@article {pmid40898211,
year = {2025},
author = {Ma, X and Shi, W and Wang, Z and Li, S and Ma, R and Zhu, W and Wu, L and Feng, X and Cong, B and Li, Y},
title = {Butyric acid and valeric acid attenuate stress-induced ferroptosis and depressive-like behaviors by suppressing hippocampal neuroinflammation.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {974},
pmid = {40898211},
issn = {1479-5876},
support = {82130055//Key Projects of the National Natural Science Foundation of China/ ; 82293651//Major Projects of the National Natural Science Foundation of China/ ; 82072109//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Depression is closely associated with stress-induced hippocampal damage and dysfunction. Emerging evidence demonstrates that the gut microbiota and its metabolites, acting as probiotics or prebiotics, can modulate brain structure and function via the gut-brain axis, thereby offering therapeutic potential for ameliorating related neurological and psychiatric disorders. This study delves into the contribution of the gut microbiota and its metabolites to stress-induced ferroptosis of hippocampal neurons and the associated molecular pathways.

METHODS: This study used time-course stress paradigms combined with ferroptosis inhibitors to identify hippocampal neuronal ferroptosis. Fecal microbiota transplantation were conducted to analyze the role of gut microbiota in this process. Subsequently, 16 S rDNA sequencing and metabolomics techniques were applied to identify key gut microbiota and metabolites. Metabolites intervention were performed to examine their causal relationship with neuronal ferroptosis. Finally, we used histochemical and molecular assays to assess both intestinal and blood-brain barrier integrity as well as inflammation in peripheral blood and hippocampal tissue, along with GPR41/RhoA/Rock1 pathway changes, to preliminarily investigate the molecular mechanisms underlying stress-induced hippocampal neuronal ferroptosis.

RESULTS: We demonstrated that stress triggered hippocampal neuronal ferroptosis and subsequent depressive-like behaviors in mice. Fecal microbiota transplantation successfully replicated the ferroptosis phenotype. Butyric acid and valeric acid were identified as key metabolites significantly reduced in the serum of acutely and chronically stressed mice, respectively. Intervention with these metabolites markedly alleviated ferroptosis. Furthermore, valerate intervention increased hippocampal GPR41 expression and significantly suppressed the pro-inflammatory RhoA/Rock1 pathway in chronically stressed mice, thereby reducing neuroinflammation and ameliorating neuronal ferroptosis. However, butyrate intervention showed no significant effect on the GPR41/RhoA/Rock1 pathway.

CONCLUSION: Stress induces ferroptosis in hippocampal neurons, where reduced abundance of short-chain fatty acid-producing bacteria plays a key role. Key metabolites butyric acid and valeric acid alleviate neuroinflammation to improve ferroptosis via the gut-brain axis in acute and chronic stress, respectively. Specifically, valeric acid exerts neuroprotective effect through the GPR41/RhoA/Rock1 pathway, whereas butyric acid-mediated protection likely operates through alternative mechanisms.},
}

@article {pmid40895486,
year = {2025},
author = {Ge, S and Zhang, S and She, L and Gu, T and Wang, S and Huang, X and Wang, L and Miao, M},
title = {Synergistic therapy of Chinese herbal medicine and gut microbiota modulation for post-stroke cognitive recovery: focus on microbial metabolite and immunoinflammation.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1623843},
doi = {10.3389/fmicb.2025.1623843},
pmid = {40895486},
issn = {1664-302X},
abstract = {Post-stroke cognitive impairment (PSCI), a common complication following stroke, significantly impacts patients' quality of life and rehabilitation. Recent studies have highlighted the role of gut microbiota and their metabolites in modulating immunoinflammation and cognitive function via the gut-brain axis. Traditional Chinese medicine (TCM) and microbiota interventions including probiotics and fecal microbiota transplantation, have shown potential in reshaping gut microbial communities and metabolite profiles. Some studies suggest that combining these approaches via identical or related therapeutic mechanisms may yield enhanced efficacy in treating Post-Stroke Cognitive Impairment (PSCI). These findings establish a theoretical foundation for future research and clinical practice. This review systematically examines the mechanistic role of gut microbial metabolites in neuroimmune modulation and comprehensively evaluates the therapeutic potential of combined TCM and microbiota-targeted therapies for PSCI, adopting a multifactorial approach that addresses neuroinflammation, microbial dysbiosis, and metabolic dysregulation.},
}

@article {pmid40895468,
year = {2025},
author = {Yang, J and Chen, J and Li, D and Wu, Q and Zhang, Y and Li, Y and Deng, Y},
title = {Hyperuricemia and the gut microbiota: current research hotspots and future trends.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1620561},
doi = {10.3389/fmicb.2025.1620561},
pmid = {40895468},
issn = {1664-302X},
abstract = {BACKGROUND: Hyperuricemia (HUA), found widely in humans and birds, is a key physiological factor responsible for the development of gout. In recent years, the relationship between the gut microbiota and HUA has garnered significant attention from researchers. This study aims to explore the current research hotspots, knowledge gaps, and future research trends regarding the gut microbiota and HUA.

METHODS: We performed a thorough search of the literature on gut flora and HUA published between 2005 and 2024 using the Web of Science and PubMed databases. The resulting data were analyzed using VOSviewer, CiteSpace, and Bibliometrix.

RESULTS: Including 735 papers in total, the study found that the number of publications in the subject increased significantly between 2020 and 2024, with 2024 being the year with the highest number of publications. The primary research countries are highlighted as China and the United States, with institutions such as the University of California, San Diego, and Qingdao University making significant contributions. Sanjay K. Nigam and Chenyang Lu have made the most important contributions as authors. Keywords analysis highlighted high-frequency terms including "gastrointestinal microbiome," "uric acid," "hyperuricemia," "inflammation," "gout," and "probiotics." In the visualization map of the keyword timeline, emerging research hotspots include "diets," "dietary fiber," "fecal microbiota transplantation," and "gut-kidney axis."

CONCLUSION: This study is the first to conduct a quantitative literature analysis in the field of gut microbiota in HUA, revealing that the core research hotspots include disease-related microbiota characteristics, probiotic therapy, microecological intervention, and the gut-distal target organ axis. The emerging hotspots focus on dietary supplementation, fecal microbiota transplantation (FMT) treatment strategies, and in-depth research on the above organ axes. Provide valuable guidance for future research directions.},
}

@article {pmid40895097,
year = {2025},
author = {Jin, Y and Wang, H and Song, J},
title = {Gut-brain axis modulation in remote rehabilitation of Parkinson's disease: reconstructing the fecal metabolome and nigral network connectivity.},
journal = {Frontiers in neurology},
volume = {16},
number = {},
pages = {1644490},
doi = {10.3389/fneur.2025.1644490},
pmid = {40895097},
issn = {1664-2295},
abstract = {The pathogenesis of Parkinson's disease (PD) is gradually evolving from a central neurodegeneration-centered concept to a multi-pathway pathological model at the gut-brain system level. Studies have shown that PD patients commonly exhibit dysbiosis, reduced short-chain fatty acids (SCFAs; microbial fermentation products of dietary fiber that play key roles in host metabolism and immune regulation), abnormal tryptophan metabolism, and impaired gut barrier function. These alterations may contribute to dopaminergic neuronal damage through mechanisms including neuroinflammation, oxidative stress, and α-synuclein (α-syn) aggregation. The vagus nerve plays a critical role in bidirectional gut-brain signaling, and its dysfunction may represent a key route for pathological protein transmission from the periphery to the brain. In response, remote rehabilitation and gut-targeted interventions-including probiotics, prebiotics, dietary modulation, fecal microbiota transplantation (FMT), and transcutaneous vagus nerve stimulation (tVNS)-have shown potential in improving neurological function and inflammation in both animal and clinical studies. Multimodal data analyses have revealed significant associations between SCFA levels in fecal metabolomics and brain imaging features. Despite ongoing challenges in mechanistic extrapolation, biomarker sensitivity, and translational implementation, the integration of metagenomics, metabolomics, neuroimaging, and digital therapeutics-collectively referred to as multi-omics and digital profiling techniques-represents an emerging research direction with the potential to inform future clinical paradigms for precision remote management of PD.},
}

@article {pmid40894980,
year = {2025},
author = {Wang, YM},
title = {How to Approach Immune Checkpoint Inhibitor Enterocolitis.},
journal = {Gastroenterology & hepatology},
volume = {21},
number = {8},
pages = {501-503},
pmid = {40894980},
issn = {1554-7914},
}

@article {pmid40894608,
year = {2025},
author = {Lopez, ML and Kang, T and Espeleta, A and Rubtsova, VI and Baek, J and Songcuan, J and Moyer, EM and Kim, J and Song, WS and Jung, S and D'Sa, N and Anica, A and Tran, E and Chun, Y and Choi, W and Jang, KH and Kelly, ME and Tamburini, IJ and Alam, YH and Le, J and Ramirez, CB and Kataru, RP and Hong, SP and Nicholas, DA and Xue, KS and Lee, G and Bae, H and Jang, C},
title = {Intestinal catabolism of dietary fructose promotes obesity and insulin resistance via ileal lacteal remodeling.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.08.18.670963},
pmid = {40894608},
issn = {2692-8205},
abstract = {UNLABELLED: High-fructose corn syrup (HFCS) consumption is a risk factor for obesity and metabolic syndrome, yet the underlying mechanisms are incompletely understood. Catabolism of dietary fructose primarily occurs in the small intestine and liver, with fructose breakdown in the liver being pathological, while small intestinal fructose clearance protects the liver. Here, we unexpectedly found that inhibition of fructose catabolism specifically in the small intestine mitigates fructose-induced obesity and insulin resistance. Mechanistically, blocking intestinal fructose catabolism reduces dietary fat absorption, which is associated with a decrease in the surface area of the ileal lacteals and alterations in gut microbiome. Fecal transplantation experiments revealed that such a microbiome stimulates the intestine-resident macrophages, promoting lacteal growth and boosting dietary fat absorption. Given the preclinical and clinical studies reporting the effect of fructose catabolism suppression on mitigating diet-induced obesity, our data suggest that such effects are partly mediated by intestinal lacteal remodeling.

SIGNIFICANCE STATEMENT: Here, we uncover a previously unappreciated link between intestinal fructose catabolism and ileal lacteal remodeling, suggesting the mechanisms by which fructose intake promotes obesity. Using mice lacking the fructose-processing enzyme specifically in the intestine, we show that blocking intestinal fructose metabolism protects against diet-induced obesity by reducing fat absorption. Changes in gut microbiome and immune cell interactions drive this effect.},
}

@article {pmid40894444,
year = {2025},
author = {Xu, P},
title = {Gut Microbiota Metabolites Targeting the Immune Response in Sepsis: Mechanisms and Therapies.},
journal = {International journal of general medicine},
volume = {18},
number = {},
pages = {4709-4734},
doi = {10.2147/IJGM.S539237},
pmid = {40894444},
issn = {1178-7074},
abstract = {Sepsis is a global health challenge, affecting millions annually and remaining a leading cause of mortality in intensive care units. Gut microbiota plays a complex role in the onset and progression of sepsis, with its alterations reflecting disease severity. Recently, modulating gut microbiota and its metabolites has emerged as a promising therapeutic strategy for sepsis. This review highlights the role of gut microbiota in sepsis and systematically identifies key immune response targets directly influenced by gut microbiota metabolites, such as short-chain fatty acids (SCFAs), bile acids, and indoleacetic acid, among other important metabolites. Additionally, it offers a full overview of current research on gut microbiota-regulated therapeutic approaches, including fecal microbiota transplantation (FMT) and artificial intelligence (AI) applications. These insights offer a novel perspective for advancing the understanding of sepsis pathogenesis and its treatment.},
}

@article {pmid40893829,
year = {2025},
author = {Allegretti, JR},
title = {Current Status of Fecal Microbiota Transplantation for Inflammatory Bowel Disease Management.},
journal = {Gastroenterology & hepatology},
volume = {21},
number = {7},
pages = {451-453},
pmid = {40893829},
issn = {1554-7914},
}

@article {pmid40891897,
year = {2025},
author = {Bertin, L and Bonazzi, E and Facchin, S and Lorenzon, G and Maniero, D and DE Barba, C and Tomasulo, A and Fortuna, A and Zingone, F and Barberio, B and Savarino, EV},
title = {The microbiota-brain connection in neurological diseases: the ubiquitous short-chain fatty acids.},
journal = {Minerva gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.23736/S2724-5985.25.03866-5},
pmid = {40891897},
issn = {2724-5365},
abstract = {The connection between the gut and brain forms a sophisticated two-way communication system where compounds produced by intestinal bacteria, especially short-chain fatty acids, play essential roles in brain-related disease processes. Evidence across multiple neurological disorders reveals convergent pathophysiological pathways involving SCFAs, which modulate neurological function via histone deacetylase inhibition, G-protein coupled receptor activation, and blood-brain barrier regulation. Clinical investigations demonstrate disorder-specific signatures: reduced butyrate-producing bacteria correlate with Parkinson's disease progression; Alzheimer's disease exhibits significant reductions in key SCFAs; and diminished butyrate production disrupts immunoregulatory homeostasis in multiple sclerosis. Additionally, neurodevelopmental disorders like autism show distinctive microbiome alterations affecting both gut and brain function. Beyond SCFAs, microbiota influence neural communication through immune modulation, neurotransmitter production, and vagus nerve signaling. Interventional studies targeting the microbiome through precision probiotics, prebiotics, and fecal microbiota transplantation demonstrate preliminary efficacy, particularly in Parkinson's disease and autism. Methodological heterogeneity and challenges establishing causality remain significant limitations. Future priorities include longitudinal characterization of microbiome dynamics preceding symptom onset, development of personalized therapeutics, and implementation of predictive computational models. Progress in these domains could transform microbiome-based approaches from experimental interventions to precision medicine applications in neurological disease management.},
}

@article {pmid40890737,
year = {2025},
author = {Lu, G and Zhang, S and Wang, R and Wu, X and Chen, Y and Wen, Q and Cui, B and Zhang, F and Li, P},
title = {Fecal microbiota transplantation improves bile acid malabsorption in patients with inflammatory bowel disease: results of microbiota and metabolites from two cohort studies.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {511},
pmid = {40890737},
issn = {1741-7015},
support = {81873548//National Natural Science Foundation of China/ ; 82100583//National Natural Science Foundation of China/ ; 2020-3//Nanjing Medical University Fan Daiming Research Funds for Holistic Integrative Medicine/ ; },
abstract = {BACKGROUND: Bile acid malabsorption (BAM) or bile acid diarrhea (BAD) complicates more than 30% of Crohn's disease (CD), yet no non-invasive biomarker reliably identifies patients who will benefit from fecal microbiota transplantation (FMT). We investigated whether serum 7α-hydroxy-4-cholesten-3-one (C4), a hepatic bile-acid synthesis precursor, can predict BAM and FMT response in inflammatory bowel disease (IBD).

METHODS: We included 106 pairs of IBD patients treated with FMT from two longitudinal cohorts of prospective trials and 24 matched healthy individuals to identify a multi-omics analysis of microbiota-metabolism and evaluate real-world effectiveness of FMT. Fecal and serum samples before and after FMT along with medical information were collected and detected through 16S rRNA amplicon sequencing and untargeted liquid chromatography mass spectrometry. Mice models were used to preliminarily verify the exacerbation of colitis through administration of primary BAs and treated by FMT.

RESULTS: Patients in BAM group tended to achieve sustained higher and stable clinical response (66.67% vs. 49.41%) and remission (52.38% vs. 40.00%) than non-BAM group at 3 months after FMT, along with a significantly decrease of C4 (P < 0.001), improvement of obvious abdominal pain and diarrhea, which was especially obvious in CD patients with ileal resection and ileal /ileocolonic type. Random forest classifiers predicted BAM in IBD patients with 18 or top 4 differential OTUs, showing an area under the curve of 0.92 and 0.83, respectively. Furthermore, results from primary bile acid-induced colitis mice models reinforced these findings.

CONCLUSIONS: Serum C4 and a minimal gut microbiota may identify IBD patients with BAM who are most likely to achieve durable remission after FMT. These translatable biomarkers can guide precision use of microbiota-directed therapy.

TRIAL REGISTRATION: ClinicalTrials.gov: NCT01790061 and NCT01793831.},
}

@article {pmid40889045,
year = {2025},
author = {Wang, H and Wang, Y and Wu, H and Shen, C and Li, Y and Bai, B and Sun, X and Liu, Y and Zhang, Q and Shi, L},
title = {High-fat diet-induced obesity-related hypertension via altered gut microbiota-mediated histone butyrylation.},
journal = {Science China. Life sciences},
volume = {},
number = {},
pages = {},
pmid = {40889045},
issn = {1869-1889},
abstract = {Hypertension is a chronic cardiovascular disease that significantly impacts human quality of life. Gut microbiota and its metabolites have been reported to be involved in lipid metabolism and blood pressure regulation, but the specific alterations and pathogenic mechanisms of gut microbiota in obesity-related hypertension (OrHTN) remain unclear. In this study, we observed a significant proliferation of Desulfobacterota and Proteobacteria, while a decrease in the abundance of several butyrate-producing bacterial genera, accompanied by decreased fecal and plasma butyrate levels in high-fat diet (HFD)-induced OrHTN rats. Histone 3 lysine 9 butyrylation (H3K9bu) modification in the kidney of OrHTN rats was reduced and downregulated the expression of the hypertension-related gene MAS1. Subsequent transplantation of cecal contents from OrHTN rats on HFD into recipient rats on a normal chow diet resulted in hypertension but without obesity. Furthermore, in vitro experiments suggested that sodium butyrate increased H3K9bu modification and the expression of MAS1 in a concentration-dependent manner. In conclusion, our findings suggest that gut microbiota may contribute to the development of OrHTN by altering the expression of hypertension-related genes through butyrate-mediated histone butyrylation. This work may provide new insights into the prevention and treatment of hypertension by targeting the regulation of gut microbiota and metabolites.},
}

@article {pmid40886868,
year = {2025},
author = {Wang, Z and Ren, X and Peng, Z and Zeng, M and Wang, Z and Chen, Q and Chen, J and Dai, X and Christian, M and Qie, X and He, Z},
title = {Flavonoid-rich extracts of Nelumbo nucifera leaves alleviate obesity in HFD-fed mice via microbiota-dependent modulation of brown fat thermogenesis.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {120513},
doi = {10.1016/j.jep.2025.120513},
pmid = {40886868},
issn = {1872-7573},
abstract = {Nelumbo nucifera Gaertn (lotus) leaf is a commonly used traditional Chinese herbal medicine with a wide range of pharmacological properties, especially lipid-lowering and weight-loss effects. Accumulating evidence highlights activation of the thermogenic program of brown adipose tissue (BAT) as a promising anti-obesity strategy. However, it remains unclear whether such beneficial metabolic effects induced by the lotus leaf are related to its regulatory role in BAT function.

