levels of Bifidobacteriaceae and Bifidobacterium. Both Akk and FMT alleviated persistent microglial activation in the hippocampus of TBI mice at 28 days. FMT prevented the reduction of 5-hydroxyindole in TBI mice, and prolonged FMT suppressed the sphingolipid signaling pathway in these animals. Furthermore, two macrophage activation-associated genes, ACx3cr1 and Cd68, were upregulated after TBI, but their expression was inhibited by FMT at 28 days. Sphingolipid metabolism was elevated in TBI mice at 7 and 28 days post-injury, and Akk treatment (p = 0.027) effectively blocked this increase at 28 days.

CONCLUSION: This study suggests that prolonged Akkermansia supplementation may mitigate post-TBI microglial activation by modulating the sphingolipid metabolic pathway. Both FMT and Akk represent potential therapeutic targets for developing novel strategies to address persistent microglial activation and chronic neuroinflammation following TBI, though their precise mechanisms require further validation.},
}

@article {pmid41618858,
year = {2026},
author = {Yang, T and Gao, Z and Huang, H and Zhang, C and Tang, Y and Qu, Q and Li, H and Ke, J and Chen, Z and Feng, M and Zhou, H and Shu, Y and Yuan, W},
title = {Gut-Metabolome-Proteome Interactions in Age-Related Hearing Loss: Insights from Fecal Microbiota Transplantation and Multi-Omics Analyses.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {13},
number = {18},
pages = {e14269},
pmid = {41618858},
issn = {2198-3844},
support = {81873702//National Natural Science Foundation of China/ ; 81470694//National Natural Science Foundation of China/ ; 82225014//National Natural Science Foundation of China/ ; 82171114//National Natural Science Foundation of China/ ; 2024NF008//National Clinical Research Center for Otolaryngologic Diseases/ ; CSTB2023TIAD-KPX0059//Chongqing Technology Innovation and Application Development Special Project/ ; 2022DBXM006//Major Programs of Chongqing Science and Health Union/ ; cstc2022ycjh-bgzxm0126//Chongqing Talent Project/ ; CSTB2022NSCQ-MSX0553//Chongqing Natural Science Foundation/ ; },
mesh = {Animals ; Mice ; Multiomics ; *Gastrointestinal Microbiome/physiology ; *Fecal Microbiota Transplantation/methods ; *Metabolome/physiology/genetics ; *Proteome/metabolism ; *Aging ; Disease Models, Animal ; Proteomics/methods ; Male ; *Hearing Loss/metabolism ; Metabolomics ; *Presbycusis/metabolism ; },
abstract = {Age-related hearing loss (ARHL) is a prevalent sensory disorder lacking disease-modifying interventions. The biological drivers, particularly the contribution of the gut microbiota and gut-inner ear crosstalk, remain poorly defined. Here, we utilize germ-free (GF) mice and fecal microbiota transplantation (FMT) to isolate microbiota-dependent effects on ARHL progression. Through integrated metagenomic, metabolomic, and proteomic profiling, we map molecular signatures of auditory aging and uncover functional gut-inner ear network, prioritizing 5-hydroxytryptophan (5-HTP) as a key intermediate metabolite within this network. Furthermore, in an aging-like House Ear Institute-Organ of Corti 1 (HEI-OC1) model, 5-HTP exhibits protective effects, potentially mediated through the PI3K/Akt-antioxidant signaling axis. Collectively, this study provides a valuable multi-omics resource and highlights microbiota-derived metabolic regulation as a promising avenue for biomarker discovery and therapeutic development in ARHL.},
}

Animals
Mice
Multiomics
*Gastrointestinal Microbiome/physiology
*Fecal Microbiota Transplantation/methods
*Metabolome/physiology/genetics
*Proteome/metabolism
*Aging
Disease Models, Animal
Proteomics/methods
Male
*Hearing Loss/metabolism
Metabolomics
*Presbycusis/metabolism

@article {pmid41620444,
year = {2026},
author = {Zhou, X and Liu, X and Peng, B and Yang, Y and Lu, H and Li, D and Deng, Y and Jiang, Z and Wu, C and Fang, W and You, Y and Kwan, HY and Zhao, X and Liu, Y},
title = {Simiao Decoction alleviates hyperuricemia-induced renal injury through regulating gut dysbiosis and decreasing gut-derived uremic toxins.},
journal = {NPJ biofilms and microbiomes},
volume = {12},
number = {1},
pages = {},
pmid = {41620444},
issn = {2055-5008},
support = {2023A1515110757//National Natural Science Foundation of China-Guangdong Joint Fund/ ; 20231800913372//Science and Technology Program of Dongguan, China/ ; U22A20365//Joint Funds of National Natural Science Foundation of China/ ; T2341019//National Natural Science Foundation of China/ ; 81830117//the Key Project of National Natural Science Foundation of China/ ; 2024B03J1343//Guangzhou Science and Technology Plan Project/ ; 20252D003//The Major scientific and technological project of Guangzhou Municipal Health Commission/ ; },
mesh = {Animals ; *Hyperuricemia/complications/drug therapy ; Rats ; *Dysbiosis/drug therapy ; *Drugs, Chinese Herbal/pharmacology ; *Gastrointestinal Microbiome/drug effects ; *Uremic Toxins/metabolism ; Disease Models, Animal ; Male ; Fecal Microbiota Transplantation ; Kidney/drug effects/injuries ; Indican/metabolism ; Tryptophan/metabolism ; Rats, Sprague-Dawley ; Epithelial-Mesenchymal Transition/drug effects ; Cresols/metabolism ; Tyrosine/metabolism ; Bacteria/classification/drug effects/metabolism ; },
abstract = {Renal injury is a common complication of hyperuricemia (HUA), which has been recognized as an independent risk factor for chronic kidney disease (CKD). The gut-kidney axis theory suggests that targeting the gut microbiota may be a potential treatment option for kidney disease. In this study, we utilized a spontaneous HUA rat model to demonstrate that Simiao decoction (SMD), a traditional Chinese medicine formula, can effectively alleviate HUA-induced renal injury by modulating gut microbiota and bacterial metabolism of tryptophan and tyrosine, thereby reducing gut-derived uremic toxins such as indoxyl sulfate (IS) and p-Cresol (PC). Fecal microbiota transplantation (FMT) further confirmed that the therapeutic effect of SMD was mediated by gut microbiota. Finally, in vitro studies revealed that IS promotes epithelial-mesenchymal transition (EMT) while PC induces cellular senescence in tubular cells. Collectively, our findings suggest that SMD can effectively alleviate HUA-induced renal injury through regulating gut dysbiosis and decreasing gut-derived uremic toxins. This study sheds light on a novel mechanism by which SMD exerts its effects on HUA-induced renal injury.},
}

Animals
*Hyperuricemia/complications/drug therapy
Rats
*Dysbiosis/drug therapy
*Drugs, Chinese Herbal/pharmacology
*Gastrointestinal Microbiome/drug effects
*Uremic Toxins/metabolism
Disease Models, Animal
Male
Fecal Microbiota Transplantation
Kidney/drug effects/injuries
Indican/metabolism
Tryptophan/metabolism
Rats, Sprague-Dawley
Epithelial-Mesenchymal Transition/drug effects
Cresols/metabolism
Tyrosine/metabolism
Bacteria/classification/drug effects/metabolism

@article {pmid41620567,
year = {2026},
author = {Yang, S and Song, J and Wang, Z and Peng, G and Tong, L and Li, X and Yang, K and Chen, Y and Zhang, H and Zhang, Q and Chen, R},
title = {eIF6 deficiency alleviates colorectal cancer by modulating the gut microbiota and related metabolites.},
journal = {Cell death and differentiation},
volume = {},
number = {},
pages = {},
pmid = {41620567},
issn = {1476-5403},
abstract = {eIF6 is overexpressed in multiple cancers. Previous work has showed that deficiency alters the gut microbiota. This study investigated the mechanism linking eIF6 deficiency, microbial dysbiosis, and colorectal cancer (CRC). eIF6 expression was assessed in human and mouse CRC samples. Functional assays were conducted in mice with AOM/DSS-induced CRC. Antibiotic treatment and faecal microbiota transplantation (FMT) were applied to evaluate microbiota-mediated effects. 16S rDNA sequencing and Dubosiella newyorkensis (D. newyorkensis) supplementation were used to identify key bacteria. Metabolites from the bacterial supernatant were analysed via targeted mass spectrometry. The effect of indole-3-carboxaldehyde (3-ICA) was tested in murine models. eIF6 expression was upregulated in CRC. Its deficiency reduced the tumour incidence and proliferation of tumours in mice and increased the abundance of beneficial bacteria such as Akkermansia and Dubosiella. FMT from eIF6 deficient mice and D. newyorkensis administration attenuated tumorigenesis and enhanced barrier function. 3-ICA, a metabolite of D. newyorkensis, also suppressed CRC progression. eIF6 deficiency exerts protective effects against CRC through the enrichment of D. newyorkensis and its metabolite 3-ICA, revealing a novel mechanism and potential therapeutic strategy for CRC.},
}