AIM OF THE STUDY: This work aims to investigate whether the lotus leaf reduces obesity by activating BAT and to elucidate whether the mechanism behind it is related to the regulation of gut microbiota.

MATERIAL AND METHODS: A mouse model of obesity was established using a high-fat diet (HFD), and the anti-obesity effect of flavonoid-rich lotus leaf extract (LLE) was determined in vivo. An animal energy metabolism monitoring system confirmed that LLE promoted energy expenditure. Then, RT-qPCR, immunohistochemistry, and Western blotting were conducted to detect the expression of genes and proteins involved in BAT thermogenesis. Subsequently, the underlying mechanisms were demonstrated by 16S rRNA gene sequencing and non-targeted metabolism analysis. Finally, fecal microbiota transplantation (FMT) was performed to investigate the LLE-dependent alleviation of obesity via the gut microbiota-BAT axis.

RESULTS: Our study demonstrated that LLE effectively reduced weight gain, ameliorated glucolipid disorders, and enhanced energy expenditure in HFD-fed mice. Notably, LLE augmented BAT activity by increasing thermogenic markers (e.g., SIRT1, PGC-1α, UCP1) and repressing inflammatory responses, potentially through activation of β3-AR/AMPK/p38 signaling pathways. Importantly, LLE could mitigate HFD-induced microbial dysbiosis (decrease in Proteobacteria, Verrucomicbiota, Acidobacteriota, Bacteroides, Dubosiella, and increase in Bilophila, Tyzzerella, Oscillibacter, Akkermansia, and Alistipes) and significantly altered 5 metabolite pathways, especially primary bile acid biosynthesis and linoleic acid metabolism. The FMT experiment confirmed that the microbial changes induced by LLE were associated with reduced body weight, enhanced energy expenditure, increased BAT activity, and thermogenesis.

CONCLUSIONS: Collectively, our findings reveal that lotus leaf promotes brown fat thermogenesis by modulating gut microbiota, identifying it as a promising new treatment target for obesity.},
}

@article {pmid40886596,
year = {2025},
author = {Li, W and Wang, N and Lyu, D and Yu, X and He, X and Yu, K and Qiu, Y and Jiao, X},
title = {Gut dysbiosis mediates neurotoxic effects of environmentally relevant tylosin exposure in adult zebrafish.},
journal = {Ecotoxicology and environmental safety},
volume = {303},
number = {},
pages = {118960},
doi = {10.1016/j.ecoenv.2025.118960},
pmid = {40886596},
issn = {1090-2414},
abstract = {Tylosin, a widely used veterinary macrolide antibiotic, raises environmental concerns due to its persistence and potential health risks. However, the neurotoxic effects of chronic low-dose tylosin exposure remain unclear. This study assessed the neurotoxicity of chronic exposure to environmentally relevant tylosin concentrations (5000 ng/L) in adult zebrafish. Behavioral tests indicated anxiety- and depression-like behaviors, including reduced exploration and increased freezing. Histopathology revealed neuronal degeneration, evidenced by decreased Nissl staining in key brain areas. Transcriptomic analysis identified significant changes in genes related to neuroinflammation, synaptic dysfunction, immune response, and steroid metabolism. Multi-omics approaches further showed substantial alterations in gut microbiota composition and metabolic profiles, particularly involving tryptophan metabolism and steroid hormone synthesis. These gut changes correlated with impaired intestinal barrier function, including fewer goblet cells and reduced tight junction and mucin-2 protein expression. Fecal microbiota transplantation confirmed the role of altered gut microbiota in inducing anxiety- and depression-like behaviors, highlighting microbiota-gut-brain axis involvement. Molecular docking identified microbial metabolites (MG 20:4, 2E-dodecenedioic acid, Ononin) interacting with critical neurodevelopmental and stress-response proteins (LRAT, BHLHE40, HSPA5), potentially linking microbiota shifts to brain dysfunction. Our results demonstrate that chronic environmental tylosin exposure induces neurotoxicity through gut dysbiosis and compromised intestinal barriers, disrupting essential neuroactive pathways. These findings emphasize the importance of considering microbiota-gut-brain axis disruption in environmental antibiotic risk assessments.},
}

@article {pmid40885910,
year = {2025},
author = {Huang, W and Chai, Y and Li, X and Zhang, Q and Yan, Z and Wang, Y and Tao, X and Zhang, J and Qiu, F},
title = {Metagenomics and metabolomics to evaluate the potential role of gut microbiota and blood metabolites in patients with cerebral infarction.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {567},
pmid = {40885910},
issn = {1471-2180},
support = {2018YFA0108601//Clinical research on intracerebral precision transplantation of neural stem cells for stroke treatment/ ; L255012//The Huairou Innovation Joint Fund Project of Beijing Natural Science Foundation/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Cerebral Infarction/microbiology/blood/metabolism ; *Metabolomics/methods ; *Metagenomics/methods ; Male ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; Middle Aged ; Female ; Aged ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Tandem Mass Spectrometry ; Adult ; Chromatography, High Pressure Liquid ; },
abstract = {Cerebral infarction, a cerebrovascular disorder, is characterized by the sudden onset of neurological deficits and clinical symptoms. It ranks among the leading causes of death and severe disability worldwide. The etiology of cerebral infarction is multifaceted, with common risk factors including dietary patterns, smoking, hypertension, and diabetes mellitus. In recent years, the role of the gut microbiota in systemic immunity and tumorigenesis has been intensively explored, thrusting the research on the gut-brain axis into the spotlight. However, there is a lack of literature investigating the relationship between the gut microbiota and blood metabolites in cerebral infarction. In this study, we employed 16S rRNA analysis and ultra-high-performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) for a comprehensive metagenomic and metabolomic analysis of fecal samples from cerebral infarction patients and the general population. Our results revealed a significant correlation between the gut microbiome and serum metabolites, highlighting the impact of the microbiome on metabolic pathways. Specifically, we found that 35 gut microbiome taxa, such as Actinobacteriota and Peptostreptococcales-Tissierellales, were significantly enriched in the control group (N group). Through Linear Discriminant Analysis Effect Size (LEfSe) analysis, 72 taxa showed significant differences between cerebral infarction patients and healthy individuals. Among them, 22 key taxa were identified as microbial biomarkers for differentiating patients from healthy controls. These findings suggest that variations in the microbiome and metabolites could potentially serve as biomarkers for future diagnostic and therapeutic strategies in cerebral infarction.},
}

Humans
*Gastrointestinal Microbiome
*Cerebral Infarction/microbiology/blood/metabolism
*Metabolomics/methods
*Metagenomics/methods
Male
RNA, Ribosomal, 16S/genetics
Feces/microbiology
Middle Aged
Female
Aged
*Bacteria/classification/genetics/isolation & purification/metabolism
Tandem Mass Spectrometry
Adult
Chromatography, High Pressure Liquid

@article {pmid40884832,
year = {2025},
author = {Chen, S and Liu, F and Han, X and Jia, D and Chen, J and Wei, Y and Yu, Z and He, L and Liao, C and Ding, K},
title = {Exposure to Bovine Viral Diarrhea Virus Disrupts Intestinal Barrier Function via NLRP3/Caspase-1-Mediated Pyroptosis and Gut Microbiota Dysbiosis.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c04854},
pmid = {40884832},
issn = {1520-5118},
abstract = {Bovine viral diarrhea virus (BVDV) is a major global pathogen that causes severe economic losses in dairy herds due to diarrhea, reproductive disorders, and reduced milk yield. Despite its well-documented systemic effects, the mechanism of BVDV-induced intestinal damage remains unclear. In our study, BVDV triggered cytopathic effects in intestinal epithelial cells, including cell death, goblet cell depletion, and disruption of barrier proteins. Although BVDV alters gut microbiota by activating the NLRP3/caspase-1 inflammasome pathway and thereby causing pyroptosis and intestinal injury, fecal microbiota transplantation mitigated those effects by suppressing NLRP3/caspase-1's activation. Those findings reveal key pathways in BVDV's pathogenesis and suggest novel therapeutic strategies to combat livestock infections.},
}

@article {pmid40882395,
year = {2025},
author = {Chen, X and Zou, J and Hong, T and Zhang, H and Yang, J and Mai, H and Shi, H and Li, X and Feng, D},
title = {Bisphenol A increases fat mass in adipose tissue by disturbing gut microbiota-dependent bile acid metabolism and TGR5/UCP1 signaling pathways in CD-1 mice.},
journal = {Ecotoxicology and environmental safety},
volume = {303},
number = {},
pages = {118922},
doi = {10.1016/j.ecoenv.2025.118922},
pmid = {40882395},
issn = {1090-2414},
abstract = {Disorder of gut microbiota-mediated bile acid (BA) metabolism plays a pivotal role in the pathogenesis of obesity. Our previous research showed that bisphenol A (BPA) exposure induced hepatic fat accumulation and gut microbiota dysbiosis. However, whether the gut microbiota-dependent BA metabolism alteration is involved in BPA-induced fat accumulation and obesity remains elusive. This study aimed to investigate the gut microbiota-dependent metabolic mechanism of obesity induced by BPA. Male CD-1 mice were exposed to a low dose of BPA (50 μg/kg/day) for six months. Our findings demonstrated that BPA exposure significantly augmented the fat mass of both brown and white adipose tissue, along with the proportion of adipose tissue weight relative to body weight. Furthermore, BPA reduced the relative abundance of Bacteroides, Parabacteroides, and Akkermansia, which are associated with BA metabolism. Additionally, serum levels of lithocholic acid, the most potent activator of Takeda G protein-coupled receptor 5 (TGR5), and TGR5 expression in adipose tissue were substantially diminished following BPA exposure. Inhibition of TGR5 reduced cyclic adenosine monophosphate levels, subsequently decreasing the expression of iodothyronine deiodinase 2 and fibroblast growth factor 21. These changes down-regulated the expression of uncoupling protein 1 (UCP1), ultimately leading to reduced energy expenditure and increased fat mass. Moreover, further fecal microbiota transplantation and microbiota elimination confirmed the role of gut microbiota in BPA-induced adverse effects. Collectively, our study demonstrated that the suppression of gut microbiota-BA-TGR5/UCP1 signaling pathways may constitute a potential mechanism underlying BPA-induced fat mass gain, providing a novel target for the prevention of BPA-induced obesity.},
}

@article {pmid40881288,
year = {2025},
author = {Pourrat, A and Baillieu, V and Ansel, S and Leonardi, M and Poiron, P and Bellais, S and Paul, M and Nebbad, B},
title = {Standardized freeze-dried FMT: is the ideal protectant out there?.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1618067},
doi = {10.3389/fmicb.2025.1618067},
pmid = {40881288},
issn = {1664-302X},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is an effective treatment for recurrent Clostridioides difficile infections. Freeze-drying offers a next-generation, more practical, and aesthetically acceptable FMT formulation that could facilitate standardized preparation methods. Viable preservation is a critical step in freeze-drying, yet no universal medium effectively protects both anaerobes and aerobes.

OBJECTIVE: This study aimed to evaluate different protectants compared to trehalose 5% (T5) after confirming its efficacy.

METHODS: A mix of inulin and glucosamine (IG5) and a High-antioxidant Matrix with trehalose (HM) were tested. Viability was assessed using colony-forming unit (CFU) enumeration and flow cytometry with a LIVE/DEAD™ staining method.

RESULTS: T5 demonstrated satisfactory bacterial recovery after freeze-drying, with viability of 84 ± 28% for anaerobes and 59 ± 39% for Bifidobacterium (BIF), confirming its efficiency in our preparation facilities. While HM showed highest results (91 ± 7% for anaerobes, 121 ± 33% for BIF), it did not significantly outperform T5. IG5, however, resulted in a significant loss of bacteria, with only 16 ± 12% viability for anaerobes (p = 0.016) and 19 ± 9% for BIF (p = 0.031).

CONCLUSION: HM and T5 both proved effective for freeze-dried FMT, with HM yielding the highest recovery but not significantly outperforming T5. Given its simplicity and consistent results, T5 may serve as a reliable standalone protectant or as a base for improved formulations. IG5 showed significant bacterial loss and is unsuitable. Further biological validation and stability data will guide the development of optimized freeze-dried oral FMT capsules.},
}

@article {pmid40880458,
year = {2025},
author = {Dinis, L and Pinheiro, H and Póvoa, P and Calhau, C and Pestana, D and Marques, C},
title = {Advancing Access to Intestinal Microbiota Transplant: Bridging the Gap Between National Practices and the European Strategy.},
journal = {Acta medica portuguesa},
volume = {},
number = {},
pages = {},
doi = {10.20344/amp.22750},
pmid = {40880458},
issn = {1646-0758},
abstract = {Clostridioides difficile is an opportunistic pathogen that can cause a range of conditions, from asymptomatic carriage to severe illness, posing a significant public health threat due to its high mortality rates and substantial healthcare costs. Traditional treatment options, including antibiotics, often fail to eradicate the infection, leading to recurrent cases that severely impact patients' lives. Intestinal microbiota transplant (IMT) has emerged as an effective strategy for decolonizing pathogenic agents, demonstrating safety and efficacy, particularly in treating recurrent Clostridioides difficile infection (rCDI). Despite its potential, access to IMT is limited due to safety concerns, logistical challenges, and a lack of proper guidance, underscoring the urgent need for structured intestinal microbiota banks (IMBs). These organized facilities are crucial for the collection, screening, processing, and distribution of intestinal microbiota preparations, thereby facilitating the clinical application of IMT. In this narrative review, we discuss the relevance of applying IMT for the treatment of rCDI in Europe, with a focus on Portugal. We highlight the existence and distribution of IMBs across Europe and their importance in improving access to IMT. This review also addresses the challenges in creating an IMB and the development of such a structure in Portugal as a centralized repository for high-quality, standardized microbiota preparations, making IMT accessible for national hospitals. Additionally, it emphasizes the need to raise awareness among healthcare providers and the public to support the broader adoption of IMT.},
}

@article {pmid40878918,
year = {2025},
author = {Liu, X and Xie, Y and Yang, S and Jiang, C and Shang, K and Luo, J and Zhang, L and Hu, G and Liu, Q and Yue, B and Fan, Z and He, Z and Li, J},
title = {Multi-omics investigation of spontaneous T2DM macaque emphasizes gut microbiota could up-regulate the absorption of excess palmitic acid in the T2DM progression.},
journal = {eLife},
volume = {14},
number = {},
pages = {},
pmid = {40878918},
issn = {2050-084X},
support = {2021YJ0136//Science and Technology Foundation of Sichuan Province/ ; 32171607//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Diabetes Mellitus, Type 2/microbiology/pathology/metabolism ; *Palmitic Acid/metabolism ; Macaca mulatta ; Mice ; Disease Models, Animal ; Male ; Gene Expression Profiling ; Metabolome ; RNA, Ribosomal, 16S/genetics ; Disease Progression ; Multiomics ; },
abstract = {Although gut microbiota and lipid metabolites have been suggested to be closely associated with type 2 diabetes mellitus (T2DM), the interactions between gut microbiota, lipid metabolites, and the host in T2DM development remains unclear. Rhesus macaques may be the best animal model to investigate these relationships given their spontaneous development of T2DM. We identified eight spontaneous T2DM macaques and conducted a comprehensive study investigating the relationships using multi-omics sequencing technology. Our results from 16 S rRNA, metagenome, metabolome, and transcriptome analyses identified that gut microbiota imbalance, tryptophan metabolism and fatty acid β oxidation disorders, long-chain fatty acid (LCFA) accumulation, and inflammation occurred in T2DM macaques. We verified the accumulation of palmitic acid (PA) and activation of inflammation in T2DM macaques. Importantly, mice transplanted with spontaneous T2DM macaque fecal microbiota and fed a high PA diet developed prediabetes within 120 days. We determined that gut microbiota mediated the absorption of excess PA in the ileum, resulting in the accumulation of PA in the serum, consequently leading to T2DM in mice. In particular, we demonstrated that the specific microbiota composition was probably involved in the process. This study provides new insight into interactions between microbiota and metabolites and confirms causative effect of gut microbiota on T2DM development.},
}

Animals
*Gastrointestinal Microbiome
*Diabetes Mellitus, Type 2/microbiology/pathology/metabolism
*Palmitic Acid/metabolism
Macaca mulatta
Mice
Disease Models, Animal
Male
Gene Expression Profiling
Metabolome
RNA, Ribosomal, 16S/genetics
Disease Progression
Multiomics