@article {pmid41621641,
year = {2026},
author = {Chen, L and Yang, Y and Zhang, Y and Yang, X and Zhang, X and Chen, L and Li, W and Zhang, S and Xiong, R and Wang, J and Xu, Z and Zhang, ZY and Pan, C and Ji, M},
title = {Tuft Cells in the Gut Limit Cognitive Disorders by Regulating Gut Homeostasis.},
journal = {Cellular and molecular gastroenterology and hepatology},
volume = {20},
number = {6},
pages = {101747},
pmid = {41621641},
issn = {2352-345X},
mesh = {Animals ; *Tuft Cells/metabolism/immunology ; Homeostasis ; Mice ; Male ; Disease Models, Animal ; Gastrointestinal Microbiome ; Intestinal Barrier Function ; *Alzheimer Disease/immunology/pathology ; Mice, Knockout ; Intestinal Mucosa/pathology ; *Cognitive Dysfunction ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; },
abstract = {BACKGROUND & AIMS: Tuft cells, a type of epithelial cell in the gut, play a pivotal role in regulating type 2 immunity and maintaining the gut barrier. However, their role in cognitive impairments remains unclear.

METHODS: We compared behavioral performance between male tuft cell-absent mice (Pou2f3[-/-]) and their wild-type (WT) littermates. We analyzed gut microbiota using fecal 16S rRNA, measured gut permeability via FITC-dextran assay, and detected CD4[+]-T cells and type 2 innate lymphoid cells by flow cytometry in both genotypes. Co-housing and fecal microbiota transplantation experiments were conducted to explore the role of gut microbiota in cognitive diseases. Single-cell RNA sequencing and fluorescence imaging were used to examine tuft cell changes in the colon of WT and Alzheimer's disease (AD) model mice. Colonic organoids were used to assess the effect of β-amyloid on tuft cell differentiation. Succinic acid, a promoter of tuft cells, was administered, and tuft cell-deficient AD mice were generated to evaluate its impact on behavior and gut homeostasis.

RESULTS: Increased gut permeability, immune imbalance, neuroinflammation, and cognitive dysfunction occurred in 10-month-old mice lacking tuft cells. These alterations were mediated by gut microbiota, evidenced by shifts in microbiota composition and abundance, and supported by co-housing and fecal microbiota transplantation experiments. AD model mice had fewer tuft cells and impaired type 2 immunity in the gut, potentially because of β-amyloid inhibiting tuft cell differentiation. Succinic acid, a tuft cell activator, restored cognitive function and gut homeostasis in AD mice.

CONCLUSIONS: Tuft cells may be necessary for maintaining gut homeostasis in cognitive disorders.},
}

Animals
*Tuft Cells/metabolism/immunology
Homeostasis
Mice
Male
Disease Models, Animal
Gastrointestinal Microbiome
Intestinal Barrier Function
*Alzheimer Disease/immunology/pathology
Mice, Knockout
Intestinal Mucosa/pathology
*Cognitive Dysfunction
Mice, Inbred C57BL
Fecal Microbiota Transplantation

@article {pmid41622931,
year = {2025},
author = {Hong, X and Deng, Y and Feng, J and Bao, C and Zhang, Y and Gao, N and Shen, H},
title = {[Fecal Microbiota Transplantation: A Promising Avenue for Lung Cancer Therapy].},
journal = {Zhongguo fei ai za zhi = Chinese journal of lung cancer},
volume = {28},
number = {11},
pages = {841-848},
pmid = {41622931},
issn = {1999-6187},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Lung Neoplasms/therapy/immunology/microbiology ; Animals ; Gastrointestinal Microbiome ; },
abstract = {As lung cancer treatment continues to advance, mainstream approaches such as surgery, radiotherapy, chemotherapy, neoadjuvant therapy, targeted therapy and immunotherapy have become widely adopted in clinical practice. However, the efficacy of these methods is still limited and they are associated with significant side effects. In recent years, the pivotal role of the gut microbiota in tumor immune regulation has become increasingly recognized, with its potential impact on tumor immunotherapy emerging as a novel therapeutic focus in lung cancer management. Against this backdrop, fecal microbiota transplantation (FMT) has been proposed as a potential immunomodulatory strategy. It enhances host immune responses and improves the tumor immune microenvironment by regulating the gut microbiota. This paper provides a systematic review of the latest research advances in FMT for lung cancer treatment. Focusing on the relationship between gut microbiota and lung cancer, the therapeutic mechanisms of FMT and clinical application studies, it provides a comprehensive exploration of the challenges and prospects for the use of FMT in lung cancer therapy. .},
}

Humans
*Fecal Microbiota Transplantation/methods
*Lung Neoplasms/therapy/immunology/microbiology
Animals
Gastrointestinal Microbiome

@article {pmid41622997,
year = {2026},
author = {Li, Y and Wang, J and Wang, H and Ma, X and Ren, D and Wang, B},
title = {A novel exopolysaccharide from Lactiplantibacillus plantarum H6 improves cholesterol metabolism via Muribaculum-mediated activation of the enterohepatic FXR-FGF15 axis.},
journal = {Gut microbes},
volume = {18},
number = {1},
pages = {2623578},
pmid = {41622997},
issn = {1949-0984},
mesh = {Animals ; *Cholesterol/metabolism ; *Fibroblast Growth Factors/metabolism/genetics ; Mice ; *Polysaccharides, Bacterial/pharmacology/administration & dosage/chemistry/isolation & purification ; *Lactiplantibacillus plantarum/chemistry/metabolism ; Liver/metabolism/drug effects ; *Receptors, Cytoplasmic and Nuclear/metabolism/genetics ; Receptor, Farnesoid X-Activated ; Male ; Mice, Inbred C57BL ; Gastrointestinal Microbiome/drug effects ; *Hypercholesterolemia/metabolism/drug therapy ; Humans ; Cholesterol 7-alpha-Hydroxylase/metabolism/genetics ; },
abstract = {Hypercholesterolemia is a major risk factor for atherosclerotic cardiovascular disease; however, current therapeutic options such as statins are limited by issues including hepatotoxicity and patient intolerance. Probiotics and their metabolites show promise in modulating cholesterol metabolism through the gut‒liver axis, yet the specific commensal bacteria and molecular mechanisms underlying these effects remain poorly understood. In this study, we isolated and characterized EPS-D1, a novel exopolysaccharide (15.003 kDa) derived from Lactiplantibacillus plantarum H6, which is composed primarily of mannose (46.10%) and glucose (33.98%) and features a highly branched structure (branching degree of 29.5%). The administration of EPS-D1 significantly reduced the serum total cholesterol (TC), triglyceride (TG), and low-density lipoprotein cholesterol (LDL-C) by 40.31%, 37.55%, and 43.15%, respectively, in high-cholesterol diet (HCD) mice. Additionally, it improved hepatic steatosis and reduced markers of liver injury. Through 16S rRNA sequencing and fecal microbiota transplantation (FMT), we identified Muribaculum as the key commensal bacterium enriched by EPS-D1. Direct administration of Muribaculum (Muribaculum intestinale) replicated the cholesterol-lowering effects, decreasing ileal and fecal cholesterol levels by 74.79% and 53.16%, respectively. Mechanistically, both EPS-D1 and M. intestinale activated the enterohepatic FXR‒FGF15 axis, which resulted in the upregulation of hepatic cholesterol 7α-hydroxylase (CYP7A1) expression and the downregulation of ileal ASBT and NPC1L1, thereby promoting bile acid synthesis and inhibiting cholesterol absorption. Furthermore, M. intestinale increased intestinal short-chain fatty acids (SCFAs), particularly acetic acid and caproic acid, by 37.88% while also modulating the composition of the bile acid pool. These findings establish M. intestinale as a precise microbial target for cholesterol management and demonstrate that EPS-D1 from L. plantarum H6 enhances cholesterol metabolism through microbiota-mediated activation of the enterohepatic FXR‒FGF15 axis, providing a novel therapeutic strategy for managing hypercholesterolemia.},
}

Animals
*Cholesterol/metabolism
*Fibroblast Growth Factors/metabolism/genetics
Mice
*Polysaccharides, Bacterial/pharmacology/administration & dosage/chemistry/isolation & purification
*Lactiplantibacillus plantarum/chemistry/metabolism
Liver/metabolism/drug effects
*Receptors, Cytoplasmic and Nuclear/metabolism/genetics
Receptor, Farnesoid X-Activated
Male
Mice, Inbred C57BL
Gastrointestinal Microbiome/drug effects
*Hypercholesterolemia/metabolism/drug therapy
Humans
Cholesterol 7-alpha-Hydroxylase/metabolism/genetics