@article {pmid40877311,
year = {2025},
author = {Wilson, BC and Zuppi, M and Derraik, JGB and Albert, BB and Tweedie-Cullen, RY and Leong, KSW and Beck, KL and Vatanen, T and O'Sullivan, JM and Cutfield, WS and , },
title = {Long-term health outcomes in adolescents with obesity treated with faecal microbiota transplantation: 4-year follow-up.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {7786},
pmid = {40877311},
issn = {2041-1723},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; Adolescent ; Male ; Female ; Follow-Up Studies ; Double-Blind Method ; *Pediatric Obesity/therapy ; Treatment Outcome ; Body Composition ; Body Mass Index ; Gastrointestinal Microbiome ; *Obesity/therapy ; Metabolic Syndrome/therapy ; Feces/microbiology ; },
abstract = {Faecal microbiota transplantation (FMT) has been explored as a potential treatment for obesity, but its long-term effects on metabolic health remain unclear. Here, we report 4-year follow-up findings from a double-blind, randomised, placebo-controlled trial assessing FMT in adolescents with obesity (ACTRN12615001351505, Australian New Zealand Clinical Trials Registry). This unblinded follow-up study evaluated 63% (55/87) of the original participants (27 FMT, 28 placebo). There was no difference in BMI between the two groups, after adjusting for sex, age, diet, and physical activity (-3.6 kg/m[2], p = 0.095). However, FMT recipients showed clinical improvements in body composition and metabolic health compared to the placebo group. Specifically, FMT recipients had smaller waist circumference (-10.0 cm, p = 0.026), total body fat (-4.8%, p = 0.024), metabolic syndrome severity score (-0.58, p = 0.003), and systemic inflammation (-68% hs-CRP, p = 0.002) and higher levels of HDL cholesterol (0.16 mmol/L, p = 0.037). No group differences were observed in glucose markers, or other lipid parameters. Shotgun metagenomic sequencing revealed sustained long-term alterations in gut microbiome richness, composition and functional capacity, with persistence of donor-derived bacterial and bacteriophage strains. These findings highlight the potential relevance of FMT as a microbiome-augmenting intervention for obesity management and metabolic health, warranting further investigation.},
}

Humans
*Fecal Microbiota Transplantation/methods
Adolescent
Male
Female
Follow-Up Studies
Double-Blind Method
*Pediatric Obesity/therapy
Treatment Outcome
Body Composition
Body Mass Index
Gastrointestinal Microbiome
*Obesity/therapy
Metabolic Syndrome/therapy
Feces/microbiology

@article {pmid40876612,
year = {2025},
author = {Xie, X and Ge, W and Luo, Y and Xing, X and Sun, X},
title = {Ginsenoside Rb3 Modulates Gut Microbiota to Alleviate Cerebral Inflammation and Ferroptosis via the NLRP3/NF-κB/GPX4 Pathway in Rats with Cerebral Ischemia/Reperfusion Injury.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {178091},
doi = {10.1016/j.ejphar.2025.178091},
pmid = {40876612},
issn = {1879-0712},
abstract = {Cerebral ischemia/reperfusion injury (CIRI) poses a significant threat to human life and health. Ginsenoside Rb3 (Rb3) is known to exhibit protective effects against myocardial ischemia, its impact on CIRI remains unclear. Therefore, we investigated the protective effects of Rb3 on CIRI and its underlying mechanisms. Our results showed that Rb3 reduced cerebral infarct volume, decreased blood-brain barrier (BBB) permeability, and improved neurological deficits in CIRI rats. Rb3 also mitigated cerebral ferroptosis and alleviated neuroinflammation, as evidenced by decreased iron levels, reduced MDA content, an improved GSH/GSSG ratio, and lower levels of TNF-α, IL-1β, and IL-6, through modulation of the NLRP3/NF-κB/GPX4 pathway. Additionally, Rb3 alleviated intestinal inflammation, improved the intestinal barrier, and corrected gut microbiota dysbiosis and reduced the microbial metabolites TMAO and LPS in CIRI rats. It is noteworthy that in pseudo germ-free rats with CIRI, fecal microbiota transplants (FMT) from Rb3-treated rats conferred similar protective effects as Rb3. Summarily, this study reveals that Rb3 reduces neuroinflammation and ferroptosis in the brains of middle cerebral artery occlusion/reperfusion (MCAO/R) rats via the NLRP3/NF-κB/GPX4 pathway in a gut microbiota-dependent manner.},
}

@article {pmid40876561,
year = {2025},
author = {de Oliveira, DG and Machado, A and Lacerda, PC and Karakikla-Mitsakou, Z and Vasconcelos, C},
title = {Systemic lupus erythematosus and the gut microbiome: To look forward is to look within - A systematic review and narrative synthesis.},
journal = {Autoimmunity reviews},
volume = {},
number = {},
pages = {103921},
doi = {10.1016/j.autrev.2025.103921},
pmid = {40876561},
issn = {1873-0183},
abstract = {BACKGROUND: Systemic lupus erythematosus (SLE) is a heterogeneous autoimmune disease shaped by complex interactions involving genetic and environmental factors. Among these, the gut microbiome is emerging as potentially modulating immune responses and influencing disease susceptibility, progression, and activity.

OBJECTIVES: To synthesize current evidence on gut microbiome changes in adult SLE patients, framed along the clinical pathway - from diagnosis to treatment - to help bridge bench and bedside for microbiome-informed SLE care and research.

METHODS: A systematic search identified primary research studies examining gut microbiota in adult SLE patients. Studies were reviewed in a stepwise manner by independent investigators. Findings were synthesized narratively, emphasizing human data.

RESULTS: SLE patients exhibit gut microbiome dysbiosis, with reduced microbial richness and altered bacterial taxa. A lower Firmicutes/Bacteroidetes ratio is frequently observed. Enrichment of specific taxa, such as Enterococcus, Lactobacillus, and Ruminococcus gnavus, is reported. Dysbiosis correlates with increased gut permeability, immune activation, and autoreactivity. Clinical associations include disease activity, flares, nephritis, and other manifestations. SLE treatments, such as hydroxychloroquine and corticosteroids, influence the microbiome. Emerging interventions such as dietary modulation and fecal microbiota transplantation show promise in early studies. However, considerable heterogeneity exists across studies in terms of patient characteristics, methodology, and taxa-level findings.

CONCLUSIONS: The gut microbiome has multifaceted associations with SLE pathogenesis, disease activity, and therapeutic response. Translation will require standardized methods, functional validation, longitudinal follow-up, and clinical integration. While uncertainties remain, the gut microbiome is increasingly relevant, and clinicians caring for patients with SLE should be aware of its emerging implications.},
}

@article {pmid40876127,
year = {2025},
author = {Cao, S and Guo, X and Xin, M and Wang, X and Huo, J and Yue, Y and Li, X and Xu, D and Liu, L},
title = {Sesamin ameliorates ulcerative colitis by modulating the DUSP1/ERK feedback loop and restoring gut microbiota homeostasis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {147},
number = {},
pages = {157188},
doi = {10.1016/j.phymed.2025.157188},
pmid = {40876127},
issn = {1618-095X},
abstract = {BACKGROUND: Sesamin (SSM), a plant-derived lignan, possesses anti-inflammatory and immunomodulatory effects. The pathogenesis of ulcerative colitis (UC) is complex and involves intestinal mucosal damage, inflammation, and dysbiosis of the gut microbiota. However, to date, the protective effects and therapeutic mechanisms of SSM in UC have hardly been investigated.

PURPOSE: The purpose of the study was to investigate the protective effects and therapeutic mechanisms of SSM in UC.

METHODS: This study utilized a dextran sulfate sodium-induced mouse model of UC to investigate the therapeutic effects of SSM and its impact on gut microbiota using molecular biology techniques, including histological staining, western blotting, proteomics, molecular docking, 16S rRNA sequencing, and fecal microbiota transplantation.

RESULTS: SM significantly alleviated inflammation, repaired intestinal mucosal barrier, and improved gut microbiota structure in mice with UC (p < 0.05). Further studies revealed that SSM upregulated dual-specificity phosphatase 1 (DUSP1) by suppressing extracellular signal-regulated protein kinase (ERK) phosphorylation, whereas DUSP1 knockdown increased p-ERK levels (p < 0.05). Additionally, SSM regulated the distribution of gut microbiota by increasing the abundance of beneficial bacteria (such as Lactobacillus), reducing the abundance of opportunistic pathogens (such as Staphylococcus), and restoring gut microbiota homeostasis (p < 0.05).

CONCLUSION: In summary, this is the first study to demonstrate that SSM exerts anti-inflammatory and intestinal barrier-restoring effects through modulating the DUSP1/ERK feedback loop and restoring gut microbiota homeostasis, thereby offering a novel therapeutic strategy for UC.},
}

@article {pmid40875477,
year = {2025},
author = {Guo, YF and Wang, Y and Wu, H and Wang, L and Miao, X},
title = {Rauvolfia Verticillata Pectic Polysaccharides Alleviate Inflammation-Associated Colorectal Cancer and Correlate with Modulation of Gut Microbiota, Short-Chain Fatty Acid Metabolism, and NF-κB/IL-6/STAT3 Signaling Pathways.},
journal = {Nutrition and cancer},
volume = {},
number = {},
pages = {1-17},
doi = {10.1080/01635581.2025.2551294},
pmid = {40875477},
issn = {1532-7914},
abstract = {Background: Colorectal cancer (CRC) is increasingly common in younger individuals and strongly linked to chronic inflammation. Gut microbiota and pathways like NF-κB/STAT3 play key roles, which highlights the therapeutic potential of natural compounds that target intestinal immunity and microbial balance. Objective: To investigate the therapeutic effects of pectic polysaccharides (PPs) from Rauvolfia verticillata in inflammation-associated CRC via the modulation of of gut microbiota and NF-κB/IL-6/STAT3 signaling pathways. Methods: C57BL/6 mice were subjected to azoxymethane (AOM)/dextran sulfate sodium (DSS)-induced CRC and treated with PP (100 mg/kg/day), the STAT3 inhibitor W2014-S (10 mg/kg), or fecal microbiota transplantation (FMT) from PP-treated donors. Histopathology, immunohistochemistry (IHC), Western blot, immunofluorescence (IF), 16S rRNA sequencing, and SCFA analysis were performed to assess inflammation, signaling pathways, gut microbiota composition, and metabolic changes. Results: PP intervention significantly mitigated AOM/DSS-induced weight loss, intestinal lesions, and disease activity index (DAI) scores while suppressing NF-κB and STAT3 activation. PP restored gut microbiota diversity, reduced pro-inflammatory genera, and regulated SCFA levels, particularly hexanoic those of and isohexanoic acids. FMT from PP-treated donors similarly attenuated colitis and inhibited NF-κB/STAT3 pathways. Conclusions: PP alleviates CRC and is associated with modulation of gut microbiota, SCFA metabolism, and NF-κB/IL-6/STAT3 signaling, offering a potential therapeutic strategy for inflammation-driven CRC.},
}

@article {pmid40873786,
year = {2025},
author = {Pinto, S and Benincà, E and Nooij, S and Terveer, EM and Keller, JJ and van der Meulen-de Jong, AE and Steyerberg, EW and Bogaards, JA},
title = {Ecological resilience in ulcerative colitis: microbial dynamics of donor and resident species in a longitudinal fecal microbiota transplantation study.},
journal = {ISME communications},
volume = {5},
number = {1},
pages = {ycaf119},
pmid = {40873786},
issn = {2730-6151},
abstract = {Fecal microbiota transplantation (FMT) is a promising treatment for the chronic immune-mediated disease ulcerative colitis (UC). However, the microbial dynamics underlying clinical remission remain poorly understood. To investigate these dynamics, we analysed data from 22 UC patients treated with four rounds of FMT donated by two healthy donors. Microbiota samples from patients were collected at nine timepoints before, during, and after treatment, covering a period of 14 weeks. Additionally, 27 donor samples were analysed. Species in the recipients' gut microbiota were categorised into ecological categories based on their origin and temporal dynamics: species already present in the recipient pre-FMT, species derived from the donor, or novel species, i.e. absent before FMT in both recipient and donor but detected during or after treatment. Overdispersed Poisson regression models were employed to model the number of species within each category over time. Furthermore, we investigated the change in relative abundance for recipient, colonising, and novel species. The results revealed that recipient species with higher relative abundances prior to FMT were more likely to persist following FMT. Notably, patients who achieved combined clinical and endoscopic remission at week 14 retained a higher number of recipient species compared to non-responders. In contrast, non-responders initially exhibited colonisation of more donor species than responders, but colonisation rate decreased over time in non-responders whereas colonisation rate remained stable in responders. These findings suggest that clinical remission following FMT is associated with controlled incorporation of donor species without replacement of resident species, which may reflect a resilient recipient gut community.},
}

@article {pmid40873717,
year = {2025},
author = {Li, D and Tao, H and Tan, X and Ling, H and Lu, Y and Zhang, H and Theany, S and Xu, H},
title = {Gut microbiota and their metabolites ameliorate acute and chronic colitis in mice via modulating Th17/Treg balance.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1643209},
pmid = {40873717},
issn = {1664-302X},
abstract = {INTRODUCTION: Ulcerative colitis (UC) is a recurrent inflammatory bowel disease affecting the colorectum, which remains a prominent research focus due to significant individual variations in clinical therapeutic outcomes. Fecal microbiota transplantation (FMT), as a therapeutic approach to restore intestinal homeostasis, has demonstrated favorable efficacy in UC management. However, given the characteristic alternating cycles of active and remission phases in UC, there remains a paucity of in-depth research regarding the optimal timing for FMT intervention. Concurrently, butyrate - a crucial microbial metabolite - ameliorates murine colitis through both direct and indirect mechanisms, while the therapeutic effectiveness of FMT in UC correlates closely with intestinal butyrate concentration.

METHODS: This study established acute and chronic UC murine models and employed FMT and butyrate interventions to monitor dynamic alterations in gut microbiota and lymphocyte subsets. Through comprehensive analyses, we aimed to elucidate the interplay between gut microbiota and host immune mechanisms, identify the optimal therapeutic timing for UC interventions, and evaluate the mechanistic role of butyrate. These findings provide theoretical foundations for personalized microbiota-targeted therapies in UC.

RESULTS: Our findings demonstrate that gut microbiota and their metabolites exert therapeutic effects on murine acute/chronic colitis through modulation of the T helper cell 17 (Th17)/T regulatory cell (Treg) ratio. Specifically, the remission phase represents a more favorable window for intestinal homeostasis modulation, with combination therapy involving microbial metabolites exhibiting superior anti-inflammatory efficacy.

DISCUSSION: The maintenance of an appropriate Th17/Treg equilibrium during microbiota restoration demonstrates therapeutic advantages. Notably, butyrate synergistically enhances microbial therapeutic effects, providing experimental evidence for personalized modulation of gut ecosystems in inflammatory bowel disease management.},
}

@article {pmid40873657,
year = {2025},
author = {Chapon, J and Scanzi, J and Sokol, H and Pereira, B and Buisson, A},
title = {Efficacy of different modalities of faecal microbiota transplantation in ulcerative colitis: systematic review and network meta-analysis.},
journal = {Therapeutic advances in gastroenterology},
volume = {18},
number = {},
pages = {17562848251369624},
pmid = {40873657},
issn = {1756-283X},
abstract = {BACKGROUND: While several small sample size randomized controlled trials suggested the superiority of faecal microbiota transplantation (FMT) over placebo in ulcerative colitis (UC), the most effective modality to perform FMT remains unknown.

OBJECTIVES: To compare the efficacy of different modalities of FMT to induce clinical remission in patients with UC.

DATA SOURCES AND METHODS: We performed a systematic review and network analysis (sources: MEDLINE, Embase, Cochrane CENTRAL; random effects model) of randomized controlled trials including at least one arm of FMT in adult patients with active UC. The primary endpoint, that is, clinical remission (total Mayo score ⩽2 with Mayo endoscopic score ⩽1), was assessed between weeks 6 and 12. Results are expressed as relative risks with 95% confidence intervals, adjusted for bowel cleansing and pre-FMT antibiotics. Ranking of FMT modalities was calculated as their surface under the cumulative ranking (SUCRA).

RESULTS: Among the 12 selected studies, patients were exclusively bio-naïve in 4 studies (4/12), while between 9% and 32% had prior biologics exposure in the other trials. The risk of bias was low across all domains in seven studies. Contrary to upper gastrointestinal tract (GI) FMT (Relative risk (RR) = 1.1 (0.2-7.7)), oral capsule (RR = 7.1 (1.8-33.3)), lower GI FMT (RR = 4.5 (1.7-12.5) and combination of both (RR = 12.5 (2.1-100)) are more effective than placebo to induce clinical remission. The combination of lower GI FMT and oral capsule was significantly more effective than upper GI FMT to induce clinical remission (RR = 10.7 (1.1-104.2)). Combination of lower GI FMT and oral capsule ranked the highest for the induction of clinical remission (SUCRA = 0.93). Multidonor FMT did not perform better than single donor FMT. Autologous FMT ranked lower than placebo (SUCRA = 0.12 vs 0.22).

CONCLUSION: The combination of lower GI and oral capsule FMT seems to be the best modality of FMT for patients with UC. In clinical trials, autologous FMT should be avoided due to a potential detrimental effect.

TRIAL REGISTRATION: PROSPERO registration number: CRD42023385511.},
}

@article {pmid40873417,
year = {2025},
author = {You, Y and Xiang, T and Yang, C and Xiao, S and Tang, Y and Luo, G and Ling, Z and Luo, F and Chen, Y},
title = {Interactions between the gut microbiota and immune cell dynamics: novel insights into the gut-bone axis.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2545417},
doi = {10.1080/19490976.2025.2545417},
pmid = {40873417},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Bone and Bones/immunology ; Dysbiosis/immunology/microbiology ; Animals ; Osteoarthritis/immunology/microbiology ; Arthritis, Rheumatoid/immunology/microbiology ; Probiotics ; Osteoporosis/immunology/microbiology ; *Bone Diseases/immunology/microbiology ; Immune System ; Gastrointestinal Tract/immunology/microbiology ; Prebiotics ; },
abstract = {Over the past few decades, accumulating evidence has demonstrated that gut microbiota engages in a sustained dialog with the immune system, leading to microbiota-driven immune responses that mediate the regulation of bone-related diseases. Despite the complexity of the dynamic interactions within the gut-immune-bone axis, advancements in high-throughput multi-omics sequencing have significantly facilitated the detailed exploration of this intricate network, thereby providing the potential to develop novel therapeutic strategies for bone-related diseases. In this review, we first summarize the variations in gut microbiota composition observed in patients with bone-related diseases, such as rheumatoid arthritis (RA), osteoarthritis (OA), and osteoporosis (OP), in comparison to healthy controls, along with the factors influencing these changes. The review that follows synthesize evidences highlighting the profound effects of gut microbial dysbiosis on immune homeostasis and bone microenvironment, respectively. We further elaborate that the gut-immune axis and gut-bone axis are not independent but three-dimensional networks, emphasizing gut microbial dysbiosis as a pivotal driver of immune dysregulation and subsequent bone homeostasis imbalance. Therapeutic strategies to manipulate the gut-immune-bone axis based on the use of probiotics as well as prebiotics, fecal microbiota transplantation, dietary modifications, and pharmacological interventions are also discussed. Finally, we discuss the challenges of current research on the gut-immune-bone axis and propose future directions for identifying novel therapeutic targets based on this axis to treat these diseases.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Bone and Bones/immunology
Dysbiosis/immunology/microbiology
Animals
Osteoarthritis/immunology/microbiology
Arthritis, Rheumatoid/immunology/microbiology
Probiotics
Osteoporosis/immunology/microbiology
*Bone Diseases/immunology/microbiology
Immune System
Gastrointestinal Tract/immunology/microbiology
Prebiotics

@article {pmid40873073,
year = {2025},
author = {, },
title = {[Expert consensus on the clinical application of gut microbiota transplant therapy in chronic liver disease (version 2025)].},
journal = {Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology},
volume = {33},
number = {8},
pages = {738-746},
doi = {10.3760/cma.j.cn501113-20250429-00163},
pmid = {40873073},
issn = {1007-3418},
support = {82470598//National Natural Science Foundation of China/ ; 2023A0505010007//Science and Technology Planning Project of Guangdong Province/ ; K-202401210//Guangdong Weiji Medical Development Foundation Specialized Research Fund for Gastroenterology/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; *Liver Diseases/therapy ; Chronic Disease ; Consensus ; Liver Cirrhosis/therapy ; Liver Neoplasms/therapy ; },
abstract = {The gut microbiota plays an important role in maintaining host health and liver function, and gut microbiota transplant (also known as fecal microbiota transplantation) has shown potential clinical benefits in the treatment of chronic liver disease. To help clinical professionals to quickly master and standardize the clinical application of gut microbiota transplant in chronic liver disease, the Group of the Liver Disease-related Gastroenterology Branch of the Chinese Medical Association organized experts in related fields to formulate the "Expert Consensus on the Clinical Application of Gut Microbiota Transplant in the Treatment of Chronic Liver Disease" such as chronic hepatitis, cirrhosis and liver cancer, including indications, contraindications, effectiveness, safety, donor selection, transplant routes, transplant precautions, prevention and treatment of adverse reactions, and other aspects to provide reference and guidance for clinicians to implement gut microbiota transplant.},
}

Humans
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
*Liver Diseases/therapy
Chronic Disease
Consensus
Liver Cirrhosis/therapy
Liver Neoplasms/therapy

@article {pmid40872257,
year = {2025},
author = {Cianci, G and Maini, G and Ferraresi, M and Pezzi, G and Bortolotti, D and Rizzo, S and Beltrami, S and Schiuma, G},
title = {Immune Modulation by Microbiota and Its Possible Impact on Polyomavirus Infection.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {8},
pages = {},
doi = {10.3390/pathogens14080747},
pmid = {40872257},
issn = {2076-0817},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Polyomavirus Infections/immunology/microbiology/virology/therapy ; *Polyomavirus/immunology ; Dysbiosis/immunology ; Fecal Microbiota Transplantation ; Animals ; Immunocompromised Host ; },
abstract = {Polyomaviruses are a family of small DNA viruses capable of establishing persistent infections, and they can pose significant pathogenic risks in immunocompromised hosts. While traditionally studied in the context of viral reactivation and immune suppression, recent evidence has highlighted the gut microbiota as a critical regulator of host immunity and viral pathogenesis. This review examines the complex interactions between polyomaviruses, the immune system, and intestinal microbiota, emphasizing the role of short-chain fatty acids (SCFAs) in modulating antiviral responses. We explore how dysbiosis may facilitate viral replication, reactivation, and immune escape and also consider how polyomavirus infection can, in turn, alter microbial composition. Particular attention is given to the Firmicutes/Bacteroidetes ratio as a potential biomarker of infection risk and immune status. Therapeutic strategies targeting the microbiota, including prebiotics, probiotics, and fecal microbiota transplantation (FMT), are discussed as innovative adjuncts to immune-based therapies. Understanding these tri-directional interactions may offer new avenues for mitigating disease severity and improving patient outcomes during viral reactivation.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Polyomavirus Infections/immunology/microbiology/virology/therapy
*Polyomavirus/immunology
Dysbiosis/immunology
Fecal Microbiota Transplantation
Animals
Immunocompromised Host

@article {pmid40871460,
year = {2025},
author = {Ren, J and Wang, Q and Hong, H and Tang, C},
title = {Fecal Microbiota Transplantation in Alzheimer's Disease: Mechanistic Insights Through the Microbiota-Gut-Brain Axis and Therapeutic Prospects.},
journal = {Microorganisms},
volume = {13},
number = {8},
pages = {},
doi = {10.3390/microorganisms13081956},
pmid = {40871460},
issn = {2076-2607},
support = {HY202411//One health Interdisciplinary Research Project, Ningbo University/ ; D16013//National 111 Project of China/ ; the Health Fund of Translational Biomedicine//the Health Fund of Translational Biomedicine/ ; },
abstract = {Alzheimer's disease (AD), a prevalent neurodegenerative disorder in the aging population, remains without definitive therapeutic solutions. Emerging insights into the gut microbiota (GM) and its bidirectional communication with the central nervous system(CNS) through the microbiota-gut-brain axis (MGBA) have unveiled potential correlative mechanisms that may contribute to AD pathogenesis, though causal evidence remains limited. Dysregulation of GM composition (dysbiosis) exacerbates AD progression via neuroinflammation, amyloid-β (Aβ) deposition, and tau hyperphosphorylation (p-tau), while restoring microbial homeostasis presents a promising therapeutic strategy. Fecal microbiota transplantation (FMT), a technique to reconstitute gut ecology by transferring processed fecal matter from healthy donors, has demonstrated efficacy in ameliorating cognitive deficits and neuropathology in AD animal models. Preclinical studies reveal that FMT reduces Aβ plaques, normalizes tau phosphorylation, suppresses inflammasome activation, and restores microglial homeostasis through modulation of microbial metabolites and immune pathways. Although clinical evidence remains limited to case reports and small-scale trials showing potential therapeutic effect, safety concerns regarding long-term effects and protocol standardization necessitate further investigation. This review synthesizes current knowledge on GM-AD interactions, evaluates FMT's mechanistic potential, and discusses challenges in translating this ancient practice into a cutting-edge AD therapy. Rigorous randomized controlled trials and personalized microbiota-based interventions are imperative to advance FMT from bench to bedside.},
}

@article {pmid40871301,
year = {2025},
author = {Chen, S and Liu, T and Chen, J and Shen, H and Wang, J},
title = {Fecal Virome Transplantation Confirms Non-Bacterial Components (Virome and Metabolites) Participate in Fecal Microbiota Transplantation-Mediated Growth Performance Enhancement and Intestinal Development in Broilers with Spatial Heterogeneity.},
journal = {Microorganisms},
volume = {13},
number = {8},
pages = {},
doi = {10.3390/microorganisms13081795},
pmid = {40871301},
issn = {2076-2607},
support = {Project No. CZ004306//"Tianshan Talent" Program/ ; Project No. XJLG-CYJSTX-10//Xinjiang Modern Agriculture Industry Technology System/ ; },
abstract = {Fecal microbiota transplantation (FMT) promotes growth performance and intestinal development in yellow-feathered broilers, but whether the virome and metabolites contribute to its growth-promoting effect remains unclear. This study removed the microbiota from FMT filtrate using a 0.45 μm filter membrane, retaining the virome and metabolites to perform fecal virome transplantation (FVT), aiming to investigate its regulatory role in broiler growth. Healthy yellow-feathered broilers with high body weights (top 10% of the population) were used as FVT donors. Ninety-six 8-day-old healthy male yellow-feathered broilers (95.67 ± 3.31 g) served as FVT recipients. Recipient chickens were randomly assigned to a control group and an FVT group. The control group was gavaged with 0.5 mL of normal saline daily, while the FVT group was gavaged with 0.5 mL of FVT solution daily. Growth performance, immune and antioxidant capacity, intestinal development and related gene expression, and microbial diversity were measured. The results showed that FVT improved the feed utilization rate of broilers (the feed conversion ratio decreased by 3%; p < 0.05), significantly increased jejunal length (21%), villus height (69%), and crypt depth (84%) (p < 0.05), and regulated the jejunal barrier: insulin-like growth factor-1 (IGF-1) (2.5 times) and Mucin 2 (MUC2) (63 times) were significantly upregulated (p < 0.05). FVT increased the abundance of beneficial bacteria Lactobacillales. However, negative effects were also observed: Immunoglobulin A (IgA), Immunoglobulin G (IgG), Immunoglobulin M (IgM), Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6), Tumor Necrosis Factor-alpha (TNF-α), and Interferon-gamma (IFN-γ) in broilers were significantly upregulated (p < 0.05), indicating immune system overactivation. Duodenal barrier-related genes Mucin 2 (MUC2), Occludin (OCLN), Claudin (CLDN1), and metabolism-related genes solute carrier family 5 member 1 (SLC5A1) and solute carrier family 7 member 9 (SLC7A9) were significantly downregulated (p < 0.05). The results of this trial demonstrate that, besides the microbiota, the gut virome and metabolites are also functional components contributing to the growth-promoting effect of FMT. The differential responses in the duodenum and jejunum reveal spatial heterogeneity and dual effects of FVT on the intestine. The negative effects limit the application of FMT/FVT. Identifying the primary functional components of FMT/FVT to develop safe and targeted microbial preparations is one potential solution.},
}

@article {pmid40870405,
year = {2025},
author = {Bibolar, AC and Nechita, VI and Lung, FC and Crecan-Suciu, BD and Păunescu, RL},
title = {Gut Feelings: Linking Dysbiosis to Depression-A Narrative Literature Review.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {61},
number = {8},
pages = {},
doi = {10.3390/medicina61081360},
pmid = {40870405},
issn = {1648-9144},
mesh = {Humans ; *Dysbiosis/complications/psychology/physiopathology/microbiology ; *Depression/microbiology/etiology/psychology/physiopathology ; *Gastrointestinal Microbiome/physiology ; Animals ; Probiotics/therapeutic use ; },
abstract = {The balance between physiological, psychological, and environmental factors often shapes human experience. In recent years, research has drawn attention to the gut microbiota as a significant contributor to brain function and emotional regulation. This narrative review examines how changes in gut microbiota may relate to depression. We selected studies that explore the link between intestinal dysbiosis and mood, focusing on mechanisms such as inflammation, vagus nerve signaling, HPA axis activation, gut permeability, and neurotransmitter balance. Most of the available data come from animal models, but findings from human studies suggest similar patterns. Findings are somewhat difficult to compare due to differences in measurement procedures and patient groups. However, several microbial shifts have been observed in people with depressive symptoms, and trials with probiotics or fecal microbiota transplant show potential. These results remain limited. We argue that these interventions deserve more attention, especially in cases of treatment-resistant or inflammation-driven depression. Understanding how the gut and brain interact could help define clearer subtypes of depression and guide new treatment approaches.},
}

Humans
*Dysbiosis/complications/psychology/physiopathology/microbiology
*Depression/microbiology/etiology/psychology/physiopathology
*Gastrointestinal Microbiome/physiology
Animals
Probiotics/therapeutic use

@article {pmid40869967,
year = {2025},
author = {Fu, Y and Bonifacio-Mundaca, J and Desterke, C and Casafont, Í and Mata-Garrido, J},
title = {Genomic Alterations and Microbiota Crosstalk in Hepatic Cancers: The Gut-Liver Axis in Tumorigenesis and Therapy.},
journal = {Genes},
volume = {16},
number = {8},
pages = {},
doi = {10.3390/genes16080920},
pmid = {40869967},
issn = {2073-4425},
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; *Liver Neoplasms/genetics/microbiology/therapy/pathology ; *Carcinoma, Hepatocellular/genetics/microbiology/therapy/pathology ; *Carcinogenesis/genetics ; Liver/pathology/metabolism/microbiology ; *Cholangiocarcinoma/genetics/microbiology/therapy ; Mutation ; Epigenesis, Genetic ; Animals ; },
abstract = {Background/Objectives: Hepatic cancers, including hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are major global health concerns due to rising incidence and limited therapeutic success. While traditional risk factors include chronic liver disease and environmental exposures, recent evidence underscores the significance of genetic alterations and gut microbiota in liver cancer development and progression. This review aims to integrate emerging knowledge on the interplay between host genomic changes and gut microbial dynamics in the pathogenesis and treatment of hepatic cancers. Methods: We conducted a comprehensive review of current literature on genetic and epigenetic drivers of HCC and CCA, focusing on commonly mutated genes such as TP53, CTNNB1, TERT, IDH1/2, and FGFR2. In parallel, we evaluated studies addressing the gut-liver axis, including the roles of dysbiosis, microbial metabolites, and immune modulation. Key clinical and preclinical findings were synthesized to explore how host-microbe interactions influence tumorigenesis and therapeutic response. Results: HCC and CCA exhibit distinct but overlapping genomic landscapes marked by recurrent mutations and epigenetic reprogramming. Alterations in the gut microbiota contribute to hepatic inflammation, genomic instability, and immune evasion, potentially enhancing oncogenic signaling pathways. Furthermore, microbiota composition appears to affect responses to immune checkpoint inhibitors. Emerging therapeutic strategies such as probiotics, fecal microbiota transplantation, and precision oncology based on mutational profiling demonstrate potential for personalized interventions. Conclusions: The integration of host genomics with microbial ecology provides a promising paradigm for advancing diagnostics and therapies in liver cancer. Targeting the gut-liver axis may complement genome-informed strategies to improve outcomes for patients with HCC and CCA.},
}

Humans
*Gastrointestinal Microbiome/genetics
*Liver Neoplasms/genetics/microbiology/therapy/pathology
*Carcinoma, Hepatocellular/genetics/microbiology/therapy/pathology
*Carcinogenesis/genetics
Liver/pathology/metabolism/microbiology
*Cholangiocarcinoma/genetics/microbiology/therapy
Mutation
Epigenesis, Genetic
Animals

@article {pmid40868265,
year = {2025},
author = {Haidar, L and Bănărescu, CF and Uța, C and Zimbru, EL and Zimbru, RI and Tîrziu, A and Pătrașcu, R and Șerb, AF and Georgescu, M and Nistor, D and Panaitescu, C},
title = {Beyond the Skin: Exploring the Gut-Skin Axis in Chronic Spontaneous Urticaria and Other Inflammatory Skin Diseases.},
journal = {Biomedicines},
volume = {13},
number = {8},
pages = {},
doi = {10.3390/biomedicines13082014},
pmid = {40868265},
issn = {2227-9059},
abstract = {Emerging evidence suggests a critical role of the gut microbiome in modulating systemic immune responses, with increasing relevance in dermatological diseases. Chronic spontaneous urticaria (CSU), traditionally viewed as an isolated cutaneous disorder, is now recognized as a systemic immune condition involving complex interactions between innate and adaptive immunity, mast cell dysregulation, and non-IgE-mediated pathways. This review explores the gut-skin axis as a unifying concept linking intestinal dysbiosis to inflammatory skin diseases, including atopic dermatitis, psoriasis, rosacea, and acne. Special emphasis is placed on CSU, where altered gut microbial composition, characterized by reduced diversity, depletion of short-chain fatty acid-producing bacteria, and expansion of Proteobacteria, may contribute to increased intestinal permeability, systemic immune activation via toll-like receptors, and heightened mast cell sensitivity. We discuss findings from animal models demonstrating that gut microbiota modulation can attenuate mast cell hyperreactivity and reduce urticarial symptoms. In parallel, we examine clinical evidence supporting the potential role of probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation as adjunctive strategies in CSU management. Despite promising findings, challenges remain in translating microbiome research into effective therapies due to interindividual variability, the complexity of host-microbiome interactions, and a lack of standardized protocols. Future research should focus on identifying predictive microbial patterns and developing personalized microbiome-targeted interventions. Understanding the bidirectional gut-skin relationship may open new therapeutic avenues beyond symptomatic treatment, positioning the microbiome as a novel target in CSU and related inflammatory dermatoses.},
}