@article {pmid41623601,
year = {2026},
author = {Koda, K and Mimura, T and Yamana, T and Ishizuka, M and Takahashi, T and Takano, S and Abe, T and Nishizawa, Y and Katsuno, H and Sato, M and Nishimura, K and Yoshida, M and Maeda, K},
title = {The Japan Society of Coloproctology Practice Guidelines for Fecal Incontinence 2024 (Revised Second Edition).},
journal = {Journal of the anus, rectum and colon},
volume = {10},
number = {1},
pages = {64-134},
pmid = {41623601},
issn = {2432-3853},
abstract = {In 2024, the second edition of the Japan Society of Coloproctology (JSCP) Practice Guidelines for Fecal Incontinence was published in Japan, followed by the release of this English version. This marks the first major revision in 7 years since the publication of the first edition. The second edition was completed over a span of 3 years, and its overview and key features are summarized below. This guideline begins with a clinical flowchart outlining the general diagnostic and therapeutic approach. A notable update is the inclusion of insertable anal and vaginal continence devices, which are now considered a form of conservative therapy under clinical research frameworks. In Chapter I-B (Epidemiology), the prevalence of anal incontinence was newly reported: among a Japanese population with an average age of 35 years, 15.5% of men and 42.7% of women were affected. In Chapter II (Diagnosis), the utility of a bowel diary for patient assessment is discussed for the first time. The guideline also provides a detailed description of the evaluation method for digital rectal examination. Additionally, a new section was added addressing incontinence-associated dermatitis (IAD), including its risks and methods of assessment. In Chapter III (Diagnostic Testing), the guideline expands upon previously established diagnostic tests by newly including detailed descriptions of ultrasound techniques-specifically, endoanal ultrasound, transperineal ultrasound, and transvaginal ultrasound. Chapter IV (Treatment) outlines conservative treatment strategies, including dietary guidance, bowel habit instruction, and care for fecal incontinence. Pharmacologic therapies are presented with itemized explanations by drug type. Pelvic floor muscle training, biofeedback therapy, and transanal irrigation are classified under "specialized conservative therapies" and discussed in detail. For surgical treatment, a new Clinical Question (CQ) addresses postpartum fecal incontinence. It recommends early referral to a specialized center when a sphincter injury is present to be repaired, whereas observation for one year may be appropriate when no injury is identified. Another new CQ discusses the mode of delivery in subsequent pregnancies following obstetric anal sphincter injuries (OASIS), emphasizing the need to evaluate fecal incontinence severity, anal sphincter function, and its integrity before making clinical decisions. Stoma creation is described in detail as one of the surgical treatment options, including its implications for improved postoperative quality of life. For the first time, regenerative therapy for the anal sphincter is introduced as a novel surgical option, reporting promising long-term outcomes from trials involving the transplantation of autologous cultured myoblasts into the external anal sphincter. Finally, Chapter V addresses special clinical scenarios in detail, including fecal incontinence associated with neurological and spinal disorders, dementia, frailty, and bedridden elderly patients.},
}

@article {pmid41623954,
year = {2025},
author = {Abtahi Froushani, SM and Hasani, SJ and Ghaderi, M and Mahmoudzadeh, L},
title = {A review of inflammatory bowel diseases in humans and pets: treatment strategies.},
journal = {Veterinary research forum : an international quarterly journal},
volume = {16},
number = {11},
pages = {601-610},
pmid = {41623954},
issn = {2008-8140},
abstract = {Inflammatory bowel disease (IBD) encompasses a group of chronic inflammatory conditions that primarily impact the gastrointestinal system. While ulcerative colitis and Crohn's disease are the principal manifestations in humans, animals frequently exhibit lymphocytic-plasmacytic enteritis/colitis and eosinophilic enteritis/colitis. Growing evidence suggests a complex interplay among genetic predisposition, gut microbiota imbalance and abnormal immune responses to intestinal microbes in susceptible individuals. This intricate involvement results in remarkably similar clinical presentations across species. Patients often experience symptoms such as diarrhea, vomiting, weight loss and anemia. Extraintestinal manifestations including uveitis, skin rash and arthritis may also occur. Endoscopy and biopsy typically serve as the gold standard for confirming the diagnosis and differentiating it from other gastrointestinal disorders in humans and animals. The treatment approach generally focuses on managing disease activity through immunosuppressive medications such as glucocorticoids, administered at appropriate dosages. However, the precise cause of IBD remains a topic of ongoing research. With the emergence of additional treatment options like herbal compounds and fecal microbiota transplantation, which have demonstrated effectiveness in restoring gut health in IBD patients, there is optimism for novel therapeutic strategies. Ultimately, conclusion is that chronic gastrointestinal conditions like IBD are complex in both human and veterinary medicine. These diseases share numerous common pathophysiological features, yet, diagnostic and treatment challenges continue to exist.},
}