@article {pmid40868053,
year = {2025},
author = {Maruyama, T and Ishikawa, D and Kurokawa, R and Masuoka, H and Nomura, K and Haraikawa, M and Orikasa, M and Odakura, R and Koma, M and Omori, M and Ishino, H and Ito, K and Shibuya, T and Suda, W and Nagahara, A},
title = {Hydrogen Gas Inhalation Improved Intestinal Microbiota in Ulcerative Colitis: A Randomised Double-Blind Placebo-Controlled Trial.},
journal = {Biomedicines},
volume = {13},
number = {8},
pages = {},
doi = {10.3390/biomedicines13081799},
pmid = {40868053},
issn = {2227-9059},
support = {None//MiZ Co., Ltd/ ; },
abstract = {Background/Objective: Dysbiosis is implicated in the pathogenesis of ulcerative colitis. Hydrogen has been reported to promote intestinal microbiota diversity and suppress ulcerative colitis progression in mice models. In this study, we investigated changes in the intestinal microbiota, therapeutic effects, and safety of hydrogen inhalation in patients with ulcerative colitis. Methods: In this randomised, double-blind, placebo-controlled trial, 10 active patients with ulcerative colitis (aged ≥20 years; Lichtiger's clinical activity index, 3-10; and Mayo endoscopic subscores ≥1) participated, and they were assigned to either a hydrogen or air inhalation group (hydrogen and placebo groups, respectively). All patients inhaled gas for 4 h every day for 8 weeks. Subsequently, we performed clinical indices and microbiota analyses using the metagenomic sequencing of stool samples before and after inhalation. Results: There was significant difference in the sum of the Mayo endoscopic subscores before and after inhalation in the clinical assessment indices. The hydrogen group showed higher α-diversity (p = 0.19), and the variation in β-diversity was markedly different, compared to the placebo group, in intestinal microbiota analysis (p = 0.02). Functional gene analysis revealed 115 significant genetic changes in the hydrogen group following treatment. No inhalation-related adverse events were observed. Conclusions: Hydrogen inhalation appeared to improve intestinal microbiota diversity; however, no clear therapeutic effect on ulcerative colitis was observed. Further studies are needed, and hydrogen inhalation may possibly lead to a logical solution combined with microbiome therapy, such as faecal microbiota transplantation, with fewer adverse events.},
}

@article {pmid40868023,
year = {2025},
author = {Kullar, R and Johnson, S and Goldstein, EJC},
title = {Clostridioides difficile in Peripartum Women: Review of Outcomes and Treatment.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {8},
pages = {},
doi = {10.3390/antibiotics14080829},
pmid = {40868023},
issn = {2079-6382},
abstract = {Background:Clostridioides difficile infection (CDI) is one of the most common healthcare-associated infections in the United States with increasing rates in younger patients and those in the community. CDI incidence may also be on the rise in peripartum women. Methods: We conducted a literature review to assess the incidence and outcomes of CDI in the peripartum population and review treatment options. Results: Peripartum patients have a high risk of complications and adverse events associated with CDI. Most patients have been treated with vancomycin or metronidazole; however, cases of patients recurring on standard treatment have been described, with patients having successful outcomes with fidaxomicin or fecal microbiota transplantation (FMT). Probiotics have been shown to be safe in peripartum women; however, the role in preventing primary and secondary CDI has not been studied. Conclusions: Peripartum women that develop CDI are at increased risk for complications. Treatment includes vancomycin, metronidazole, or fidaxomicin or FMT for recurrent cases.},
}

@article {pmid40867077,
year = {2025},
author = {Ebadi, M and Reddi, S and Senyshyn, L and Minot, SS and Gooley, T and Kabage, AJ and Lee, SJ and Hill, GR and Khoruts, A and Rashidi, A},
title = {Effect of fecal microbiota transplantation on gut microbiota functional profile in recipients of allogeneic hematopoietic cell transplantation.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2551882},
doi = {10.1080/19490976.2025.2551882},
pmid = {40867077},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; *Hematopoietic Stem Cell Transplantation/adverse effects ; *Gastrointestinal Microbiome ; Male ; Middle Aged ; Female ; Adult ; Bacteria/classification/genetics/isolation & purification/metabolism ; *Dysbiosis/therapy/microbiology ; Transplantation, Homologous ; Feces/microbiology ; Aged ; },
abstract = {Intestinal dysbiosis has been associated with both the effectiveness and toxicity of immunotherapy in cancer patients, inspiring multiple trials investigating fecal microbiota transplantation (FMT) in these patients. FMT restores microbial community structures damaged by antibiotics and enriches the microbiota with beneficial bacteria. However, the precise mechanism through which FMT exerts its effects and provides clinical benefits remains incompletely understood. Efforts to date have primarily focused on characterizing taxonomic changes following FMT. We hypothesized that FMT may also modify the functional pathways and metabolic capabilities of the gut microbiota, with possible clinical impact. To investigate this, we conducted a study involving 17 patients with blood disorders who received prophylactic FMT from one of the three healthy donors shortly after hematopoietic cell transplantation (HCT). By analyzing shotgun metagenomic profiles of the baseline, pre-FMT, and post-FMT gut microbiota, we demonstrate that FMT effectively restored pathways that had been depleted following HCT. However, it did not significantly reduce pathways that had expanded, indicating that FMT operates primarily through a restorative mechanism, reestablishing lost functional capabilities in the microbiota rather than suppressing overactive pathways. These findings highlight the potential for optimizing FMT protocols and identifying patient populations where FMT may be particularly beneficial.},
}

Humans
*Fecal Microbiota Transplantation
*Hematopoietic Stem Cell Transplantation/adverse effects
*Gastrointestinal Microbiome
Male
Middle Aged
Female
Adult
Bacteria/classification/genetics/isolation & purification/metabolism
*Dysbiosis/therapy/microbiology
Transplantation, Homologous
Feces/microbiology
Aged

@article {pmid40866789,
year = {2025},
author = {Kusakabe, S and Kurashige, R and Fukushima, K and Shimizu, K and Yoshihara, T and Motooka, D and Nakamura, S and Kurashige, M and Nakata, K and Hino, A and Kasahara, H and Ueda, T and Fujita, J and Hosen, N and Takehara, T and Oda, J},
title = {Fecal microbiota transplantation for Crohn's disease-like intestinal lesions arising after allogeneic stem cell transplantation.},
journal = {International journal of hematology},
volume = {},
number = {},
pages = {},
pmid = {40866789},
issn = {1865-3774},
abstract = {Several cases of inflammatory bowel disease (or similar gastrointestinal lesions) arising after allogeneic hematopoietic stem cell transplantation have been reported, but the effect of intestinal dysbiosis on development of these lesions remains unclear. We performed fecal microbiota transplantation (FMT) and 16S rRNA microbiome analysis in a patient who developed Crohn's disease-like lesions after allogeneic transplantation. A 62-year-old woman underwent haploidentical stem cell transplantation from her daughter to treat double-hit lymphoma relapsed after chimeric antigen receptor T-cell therapy, and achieved remission without developing acute graft-versus-host disease. Eight months later, she developed Crohn's disease-like intestinal lesions after cytomegalovirus enteritis. Her condition did not improve with the conventional treatment, so she underwent FMT from her daughter as part of a clinical trial. Diarrhea gradually improved, and follow-up endoscopy 4 months after the FMT showed ulcer healing and scarring. The 16S rRNA analysis revealed a reduction in the relative abundance of the Enterococcus genus after FMT, suggesting that dysbiosis may have contributed to lesion development. The patient is currently on a regular diet, with no symptom recurrence, and the primary disease remains in remission. Although this outcome suggests that FMT is effective, careful patient selection is required to reduce the risk of FMT-associated sepsis.},
}

@article {pmid40865967,
year = {2025},
author = {Jee, JJ and Park, S and Kim, J and Lee, H and Koh, H and Koo, BN},
title = {Bacterial extracellular vesicle as a predictive biomarker for postoperative delirium status after spinal surgery: a prospective cohort study.},
journal = {International journal of surgery (London, England)},
volume = {},
number = {},
pages = {},
doi = {10.1097/JS9.0000000000003024},
pmid = {40865967},
issn = {1743-9159},
abstract = {BACKGROUND: Prognostic factors significantly associated with postoperative delirium (POD) have been reported discordantly, possibly due to heterogeneous cohorts. Here, bacteria extracellular vesicles (BEVs) were introduced to predict the POD status of a unique patient cohort.

METHODS: One hundred twenty-eight patients who underwent spinal surgery participated in this prospective cohort study. Significant preoperative factors (i.e., baseline characteristics, and sequences of 16s rRNA genes from bloods and stools) between patients with and without delirium were subjected to random forest classifiers for prediction model, and potential metabolites that regulate the POD were inferred in silico.

RESULTS: No significant differences were found between patients with and without delirium in terms of demographics, anthropometrics, intervention history or preoperative cognitive function scores, except for circulating BEVs; delirium group had less diverse BEVs dominated with EVs from Gammaproteobacteria, whereas more diverse BEVs enriched with EVs from Bacilli and Alphaproteobacteria were significantly associated with non-delirium. Compared to that with baseline characteristics or gut microbiome, prediction model using random forest classifier with the significant BEVs yielded the lowest error rate of 21.59%, and was validated with an independent data set, resulting in 80% accuracy. Moreover, EVs from Moraxellaceae and Acinetobacter showed the highest probabilities of prediction of the POD despite their low relative abundance, indicating the most significant prognostic markers for the POD. As the inference of a potential metabolites that regulate the POD, succinate and enterobacterial common antigens delivered from BEV cargo were expected to participate in pathogenic events, whereas S-methyl-5'-thioadenosine, 2-oxoglutarate, pyruvate, acetate and butyrate may play a neuroprotective role in the POD.

CONCLUSIONS: The profile of circulating preoperative BEVs is the key prognostic factor for distinguishing POD in elderly surgical patients with controlled baseline conditions. Metabolites of defensive and offensive mechanisms inferred from BEVs will be essential for developing next-generation POD prevention strategies.},
}

@article {pmid40865561,
year = {2025},
author = {Wei, S and Lu, J},
title = {Microbial Modulation of the Gut-Liver Axis in Autoimmune Liver Diseases.},
journal = {Seminars in liver disease},
volume = {},
number = {},
pages = {},
doi = {10.1055/a-2679-3641},
pmid = {40865561},
issn = {1098-8971},
abstract = {Autoimmune liver diseases (AILDs), including autoimmune hepatitis, primary biliary cholangitis, and primary sclerosing cholangitis, are chronic inflammatory conditions influenced by complex interactions among genetic, environmental, and immunological factors. Recent studies have highlighted the critical role of the gut microbiota in regulating immune responses beyond the gastrointestinal tract via the gut-liver axis. This review examines the interactions between intestinal microecology and AILDs, with a focus on mechanisms such as bacterial translocation, disruption of the intestinal barrier, and modulation of microbial metabolites. Dysbiosis, involving alterations in both bacterial and fungal communities, has been associated with immune dysregulation and hepatic inflammation. Evidence indicates that short-chain fatty acids, bile acids, and microbial products such as lipopolysaccharides influence hepatic immune tolerance and inflammatory signaling pathways. Several diagnostic and therapeutic approaches, including probiotics, fecal microbiota transplantation, and bile acid regulation, have shown potential to slow or alter disease progression. However, the clinical translation of these findings remains limited due to interindividual variability and the complex nature of the gut-liver axis. Continued research is needed to develop precision medicine strategies that can harness intestinal microecology for improved management of AILDs.},
}

@article {pmid40865528,
year = {2025},
author = {Shi, Y and Li, Y and Li, H and Haerheng, A and Marcelino, VR and Lu, M and Lemey, P and Tang, J and Bi, Y and Pettersson, JH and Bohlin, J and Klaps, J and Wu, Z and Wan, W and Sun, B and Kang, M and Holmes, EC and He, N and Su, S},
title = {Extensive cross-species transmission of pathogens and antibiotic resistance genes in mammals neglected by public health surveillance.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2025.08.016},
pmid = {40865528},
issn = {1097-4172},
abstract = {Non-traditional farmed and wild mammals are often neglected in pathogen surveillance. Through metagenomic and metatranscriptomic sequencing of fecal and tissue samples from 973 asymptomatic mammals, we identified 128 viruses (30 novel), including a new coronavirus genus, 10,255 bacterial species (over 7,000 undescribed), 201 fungi, and 7 parasites. Farmed and wild mammals shared 13.3% of virus species, including canine coronavirus in Asiatic black bears and Getah virus in rabbits, while the 2.3.4.4b clade of H5N1 avian influenza virus was found in a wild leopard cat. We identified potential bacterial pathogen transmission between farmed and wild mammals and bacterial strains with high genetic similarity to those found in humans. We observed 157 clinically prioritized antibiotic resistance genes (ARGs) in mammalian microbiomes with greater than 99% identity to ARGs from human microbiomes, often co-occurring with mobile genetic elements. Overall, this work highlights cross-species risks at the human-animal interface.},
}

@article {pmid40865242,
year = {2025},
author = {Zhang, Y and Chen, Q and Xu, Y and Lv, Y and Wang, Y and Shi, XY and Liu, J and Wen, J and Li, X and Li, B},
title = {Soy isoflavones mitigate atrazine-induced dopaminergic neuron damage via reshaping short-chain fatty acid-producing bacteria in gut microbiota and modulating the GPR43/GLP-1/GLP-1R axis.},
journal = {Ecotoxicology and environmental safety},
volume = {303},
number = {},
pages = {118938},
doi = {10.1016/j.ecoenv.2025.118938},
pmid = {40865242},
issn = {1090-2414},
abstract = {Atrazine (ATR), a widely used herbicide, is linked to dopaminergic neurotoxicity and persistent gut microbiota dysbiosis after early life exposure. However, whether the gut microbiota mediates ATR-induced loss of dopaminergic neurons remains unclear. Mice were exposed to ATR from juvenility (4th week) until adulthood (12th week), after which exposure ceased until the 20th week. The role of gut microbiota was confirmed through fecal microbiota transplantation (FMT), which was classified into different groups based on the donor's ATR treatment status. 16S rRNA sequencing revealed that Akkermansia, which exhibited significant differences across FMT groups, is a classic short-chain fatty acid (SCFA)-producing bacteria. FMT recipients receiving ATR-donor microbiota exhibited reduced colonic G Protein-Coupled Receptor 43 (GPR43), serum Glucagon-like Peptide-1 (GLP-1), and substantia nigra Glucagon-like Peptide-1 receptor (GLP-1R)/Tyrosine hydroxylase (TH) levels. Soy isoflavones (SIF), selected for their dual prebiotic and neuroprotective effects, attenuated ATR-induced dopaminergic neurotoxicity by enriching SCFA-producing gut microbiota and the level of SCFAs, thereby activating the GPR43/GLP-1/GLP-1R axis and reducing neuronal loss. These findings demonstrate the critical role of gut microbiota in ATR-induced dopaminergic neurodegeneration, positioning SIF-mediated microbiota modulation as a promising therapeutic approach within the "food-medicine homology" framework.},
}

@article {pmid40863733,
year = {2025},
author = {Alaeddin, S and Ko, Y and Steiner-Lim, GZ and Jensen, SO and Roberts, TL and Ho, V},
title = {The Effect of Faecal Microbiota Transplantation on Cognitive Function in Cognitively Healthy Adults with Irritable Bowel Syndrome: Protocol for a Randomised, Placebo-Controlled, Double-Blinded Pilot Study.},
journal = {Methods and protocols},
volume = {8},
number = {4},
pages = {},
pmid = {40863733},
issn = {2409-9279},
abstract = {Faecal microbiota transplantation (FMT) is an emerging therapy for gastrointestinal and neurological disorders, acting via the microbiota-gut-brain axis. Altering gut microbial composition may influence cognitive function, but this has not been tested in cognitively healthy adults. This randomised, double-blinded, placebo-controlled pilot trial investigates whether FMT is feasible and improves cognition in adults with irritable bowel syndrome (IBS). Participants receive a single dose of FMT or placebo via rectal retention enema. Cognitive performance is the primary outcome, assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Secondary outcomes include IBS symptom severity and mood. Tertiary outcomes include microbiome composition and plasma biomarkers related to inflammation, short-chain fatty acids, and tryptophan metabolism. Outcomes are assessed at baseline and at one, three, six, and twelve months following treatment. We hypothesise that FMT will lead to greater improvements in cognitive performance than placebo, with benefits extending beyond practice effects, emerging at one month and persisting in the long term. The findings will contribute to evaluating the safety and efficacy of FMT and enhance our understanding of gut-brain interactions.},
}

@article {pmid40861872,
year = {2025},
author = {Baydoun, H and Hussain, N and Wu, KO and Kelly, CR and Fischer, M},
title = {What's New and What's Next in Fecal Microbiota Transplantation?.},
journal = {Biologics : targets & therapy},
volume = {19},
number = {},
pages = {481-496},
pmid = {40861872},
issn = {1177-5475},
abstract = {Fecal microbiota transplantation (FMT) has evolved from a niche therapy to a cornerstone in the treatment of recurrent Clostridioides difficile infection (rCDI). Initially introduced in the 1950s, its relevance has surged with the emergence of virulent and antibiotic-resistant C. difficile strains. In recent years, the FDA approved two standardized microbiota-based therapeutics-Rebyota™ (fecal microbiota, live-jslm) and Vowst™ (fecal microbiota spores, live-brpk)-for rCDI prevention. Multiple pivotal trials support the efficacy and safety of both traditional FMT and the FDA-approved prescription FMTs, with sustained response rates surpassing 80% in select populations. In parallel, live biotherapeutic products (LBPs)-donor independent, well-defined microbial consortia produced in laboratory setting are under development. Examples include VE303 and NTCD-M3, a single non-toxigenic C. difficile strain (M3). Beyond the FDA approved therapeutics, conventional FMT is gaining traction as a potential treatment for severe or fulminant CDI, especially in patients not responding to antibiotics and ineligible for surgery. Investigational indications include decolonizing multidrug-resistant organisms and treatment of noninfectious conditions such as inflammatory bowel disease, irritable bowel syndrome, liver disease, and metabolic syndrome. Given the differing pathophysiology of these conditions, a tailored approach supported by rigorous clinical trials is essential. Although there is a growing shift, particularly in the United States, toward the use of FDA-approved FMTs, global practices remain heterogeneous, with conventional FMT still widely employed. Meanwhile, regulatory pathways and clinical guidelines for microbiota-derived biologics and live biotherapeutic products continue to evolve. In this manuscript, we provide an update on the emerging use of FDA-approved prescription microbiota-derived therapeutics for the prevention of rCDI, review data on investigational agents including both donor dependent and donor independent microbial products, and summarize current evidence on the use of conventional FMT for indications beyond prevention of rCDI.},
}

@article {pmid40861794,
year = {2025},
author = {Wang, B and Stephen, SJ and Cyphert, EL and Liu, C and Hernandez, CJ and Vashishth, D},
title = {Fecal microbiota transplantation in mice improves bone material properties through altered mineral quality.},
journal = {JBMR plus},
volume = {9},
number = {9},
pages = {ziaf115},
pmid = {40861794},
issn = {2473-4039},
abstract = {Disruptions of the composition of the gut microbiome are linked to impaired bone tissue strength. Fecal microbiota transplantation (FMT) is an established clinical therapy that can restore a healthy gut microbiome and reduce systemic inflammation. However, whether FMT from a healthy donor could rescue bone fragility is unknown. As induced inflammation causes mineralization defects, we hypothesize that manipulations of the gut microbiota alter bone fracture resilience through changes in mineral quality. Here, we altered the compositions of the gut microbiome in mice via antibiotics (ampicillin and neomycin) and FMT. Mice were allocated to 5 groups (M/F, N = 13-18/group): Unaltered, Continuous (dosed 4-24 wk), Initial (dosed 4-16 wk), Reconstituted (dosed 4-16 wk with subsequent FMT from age- and sex-matched mice with unaltered gut microbiota), and Delayed (dosed 16-24 wk). Fracture toughness testing and Raman spectroscopy were conducted on the femora. The maximum toughness was greater in the Reconstituted group (for females, p < .05 compared to Continuous, Unaltered, and Delayed groups; for males, p < .05 compared to groups with antibiotic dosing). The Reconstituted group showed lower type-B carbonate substitution in the bone mineral (all p < .01 for both sexes), and lower mineral-to-matrix ratio (all p < .01 for males, for females, p < .01 compared to Unaltered, Initial, and Delayed groups). In females, mineral crystallinity was higher in the Reconstituted group than those dosed with antibiotics (all p < .05). Serum inflammation marker TNF-α was positively correlated with type-B carbonate substitutions (ρ = 0.66), mineral-to-matrix ratio (ρ = 0.71), and carboxymethyl-lysine (CML) in bone matrix (ρ = 0.43). Enhanced bone maximum fracture toughness was associated with reduced type-B carbonate substitution (r = -0.45), decreased mineral-to-matrix ratio (r = -0.40), increased mineral crystallinity (r = 0.33), and lower levels of bone CML (r = -0.49, all p < .01). These results suggest that the introduction of more beneficial gut microbiota can increase fracture resistance by modifying mineral composition and quality, likely through the reduction of systemic inflammation.},
}

@article {pmid40861764,
year = {2025},
author = {Mishra, AP and Marrelli, LM and Bonner-Reid, FT and Shekhawat, P and Toney, R and Benipal, IK and Dias, HA and Kandi, A and Siddiqui, HF},
title = {Gut-Brain Axis: Understanding the Interlink Between Alterations in the Gut Microbiota and Autism Spectrum Disorder.},
journal = {Cureus},
volume = {17},
number = {7},
pages = {e88579},
pmid = {40861764},
issn = {2168-8184},
abstract = {Autism spectrum disorder (ASD) is an umbrella term used for a complex neurobehavioral disorder. ASD is a multifactorial condition, with significant roles played by environmental, immunological, and genetic factors. The microbiota-gut-brain axis has been implicated in the pathophysiology of ASD in recent years. This review article aims to explore the correlation between gut dysbiosis and autism, and its potential impact on management strategies. Gastrointestinal (GI) symptoms, including diarrhea, constipation, and bloating, are prevalent among children with ASD. These disorders are commonly linked to increased behavioral symptoms, such as social disengagement, anxiety, and irritability. Increased gut permeability, attributable to gut dysbiosis, plays a significant role in disrupting the gut-brain axis, which is coordinated by neurological, immunological, and endocrinological routes. Elevated levels of inflammatory cytokines, changes in the generation of neurotransmitters, and disturbances in gut-derived metabolites are all considered direct consequences of dysbiosis. Treatment options, including probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary changes, have shown promising results. However, the effectiveness and long-term safety of these therapies are still being studied. It is imperative to explore this perplexing interaction through further research to encourage clinicians to adopt therapeutic approaches targeting the gut microbiota in patients with ASD.},
}

@article {pmid40861492,
year = {2025},
author = {Yu, X and Yu, X and Wang, Y and Guo, X and Wang, C and Wang, F},
title = {Respiratory diseases and the gut microbiota: an updated review.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1629005},
pmid = {40861492},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Dysbiosis/microbiology ; COVID-19/microbiology ; Lung/microbiology/immunology ; *Respiratory Tract Diseases/microbiology ; SARS-CoV-2 ; Probiotics ; Animals ; Pulmonary Disease, Chronic Obstructive/microbiology ; },
abstract = {The gut microbiota constitutes a vital ecosystem within the human body playing a pivotal role in immune regulation and metabolic homeostasis. Emerging research underscores a sophisticated interplay between the gut and lungs, termed the "gut-lung axis." Gut microbes exert influence over pulmonary immunity and metabolism via immune mediators (e.g., cytokines and interleukins), metabolites (e.g., short-chain fatty acids) and direct microbial translocation. Dysbiosis of the gut microbiota has been implicated in a spectrum of respiratory diseases, including asthma, chronic obstructive pulmonary disease (COPD), acute lung injury (ALI), Coronavirus Disease 2019 (COVID-19), lung cancer, idiopathic pulmonary fibrosis (IPF), pulmonary arterial hypertension (PAH), acute lower respiratory infection (ALRI) and tuberculosis (TB). Although multi-omics technologies have elucidated certain mechanisms underlying the gut-lung axis, numerous pathways remain to be fully delineated. This review synthesizes current knowledge on the role of gut microbiota and their metabolites in respiratory diseases and assesses their therapeutic potential. Future investigations should prioritize strategies to restore and maintain microbial homeostasis, such as dietary modifications, probiotic supplementation and fecal microbiota transplantation to pioneer novel preventive and therapeutic approaches. These summaries of advances in gut microbiology research promise better management and exploration of therapeutic strategies for respiratory diseases.},
}

Humans
*Gastrointestinal Microbiome/physiology
Dysbiosis/microbiology
COVID-19/microbiology
Lung/microbiology/immunology
*Respiratory Tract Diseases/microbiology
SARS-CoV-2
Probiotics
Animals
Pulmonary Disease, Chronic Obstructive/microbiology

@article {pmid40861487,
year = {2025},
author = {Tao, W and Yu, Y and Tan, D and Huang, X and Huang, J and Lin, C and Yu, R},
title = {Microbiota and enteric nervous system crosstalk in diabetic gastroenteropathy: bridging mechanistic insights to microbiome-based therapies.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1603442},
pmid = {40861487},
issn = {2235-2988},
mesh = {Humans ; *Enteric Nervous System/physiopathology ; *Gastrointestinal Microbiome/physiology ; Dysbiosis/microbiology ; Animals ; *Gastrointestinal Diseases/microbiology/therapy ; *Diabetes Complications/microbiology/therapy ; },
abstract = {Diabetes mellitus has emerged as a global public health crisis, with over half of patients experiencing gastrointestinal (GI) symptoms that exacerbate glucose fluctuations and impair quality of life. While prior research on the pathophysiology of diabetic gastroenteropathy (DGE) focused primarily on autonomic neuropathy, particularly involving the vagus nerve, recent studies have shifted toward the impairment of the enteric nervous system (ENS). As the largest autonomous neural network governing GI motility independent of central control, structural and functional abnormalities of the ENS constitute the fundamental pathological basis for DGE. This review first delineates gut microbial alterations in diabetes and mechanisms by which dysbiosis compromises the integrity of the ENS. Second, we analyze how microbiota-derived metabolites (short-chain fatty acids, bile acids, tryptophan), gut hormones (glucagon-like peptide-1, ghrelin), and neurotransmitters (acetylcholine, vasoactive intestinal peptide, nitric oxide) multitarget the ENS-collectively establishing the "microbiota-ENS axis" as the central hub for GI sensorimotor control. Finally, we provide an overview of preclinical and clinical evidence for microbiome-targeted therapies (probiotics, prebiotics, fecal microbiota transplantation) in alleviating DGE symptoms and repairing ENS while outlining translational challenges and future research priorities.},
}

Humans
*Enteric Nervous System/physiopathology
*Gastrointestinal Microbiome/physiology
Dysbiosis/microbiology
Animals
*Gastrointestinal Diseases/microbiology/therapy
*Diabetes Complications/microbiology/therapy

@article {pmid40860437,
year = {2025},
author = {Ma, C and He, H and Wang, K and Guo, J and Liu, L and Chen, Y and Li, B and Xiao, H and Li, X and Lu, X and Wang, T and Wen, Y and Wang, H and Chen, L},
title = {Maternal gut microbiota-derived daidzein prevents osteoporosis in female offspring following prenatal prednisone exposure.},
journal = {iMeta},
volume = {4},
number = {4},
pages = {e70037},
pmid = {40860437},
issn = {2770-596X},
abstract = {Prenatal exposure to glucocorticoids is linked to long-term health risks in offspring, but the role of maternal gut microbiota in mediating these effects remains unclear. Here, we demonstrate that prenatal prednisone therapy (PPT) in humans and prenatal prednisone exposure (PPE) in rats result in sex-specific long bone dysplasia in offspring, including reduced peak bone mass (PBM) and heightened osteoporosis risk in female offspring. Multi-omics profiling and fecal microbiota transplantation show that PPE alters maternal gut microbiota composition and depletes the microbial metabolite daidzein (DAI). DAI deficiency suppresses Hoxd12 expression, impairs osteogenesis, and leads to PBM decline in female offspring. In bone marrow-derived mesenchymal stem cells from PPE female offspring, DAI promoted Hoxd12 expression and osteogenic differentiation. Notably, DAI supplementation restored H3K9ac levels, enhanced Hoxd12 expression, and promoted osteogenic differentiation through the ERβ/KAT6A pathway. Furthermore, maternal DAI supplementation during pregnancy prevented osteoporosis susceptibility in PPE female offspring and alleviated functional abnormalities in multiple organs, including the liver, hippocampus, ovary, and adrenal gland. In conclusion, PPE induces multiorgan dysplasia and increases disease predisposition (e.g., osteoporosis) in female offspring by disrupting maternal gut microbiota and depleting DAI. Maternal DAI supplementation provides a promising preventive strategy to counteract these adverse outcomes.},
}

@article {pmid40860435,
year = {2025},
author = {Wang, C and Liu, Z and Zhou, T and Wu, J and Feng, F and Wang, S and Chi, Q and Sha, Y and Zha, S and Shu, S and Qu, L and Du, Q and Yu, H and Yang, L and Malashicheva, A and Dong, N and Xie, F and Wang, G and Xu, K},
title = {Gut microbiota-derived butyric acid regulates calcific aortic valve disease pathogenesis by modulating GAPDH lactylation and butyrylation.},
journal = {iMeta},
volume = {4},
number = {4},
pages = {e70048},
pmid = {40860435},
issn = {2770-596X},
abstract = {The involvement of gut microbiota in calcific aortic valve disease (CAVD) pathogenesis remains underexplored. Here, we provide evidence for a strong association between the gut microbiota and CAVD development. ApoE[-/-] mice were stratified into easy- and difficult- to calcify groups using neural network and cluster analyses, and subsequent faecal transplantation and dirty cage sharing experiments demonstrated that the microbiota from difficult-to-calcify mice significantly ameliorated CAVD. 16S rRNA sequencing revealed that reduced abundance of Faecalibacterium prausnitzii (F. prausnitzii) was significantly associated with increased calcification severity. Association analysis identified F. prausnitzii-derived butyric acid as a key anti-calcific metabolite. These findings were validated in a clinical cohort (25 CAVD patients vs. 25 controls), where serum butyric acid levels inversely correlated with disease severity. Functional experiments showed that butyric acid effectively hindered osteogenic differentiation in human aortic valve interstitial cells (hVICs) and attenuated CAVD progression in mice. Isotope labeling and [13]C flux analyses confirmed that butyric acid produced in the intestine can reach heart tissue, where it reshapes glycolysis by specifically modifying GAPDH. Mechanistically, butyric acid-induced butyrylation (Kbu) at lysine 263 of GAPDH competitively inhibited lactylation (Kla) at the same site, thereby counteracting glycolysis-driven calcification. These findings uncover a novel mechanism through which F. prausnitzii and its metabolite butyric acid contribute to the preservation of valve function in CAVD, highlighting the gut microbiota-metabolite-glycolysis axis as a promising therapeutic target.},
}

@article {pmid40860180,
year = {2025},
author = {Pan, Z and Jin, X and Li, Q and Zhou, Y and Zeng, Y and Wang, X and Jin, Y and Chen, Y and Li, D and Ling, W},
title = {Citrus Pectin Supplementation Alleviated Hepatic Lipid Accumulation through Gut Microbiota Indole Lactic Acid Promoting Hepatic Bile Acid Synthesis and Excretion.},
journal = {International journal of biological sciences},
volume = {21},
number = {11},
pages = {5015-5033},
pmid = {40860180},
issn = {1449-2288},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Pectins/pharmacology ; Mice ; *Bile Acids and Salts/metabolism/biosynthesis ; Male ; *Liver/metabolism/drug effects ; Mice, Inbred C57BL ; *Lipid Metabolism/drug effects ; *Indoles/metabolism ; Diet, High-Fat ; Dietary Supplements ; },
abstract = {Metabolic-associated fatty liver disease (MAFLD) represents a critical global health challenge. A few studies have suggested that citrus pectin may confer protective effects against MAFLD; however, the underlying mechanism remains unclear. The gut microbiota and its metabolites strongly contribute to MAFLD regulation by the gut‒liver axis. The present study explored the influence of pectin intervention on liver lipid accumulation in high-fat and high-sugar diet-fed mouse models. Pectin supplementation alleviated hepatic lipid accumulation and substantially restructured the gut microbial communities, particularly enhancing the proliferation of Akkermansia muciniphila (A. muciniphila) and Escherichia coli (E. coli), which subsequently increased indole-3-lactic acid (ILA) production. Mechanistic investigations revealed that ILA upregulated hepatic CYP7A1 and FXR-BSEP expression, stimulating hepatic bile acid biosynthesis and biliary excretion to alleviate liver steatosis. Results of previous fecal microbiota transplantation (FMT) and antibiotic-mediated microbial dysbiosis studies have confirmed the microbiota-dependent nature of the therapeutic effects of pectin. Furthermore, the administration of exogenous ILA has been demonstrated to be an effective intervention for the rescue of metabolic dysregulation in dysbacteriosis mouse models. This work delineated an unrecognized dietary pectin-microbiota-ILA-hepatic bile acid synthesis and excretion regulatory axis for the improvement of MAFLD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Pectins/pharmacology
Mice
*Bile Acids and Salts/metabolism/biosynthesis
Male
*Liver/metabolism/drug effects
Mice, Inbred C57BL
*Lipid Metabolism/drug effects
*Indoles/metabolism
Diet, High-Fat
Dietary Supplements

@article {pmid40859356,
year = {2025},
author = {Yang, K and Du, J and Huang, F and Si, Y and Gu, Y and Xu, N and Fan, Z and Xue, R and Wang, P and Yao, X and Liu, H and Li, X and Xu, J and Wang, Z and Sun, J and Chen, Y and Xuan, L and Liu, Q},
title = {Fecal microbiota transplantation for refractory chronic graft-versus-host disease after allogeneic hematopoietic cell transplantation: a pilot open-label, non-placebo-controlled study.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {498},
pmid = {40859356},
issn = {1741-7015},
support = {2023M741581, 2024T170387, GZC20231061//China Postdoctoral Science Foundation/ ; 2023KF04//Open Research Funds of the State Key Laboratory of Ophthalmology/ ; 2025A1515010737//GuangDong Basic and Applied Basic Research Foundation/ ; 82293634, 82170213, 82370216//Major Program of National Natural Science Foundation of China/ ; 2022YFA1105003, 2022YFC2502600-5//National Key Research and the Development Program of China/ ; },
mesh = {Humans ; *Graft vs Host Disease/therapy/etiology/microbiology ; *Fecal Microbiota Transplantation/methods ; Male ; Female ; Middle Aged ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Pilot Projects ; Adult ; Gastrointestinal Microbiome ; Chronic Disease ; Transplantation, Homologous ; Young Adult ; Treatment Outcome ; Feces/microbiology ; },
abstract = {BACKGROUND: Dysbiosis of the intestinal microbiota plays a crucial role in the initiation and development of graft-versus-host disease (GVHD). Fecal microbiota transplantation (FMT) has been reported to be effective for refractory acute GVHD; however, whether FMT is effective for refractory chronic GVHD (cGVHD) remains unknown.

METHODS: To investigate the efficacy and safety of FMT for refractory cGVHD and the underlying mechanism, 12 patients with refractory cGVHD received FMT via colonoscopy, and the response was evaluated at 12 weeks after FMT.

RESULTS: Among the 12 patients who underwent FMT, 1 patient achieved a complete response, and 5 patients achieved a partial response. Patients with refractory cGVHD presented lower α diversity and higher abundance of Escherichia-Shigella and Enterobacteriaceae. FMT increased gut microbial diversity, increased the abundance of short-chain fatty acid (SCFA)-producing bacteria, and decreased the abundance of Escherichia-Shigella and Enterobacteriaceae in responder patients. Moreover, it increased SCFA levels in fecal samples from the responder group and promoted the expansion of peripheral CD4[+]CD127[-] regulatory T (Treg) cells. Colon pathological examination revealed that CD4[+] T and CD19[+] B cell infiltration decreased and that CD4[+] Treg infiltration increased after FMT.

CONCLUSIONS: The results of the present study suggest that FMT is feasible and deserves further investigation for use in patients with refractory cGVHD.

TRIAL REGISTRATION: ClinicalTrials.gov (NCT06938165).},
}

Humans
*Graft vs Host Disease/therapy/etiology/microbiology
*Fecal Microbiota Transplantation/methods
Male
Female
Middle Aged
*Hematopoietic Stem Cell Transplantation/adverse effects
Pilot Projects
Adult
Gastrointestinal Microbiome
Chronic Disease
Transplantation, Homologous
Young Adult
Treatment Outcome
Feces/microbiology

@article {pmid40858171,
year = {2025},
author = {Lin, W and Wang, X and Zhuang, T and Wang, Z and Yang, L and Wang, X and Ding, L and Tao, F},
title = {Lithospermum erythrorhizon polysaccharide alleviates obesity via gut microbiota-mediated reprogramming of bile acid and short-chain fatty acid metabolism.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {147082},
doi = {10.1016/j.ijbiomac.2025.147082},
pmid = {40858171},
issn = {1879-0003},
abstract = {Lithospermum erythrorhizon, a traditional Chinese medicinal herb and functional food ingredient, contains bioactive soluble polysaccharide with documented anti-obesity and metabolic regulatory properties. However, the precise mechanisms underlying the anti-obesity effects of Lithospermum erythrorhizon polysaccharide (LEP) fraction remain poorly characterized. In this study, diet-induced obese (DIO) mice treated with LEP exhibited significant suppression of body weight gain and hepatic lipid deposition, accompanied by improved liver function and elevated systemic energy expenditure. Mechanistic investigations revealed that LEP administration selectively suppressed the intestinal colonization of bile salt hydrolase (BSH)-producing bacterial taxa, leading to increased circulating levels of taurine-conjugated bile acids and enhanced cecal short-chain fatty acids (SCFAs) production. Concurrently, LEP activated adipose tissue thermogenesis, as evidenced by upregulated expression of thermogenic markers. Antibiotic-induced gut microbiota ablation abolished these metabolic benefits, whereas fecal microbiota transplantation from LEP-treated mice recapitulated the anti-obesity phenotype in recipient animals. These results establish that LEP ameliorates obesity through a gut microbiota-dependent mechanism involving BSH inhibition, taurine-conjugated bile acid accumulation, SCFAs elevation, and subsequent activation of adipose thermogenic pathways. These findings highlight the potential of LEP as a dietary supplement or microbiota-targeted intervention for obesity management.},
}

@article {pmid40856929,
year = {2025},
author = {Yan, C and Chen, Y and Tian, Y and Hu, S and Wang, H and Zhang, X and Chu, Q and Huang, S and Sun, W},
title = {The emerging role of microbiota in lung cancer: a new perspective on lung cancer development and treatment.},
journal = {Cellular oncology (Dordrecht, Netherlands)},
volume = {},
number = {},
pages = {},
pmid = {40856929},
issn = {2211-3436},
support = {Y-2023AZMETQN-0066//Beijing Xisike Clinical Oncology Research Foundation/ ; 62131009//National Natural Science Foundation of China/ ; },
abstract = {Lung cancer remains the leading cause of cancer-related mortality worldwide, with limited treatment efficacy and frequent resistance to conventional therapies. Recent advances have uncovered the critical influence of the human microbiota-complex communities of bacteria, viruses, fungi, and other microorganisms-on lung cancer pathogenesis and therapeutic responses. This review synthesizes current knowledge on the compositional and functional roles of microbiota across multiple body sites, including the gut, lung, tumor microenvironment, circulation, and oral cavity, highlighting their contributions to tumor initiation, progression, metastasis, and immune regulation. We emphasize the bidirectional communication between microbial metabolites and host immune pathways, particularly the gut-lung axis, which modulates systemic and local antitumor immunity. Importantly, microbiota composition has been linked to differential responses and toxicities in chemotherapy, radiotherapy, targeted therapy, and immune checkpoint blockade. Microbiota-targeted interventions, such as probiotics, fecal microbiota transplantation, and selective antibiotics, show promising potential to enhance treatment efficacy and mitigate adverse effects. However, challenges remain in clinical translation due to interindividual microbiome variability, mechanistic complexities, and limited longitudinal data. Future research integrating multi-omics, microbial functional profiling, and controlled clinical trials is essential to harness the microbiome as a precision medicine tool in lung cancer management. This review provides a comprehensive overview of the emerging role of microbiota in lung cancer development and therapy, offering new perspectives for innovative therapeutic strategies.},
}

@article {pmid40852996,
year = {2025},
author = {Zhou, Y and Lei, M and Cai, W and Chang, Z and An, L and Zhang, S and Wei, D and Jiao, R and Gao, J and Xu, Y and Yang, H and Zhu, M and Cao, J and Li, S and Duan, X and Wu, W},
title = {Human fecal microbiota transplantation attenuates high dietary oxalate-induced renal calcium oxalate crystal depositions in rats via repairing Allobaculum-related gut barrier damage.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0081025},
doi = {10.1128/msystems.00810-25},
pmid = {40852996},
issn = {2379-5077},
abstract = {UNLABELLED: High dietary oxalate (HDOx) diet is a key factor in kidney stone formation, with gut microbiota playing a significant role. Although several studies have indicated that fecal microbiota transplantation from healthy animals can effectively reduce renal calcium oxalate (CaOx) depositions in rats, the gut microbiota composition between human and animal still remains different. This study aims to explore the effect and underlying mechanisms of healthy human-source fecal microbiota transplantation (hFMT) on CaOx crystal depositions, providing new evidence for its potential clinical application in hyperoxaluria and kidney stone treatment. First, fecal microbiota were screened and collected from healthy individuals and transplanted into rats fed with hydroxyproline. We found that hFMT effectively inhibited crystal depositions and kidney injury induced by HDOx diet, regardless of antibiotic pretreatment. Additionally, 16S rDNA sequencing of gut microbiota identified that hFMT treatment reversed HDOx-induced gut microbiota composition change, particularly restoring the abundance and ecological network of Allobaculum, which was a key indicator genus associated with CaOx crystal depositions. Compared to controls, the abundance of Allobaculum was increased in fecal samples from kidney stone patients and another rat model fed with potassium oxalate. Mechanistically, hFMT markedly attenuated HDOx-induced intestinal barrier disruption to reverse the formation of CaOx crystallization. These findings suggest that HDOx diets could significantly influence the rat gut microbiota. hFMT effectively reduces HDOx-induced renal CaOx crystal depositions and kidney injury via repairing Allobaculum-related gut barrier damage in rats. These findings underscore the potential of hFMT as a therapeutic strategy for hyperoxaluria and kidney stone treatment.

IMPORTANCE: This study investigated that healthy hFMT could serve as a novel strategy to inhibit kidney CaOx deposition induced by HDOx diet. By transplanting healthy human gut microbiota into HDOx rats, we found that hFMT significantly reduced CaOx crystal depositions and kidney damage. The treatment also restored the gut microbiota composition, particularly the abundance of Allobaculum, a genus closely associated with CaOx crystal depositions. Importantly, hFMT restored intestinal barrier function, providing a new mechanistic insight into the gut-kidney axis in kidney stone formation. These findings highlight hFMT's potential as a therapeutic strategy for managing hyperoxaluria and kidney stone, offering a promising alternative to traditional treatment.},
}

@article {pmid40852937,
year = {2025},
author = {Ullern, A and Holm, K and Andresen, NK and Røssevold, AH and Bang, C and Naume, B and Hov, JR and Kyte, JA},
title = {Gut microbiota diversity is prognostic in metastatic hormone receptor-positive breast cancer patients receiving chemotherapy and immunotherapy.},
journal = {Molecular oncology},
volume = {},
number = {},
pages = {},
doi = {10.1002/1878-0261.70117},
pmid = {40852937},
issn = {1878-0261},
support = {802544/ERC_/European Research Council/International ; CA209-9FN//Bristol Myers Squibb Foundation/ ; 214972/WT_/Wellcome Trust/United Kingdom ; 272910//Norwegian Cancer Society/Norwegian Breast Cancer Society/ ; 2018090//Norwegian Health Region South-East/ ; 2017100//Norwegian Health Region South-East/ ; },
abstract = {Immune checkpoint blockade (ICB) is standard treatment in several cancer types, despite not being proven efficacious in metastatic hormone receptor-positive breast cancer (HR+ mBC). The gut microbiota is associated with patient outcome and toxicity from cancer therapy, although limited data are available for breast cancer. In the randomized phase 2b trial ICON, immunomodulating chemotherapy was investigated in combination with dual ICB in HR+ mBC. To determine whether gut microbiota could inform prognosis, we performed 16S (V3-V4) rRNA sequencing on fecal samples collected at baseline and after 8 weeks of study treatment. We showed that high alpha diversity before treatment was associated with prolonged progression-free survival (PFS; primary trial endpoint) and overall survival. Alpha diversity was lower in patients with prior chemotherapy in the metastatic setting. However, alpha diversity remained significantly associated with PFS after correcting for prior chemotherapy and other factors in bivariate analyses. High-grade immune-related toxicity was also associated with high alpha diversity. These findings suggest that high alpha diversity should be further investigated as a positive prognostic factor in HR+ mBC and approaches to increase alpha diversity could potentially improve clinical outcome.},
}

@article {pmid40851996,
year = {2025},
author = {Nebieridze, A and Abu-Bakr, A and Nazir, A and Ghosson, A and Minova, A and Uwishema, O},
title = {Microbiome and cardiovascular health unexplored frontiers in precision cardiology: a narrative review.},
journal = {Annals of medicine and surgery (2012)},
volume = {87},
number = {7},
pages = {4255-4261},
pmid = {40851996},
issn = {2049-0801},
abstract = {BACKGROUND AND PURPOSE: Gut microbiota has a symbiotic relationship with their host. It is known that the gut microbiome has the potential to affect the host and vice versa. Cardiovascular disease and its comorbidities are the leading cause of death worldwide. Patients with various heart conditions have been observed to have a different composition of the gut microbiome. It has been postulated that the gut microbiome and its derivatives exert various effects on the cardiovascular system, termed the gut-heart axis. In this study, we aim to explore how the gut microbiome and the active metabolites produced by these microorganisms affect patient cardiovascular health. Additionally, we will discuss how gut microbiota can become a target for the new era of precision cardiology.

METHODS: Data were collected through the online databases PubMed, Google Scholar, Ovid MEDLINE, and ScienceDirect. Articles regarding cardiovascular health and pathology as well as its overlap with gut microbiome and health were used.

RESULTS: Emerging evidence suggests that gut microbiome has a significant influence on cardiovascular disease through its metabolites, such as trimethylamine N-oxide and short-chain fatty acids, which impact cholesterol metabolism, systemic inflammation, and plaque stability. Targeting said derivatives has proven to provide beneficial results for patients suffering from cardiovascular disease.

CONCLUSIONS: Finding reported here highlights the importance of microbiome in cardiovascular disease and health and suggest that microbiome-based interventions hold promise for prevention and treatment of cardiovascular disease. More research needs to be conducted to study more concrete effects of specific microorganisms on cardiovascular health. Multicenter, longitudinal studies with a large sample size will provide the best evidence for clinically significant findings. Using precision cardiology, to target the gut microbiome and its derivatives, with medications like antibiotics, and nonpharmacologic interventions like lifestyle modification and fecal transplantation can positively influence cardiovascular health and help with the effective management of ongoing diseases.},
}

@article {pmid40851483,
year = {2025},
author = {Kurhaluk, N and Kamiński, P and Tkaczenko, H},
title = {Role of Gut Microbiota in Modulating Oxidative Stress Induced by Environmental Factors.},
journal = {Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology},
volume = {59},
number = {S2},
pages = {2-52},
doi = {10.33594/000000799},
pmid = {40851483},
issn = {1421-9778},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Oxidative Stress/drug effects ; Animals ; Dysbiosis ; Signal Transduction/drug effects ; *Environmental Pollutants/toxicity ; Probiotics/therapeutic use ; Reactive Oxygen Species/metabolism ; },
abstract = {The widespread presence of environmental pollutants, including toxic metals, microplastics, and antibiotics, has significantly altered gut microbiota composition and functionality, leading to dysbiosis and oxidative stress. These changes contribute to various adverse physiological effects, including systemic inflammation, mitochondrial dysfunction, and intestinal barrier dysfunction. This review provides a comprehensive analysis of the molecular mechanisms by which these environmental factors induce oxidative damage, emphasising the importance of redox imbalance, the overproduction of reactive oxygen species, and inflammatory signalling pathways. Key pathways involved include NF-κB, Nrf2/Keap1, PI3K/AKT, p38-MAPK, JAK/STAT and TLR4/MyD88. These pathways collectively contribute to the progression of chronic inflammatory conditions. Furthermore, this article synthesises findings from 354 studies published between 2016 and 2024, integrating human and animal research evidence. Existing literature suggests that gut dysbiosis exacerbates oxidative stress through impaired short-chain fatty acid production, downregulation of peroxisome proliferator-activated receptor gamma, and disruption of antioxidant enzyme activity. This review explores these mechanisms in more detail. Additionally, the review evaluates studies investigating microbiota-targeted therapeutic interventions to mitigate oxidative stress. These interventions include probiotics, prebiotics, polyphenols, and postbiotics, focusing on their reported modulation of Nrf2 and AMPK signalling pathways. The potential of faecal microbiota transplantation as an innovative approach to restoring a healthy gut ecosystem and counteracting pollutant-induced oxidative damage is also discussed. In light of the growing global exposure to environmental pollutants and their associated long-term health implications, it is imperative to gain a deeper understanding of their impact on gut microbiota and oxidative stress. This topic remains at the forefront of biomedical research due to its implications for public health, disease prevention, and developing novel therapeutic strategies.},
}

Humans
*Gastrointestinal Microbiome/drug effects
*Oxidative Stress/drug effects
Animals
Dysbiosis
Signal Transduction/drug effects
*Environmental Pollutants/toxicity
Probiotics/therapeutic use
Reactive Oxygen Species/metabolism

@article {pmid39862395,
year = {2025},
author = {Allegretti, JR and Feuerstadt, P and Knapple, WL and Orenstein, R and Pinton, P and Sheh, A and Khanna, S},
title = {Safety and Efficacy of Fecal Microbiota, Live-jslm (REBYOTA®), for the Prevention of Recurrent Clostridioides difficile Infection in Participants With Inflammatory Bowel Disease in PUNCH CD3-OLS.},
journal = {Inflammatory bowel diseases},
volume = {31},
number = {8},
pages = {2112-2122},
pmid = {39862395},
issn = {1536-4844},
support = {//Ferring Pharmaceuticals/ ; },
mesh = {Humans ; Female ; Male ; Adult ; *Fecal Microbiota Transplantation/methods/adverse effects ; *Clostridium Infections/prevention & control/microbiology ; *Inflammatory Bowel Diseases/microbiology/complications ; Middle Aged ; *Feces/microbiology ; *Clostridioides difficile ; Treatment Outcome ; Secondary Prevention/methods ; Young Adult ; Prospective Studies ; Gastrointestinal Microbiome ; Recurrence ; },
abstract = {BACKGROUND: Fecal microbiota, live-jslm (RBL; REBYOTA®), is the first single-dose, broad consortia, microbiota-based live biotherapeutic approved by the US Food and Drug Administration to prevent recurrent Clostridioides difficile infection (rCDI) in adults following standard-of-care antimicrobials. Inflammatory bowel disease (IBD) is a common risk factor for rCDI, yet patients with IBD are often excluded from prospective trials. This subgroup analysis of PUNCH CD3-OLS (NCT03931941) evaluated the safety and efficacy of RBL in participants with rCDI and IBD.

METHODS: Participants with IBD (ulcerative colitis [UC], Crohn's disease [CD], or unspecified) who had rCDI were included. Treatment-emergent adverse event (TEAE) data were collected for up to 6 months following RBL administration. Efficacy outcomes included treatment success at 8 weeks and sustained clinical response at 6 months.

RESULTS: Overall, 793 participants were enrolled, and 697 received RBL; 74 had IBD (UC: n = 45; CD: n = 25; unspecified IBD: n = 4). TEAEs within 8 weeks of administration were reported by 45.9% and 47.5% of participants with and without IBD, respectively; most were mild or moderate gastrointestinal symptoms. Serious TEAEs within 8 weeks of administration were reported by 1.4% and 4.2% of participants with and without IBD, respectively. The treatment success rate at 8 weeks was 78.9%, and the sustained clinical response rate at 6 months was 91.1% in participants with IBD, similar to rates in participants without IBD (73.2% and 91.0%, respectively).

CONCLUSIONS: The results of this subgroup analysis of PUNCH CD3-OLS suggest RBL is safe and efficacious in patients with IBD.},
}

Humans
Female
Male
Adult
*Fecal Microbiota Transplantation/methods/adverse effects
*Clostridium Infections/prevention & control/microbiology
*Inflammatory Bowel Diseases/microbiology/complications
Middle Aged
*Feces/microbiology
*Clostridioides difficile
Treatment Outcome
Secondary Prevention/methods
Young Adult
Prospective Studies
Gastrointestinal Microbiome
Recurrence

@article {pmid40851072,
year = {2025},
author = {Zhang, L and Wang, S and Wong, MCS and Mok, CKP and Ching, JYL and Mak, JWY and Chen, C and Huo, B and Yan, S and Cheung, CP and Chiu, EOL and Fung, EYT and Cheong, PK and Chan, FKL and Ng, SC},
title = {The resident gut microbiome modulates the effect of synbiotics on the immunogenicity after SARS-COV-2 vaccination in elderly and diabetes patients.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {171},
pmid = {40851072},
issn = {2055-5008},
support = {COVID19F07//Health Bureau, The Government of the Hong Kong Special Administrative Region/ ; COVID19F07//Health Bureau, The Government of the Hong Kong Special Administrative Region/ ; COVID19F07//Health Bureau, The Government of the Hong Kong Special Administrative Region/ ; COVID19F07//Health Bureau, The Government of the Hong Kong Special Administrative Region/ ; NCI202346//New Cornerstone Science Foundation/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Aged ; *Synbiotics/administration & dosage ; SARS-CoV-2/immunology ; Female ; Male ; *COVID-19/prevention & control/immunology ; *COVID-19 Vaccines/immunology/administration & dosage ; Feces/microbiology ; Bifidobacterium ; *Immunogenicity, Vaccine ; *Diabetes Mellitus/immunology/microbiology ; Vaccination ; BNT162 Vaccine/immunology ; Middle Aged ; Antibodies, Viral/blood ; },
abstract = {The study aims to tackle the seed and soil microbiome and mechanisms that contribute to the effect of synbiotics in enhancing immunogenicity after SARS-CoV-2 vaccination in elderly and diabetic patients. Among 369 subjects who received 3 months of SIM01, a gut microbiota-derived synbiotic formula of three Bifidobacterium strains (B. adolescentis, B. bididum, and B. longum) or a placebo after the SARS-CoV-2 vaccines (mRNA vaccine BNT162b2 (Pfizer-BioNTech) or the inactivated vaccine Sinovac-CoronaVac), we performed metagenomic sequencing in stool samples of 280 vaccinees collected at baseline and 3-month postvaccination and metabonomic sequencing in 276 vaccinees collected at baseline and 1-month postvaccination. The open niche of autochthonous gut microbiota (lower levels of Bifidobacterium and decreased functional potential for carbohydrate metabolism) was associated with enhancing SIM01-contained species. The enrichment of three bifidobacterial species after 3 months of SIM01 intervention (BABBBL_fc) was positively correlated with the level of neutralizing antibodies to the BNT162b2 vaccine at 6-month postvaccination. The fold change of benzoic acid was positively correlated with BABBBL_fc in the BNT162b2 vaccinees, which was also implicated with SARS-CoV-2 surrogate virus neutralization test (sVNT)% levels at 1-month postvaccination. Importantly, SIM01 strain engraftment assessed by StrainPhlAn (A metagenomic strain-level population genomics tool) was associated with a higher fold change of three bifidobacterial species and could be predicted based on the baseline gut microbiome. Therefore, the resident gut microbiome affected the SIM01 engraftment, which was associated with the immunogenicity of SARS-CoV-2 BNT162b2 vaccines.},
}

Humans
*Gastrointestinal Microbiome/immunology
Aged
*Synbiotics/administration & dosage
SARS-CoV-2/immunology
Female
Male
*COVID-19/prevention & control/immunology
*COVID-19 Vaccines/immunology/administration & dosage
Feces/microbiology
Bifidobacterium
*Immunogenicity, Vaccine
*Diabetes Mellitus/immunology/microbiology
Vaccination
BNT162 Vaccine/immunology
Middle Aged
Antibodies, Viral/blood

@article {pmid40850941,
year = {2025},
author = {Zhang, X and Yang, Y},
title = {Gut: The gate and key to brain.},
journal = {Chinese medical journal},
volume = {},
number = {},
pages = {},
pmid = {40850941},
issn = {2542-5641},
abstract = {Brain science is the frontier of modern science, and new advances have been made in brain-like designs and brain-computer interfaces to simulate or develop brain functions. However, given that the brain is hermetically sealed within the skull, exploration and deciphering of the brain structure and functions are limited. Growing evidence suggests that the gut is not just a digestive organ. It not only provides essential nutrients and electrolytes for brain neurodevelopment and the maintenance of brain function, but it also transmits external environmental and intestinal wall signals from the intestinal lumen to the central nervous system through multiple pathways to regulate brain activity, function, and structure. A variety of gut-brain interaction pathways have been identified, including neural pathways, neuroimmune signaling, endocrine pathways, and biochemical messengers produced by gut microbes. Gut microbes interact with food and the gut to modulate gut-brain communication. The gut's important role and potential in neurodevelopment, maintenance of normal function, and disease development make it an increasingly important area of research in brain science and neuropsychiatric disorders. The gut's unique role in brain functions and its accessibility for research (compared to direct brain studies) establish it as a critical gate to understanding the mysteries of brain science. Crucially, intestinal nutrients and microbes provide two unique keys to unlock this gate-enabling neural regulation and novel treatments for neuropsychiatric diseases.},
}

@article {pmid40850681,
year = {2025},
author = {Wei, Z and Gao, G and He, Q and Kwok, LY and Sun, Z},
title = {The gut-tumor connection: the role of microbiota in cancer progression and treatment strategies.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2025.08.038},
pmid = {40850681},
issn = {2090-1224},
abstract = {BACKGROUND: The tumor microenvironment (TME) has become a critical focus in the diagnosis and treatment of cancer. The involvement of the microbiome in tumor initiation and progression underscores its potential as a promising biomarker and therapeutic target. Furthermore, microorganisms in the gut and other ecological niches play pivotal roles in shaping cancer immune surveillance and modulating responses to immunotherapy, acting as key mediators connecting gut health to cancer progression. Thus, investigating the intricate interplay between the TME and gut microbiota could offer valuable insights to advance personalized cancer therapies.

AIM OF REVIEW: This comprehensive review explores the complex interactions between the gut microbiota, tumor-associated microbiota, and TME, examining their origins, diversity, connections, and therapeutic implications. We investigate the potential for gut microbiota to translocate to tumors, where they may directly impact the TME and influence cancer progression. We compile the current knowledge on the diversity of intratumoral microbiota across various cancer types and its effects on cellular, immune, and spatial heterogeneity within the TME. Furthermore, we assess the efficacy of various methods for characterizing and identifying intratumoral microbiome, emphasizing their importance in understanding their composition and function in the TME. We also explore the therapeutic potential of modulating the gut microbiota, highlighting strategies such as dietary interventions, fecal microbiota transplantation, probiotics, prebiotics, and synthetic biology approaches. We then address the challenges and future directions in this emerging field, emphasizing the need for standardized protocols, advanced sequencing technologies, and refined animal models to enhance our understanding of microbiota-cancer interactions. In conclusion, the gut microbiota represents a promising therapeutic target for cancer treatment. Harnessing the power of gut microbial modulation could lead to novel combinatorial strategies that improve clinical outcomes for cancer patients. Nevertheless, further research is essential to surmount existing challenges and translate these insights into impactful, personalized cancer therapies.},
}

@article {pmid40849919,
year = {2025},
author = {Li, S and Wu, W and Zhou, Y and Zhang, S and Wei, D and Zhu, M and Ying, X and Sun, X and Liu, H and Zhu, W and Tang, D and Jiao, R and Zeng, G and Duan, X and Liu, J and Wu, W},
title = {Gut microbiota-regulated unconjugated bilirubin metabolism drives renal calcium oxalate crystal deposition.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2546158},
doi = {10.1080/19490976.2025.2546158},
pmid = {40849919},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Calcium Oxalate/metabolism/chemistry ; *Bilirubin/metabolism ; Rats ; Humans ; Dysbiosis/metabolism/microbiology ; Male ; *Kidney/metabolism/pathology ; *Kidney Calculi/metabolism ; Rats, Sprague-Dawley ; Fecal Microbiota Transplantation ; Disease Models, Animal ; Drosophila ; Bacteria/classification/metabolism/genetics/isolation & purification ; },
abstract = {Gut microbial dysbiosis and the resultant metabolic disorder are intimately associated with calcium oxalate (CaOx) stone formation. Renal CaOx crystal deposition is one of the primary initiating factors of CaOx formation; however, the critical signaling metabolites communicating along the gut-kidney axis, and their regulation on renal CaOx crystal deposition remain unclear. Here, we investigate the role of gut microbiota-associated unconjugated bilirubin (UCB) metabolism in renal CaOx crystalline pathogenesis. The UCB was first distinguished as a significant risk factor of renal CaOx crystal deposition, by transplantation of fecal microbiota derived from healthy rat (healthy-FMT) to alleviate the renal CaOx crystal deposition in rat models, which was also testified in CaOx stone patients. Further experiments showed that UCB could increase renal CaOx crystal deposition significantly in both rat and Drosophila models. Mechanistically, UCB can promote apoptosis in renal tubular epithelial cells, enhance oxalate secretion by upregulating Slc26a6 expression, and facilitate CaOx crystal nucleation and aggregation, all of which contribute to renal CaOx crystalline pathogenesis. Furthermore, we identified significant gut microbiota dysbiosis in renal CaOx crystal deposition rats, particularly in β-glucuronidase (β-GD) and bilirubin reductase (BilR)-related dysbiosis, which modulate UCB levels and its enterohepatic circulation. These findings suggest that UCB is a novel regulator of renal CaOx crystal deposition, and targeting its metabolism via modulation of the gut microbiota may offer a promising therapeutic strategy for preventing renal CaOx crystal deposition-related nephropathy.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Calcium Oxalate/metabolism/chemistry
*Bilirubin/metabolism
Rats
Humans
Dysbiosis/metabolism/microbiology
Male
*Kidney/metabolism/pathology
*Kidney Calculi/metabolism
Rats, Sprague-Dawley
Fecal Microbiota Transplantation
Disease Models, Animal
Drosophila
Bacteria/classification/metabolism/genetics/isolation & purification

@article {pmid40849632,
year = {2025},
author = {Jang, S and Lee, EJ and Park, S and Lim, H and Ahn, B and Huh, Y and Koh, H and Park, YR},
title = {Spatial host-microbiome profiling demonstrates bacterial-associated host transcriptional alterations in pediatric ileal Crohn's disease.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {189},
pmid = {40849632},
issn = {2049-2618},
abstract = {BACKGROUND: Crohn's disease (CD) is a chronic inflammatory bowel disease involving complex relationships between the gut microbiome and host immune system. However, the spatial relationships between tissue-resident bacteria and host cells in CD pathogenesis remain poorly understood. We developed a spatial host-microbiome profiling approach to simultaneously detect host transcriptomics and bacterial species at high taxonomic resolution in pediatric ileal CD tissues.

RESULTS: In this prospective case-control study, we analyzed 14 terminal ileal tissue samples from six pediatric patients with ileal CD and two controls. Spatial host-microbiome sequencing, combined spatial transcriptomics and in-situ polyadenylation, and bulk shotgun metagenome sequencing were performed. We developed a comprehensive bioinformatics pipeline to identify bacterial species and analyze host-microbiome interactions at cellular resolution, resulting in 13,876 analyzed cells. Our approach revealed increased bacterial abundance in CD tissues compared with controls. The extent of bacterial infiltration at diagnosis correlated with disease prognosis and severity of endoscopic findings. We identified 16 potentially beneficial and nine pathogenic microbiome members in ileal CD, including several newly discovered risk-modulating bacterial species. Cell-type-specific host gene expression analysis revealed transcriptome alterations related to bacterial defense mechanisms in the presence of various bacterial species.

CONCLUSIONS: Our spatial host-microbiome profiling approach enables simultaneous species-level identification of bacteria and host transcriptomics. It reveals the intricate interactions between host cells and bacteria, providing cellular-level insights into CD pathogenesis. Our approach offers a powerful tool for investigating host-microbiome interactions in various microbiome-associated diseases to direct new strategies for microbiome-based therapeutics and prognostic markers. Video Abstract.},
}

@article {pmid40848995,
year = {2025},
author = {Wang, J and Xue, L and Zhang, M and Shen, P and Zhao, W and Tong, Q and Wu, S and Dai, W and Yang, X and Wang, H},
title = {Colonoscopic fecal microbiota transplantation for Mild-to-Moderate Parkinson's Disease: A randomized controlled trial.},
journal = {Brain, behavior, and immunity},
volume = {},
number = {},
pages = {106086},
doi = {10.1016/j.bbi.2025.106086},
pmid = {40848995},
issn = {1090-2139},
abstract = {OBJECTIVE: Growing evidence supports the efficacy and safety of fecal microbiota transplantation (FMT) in treating Parkinson's disease (PD). Fecal microbiota are commonly transplanted via oral capsules, a nasojejunal tube, or colonoscopy, but freezing often decreases the diversity and viability of transplanted microbiota. This single-center, double-blind, randomized, placebo-controlled trial aims to explore the efficacy and safety of fresh FMT via colonoscopy in dealing with PD.

METHODS: Thirty patients with mild-to-moderate PD (Hoehn-Yahr stage I-III) were randomly assigned into the FMT group (fresh FMT via colonoscopy) and placebo group (saline injection via colonoscopy) in a 1:1 ratio. Motor and non-motor symptoms, constipation, quality of life, cognitive function, emotional state and sleep quality were assessed using relevant scales. Fecal samples were harvested before and at 4, 8 and 12 weeks after treatment for metagenomic and metabolomics analyses.

RESULTS: A total of 30 patients with mild-to-moderate PD were enrolled in the present study, involving 18 males and 12 females with a median age of 68 years, a median age of onset of 63.5 years, and a median disease duration of 3 years. At 12 weeks, scores of the UPDRS Ⅲ (group × time effect, B =  - 8.80 [-13.79, -3.81]), PAC-QOL (group × time effect, B =  - 29.67 [-45.35, -13.98]), UPDRS Ⅱ (group × time effect, B =  - 5.07 [-8.85, -1.28]), NMSS (group × time effect, B =  - 35.60 [-53.59, -17.61]), PDQ-39 (group × time effect, B =  - 17.80 [-28.21, -7.39]), HAMA (group × time effect, B =  - 1.66 [-2.92, -0.40]), and HAMD (group × time effect, B =  - 1.33 [-2.49, -0.16]) were significantly reduced in the FMT group, while CSBM per week (group × time effect, B = 3.03 [1.42, 4.63]) and the Bristol Stool Scale score (group × time effect, B = 1.95 [0.12, 3.79]) significantly increased (all P < 0.05). Significant alterations were seen in the gut microbiota and fecal metabolites in the FMT group. No adverse events were observed during the follow-up period.

CONCLUSION: Fresh FMT via colonoscopy is a safe and well-tolerated procedure for treating mild-to-moderate PD. It effectively alleviates motor and non-motor symptoms, thus facilitating defecation and improving the quality of life. These effects can be maintained for a minimum of 12 weeks and may be attributed to the optimization of gut microbiota and fecal metabolites.},
}

@article {pmid40847330,
year = {2025},
author = {Stefansson, M and Bladh, O and Nowak, P and Rombo, L and Hedenstierna, M and Ursing, J},
title = {Risk factors for further recurrences of Clostridioides difficile infection at the first and second recurrence: a retrospective cohort.},
journal = {BMC infectious diseases},
volume = {25},
number = {1},
pages = {1057},
pmid = {40847330},
issn = {1471-2334},
mesh = {Humans ; *Clostridium Infections/epidemiology/microbiology/therapy ; Female ; Male ; Retrospective Studies ; Risk Factors ; Aged ; Recurrence ; Aged, 80 and over ; *Clostridioides difficile ; Fecal Microbiota Transplantation ; Sweden/epidemiology ; },
abstract = {BACKGROUND: Recurrent Clostridioides difficile infection is most effectively treated with faecal microbiota transplantation. Swedish and European guidelines suggest faecal microbiota transplantation after a first or second recurrence, respectively. The aims of this study were to evaluate risk factors for further relapses at the first and second recurrence, related to treatment recommendations.

METHODS: Patients aged ≥ 18 years with two positive tests for C. difficile within eight weeks and treated at the study hospitals during 2014-2022 were eligible for inclusion. Retrospectively collected data included age, sex, treatment, and clinical characteristics for each episode. Risk factors for further recurrences at the first and second recurrence were identified using multivariable logistic regression analysis.

RESULTS: The median age in the total cohort (n = 231) was 76 (IQR 67-84) years, 52% were females and 15% were healthy without comorbidities. One recurrence only occurred in 110 patients (48%), however, no clinically significant risk factors predicting more than one recurrence were identified. Two or more recurrences occurred in 110 patients, of whom, 44 (40%) had further recurrences. Frailty (Clinical Frailty Scale ≥ 4) was significantly associated with more than two recurrences (p = 0.03). The respective median times between the first and the second recurrences were 12 and 17 days in patients with more than two recurrences compared to two recurrences only (p = 0.02).

CONCLUSIONS: Patients experiencing a second recurrence of C. difficile infection who were frail and relapsed in a shorter time span after the first recurrence had a significantly increased risk of further recurrences.},
}

Humans
*Clostridium Infections/epidemiology/microbiology/therapy
Female
Male
Retrospective Studies
Risk Factors
Aged
Recurrence
Aged, 80 and over
*Clostridioides difficile
Fecal Microbiota Transplantation
Sweden/epidemiology

@article {pmid40846688,
year = {2025},
author = {Ding, SQ and Lei, Y and Zhao, ZM and Li, XY and Lang, JX and Zhang, JK and Li, YS and Zhang, CD and Dai, DQ},
title = {Crosstalk Between Microbiome and Ferroptosis in Diseases: From Mechanism to Therapy.},
journal = {Comprehensive Physiology},
volume = {15},
number = {4},
pages = {e70042},
doi = {10.1002/cph4.70042},
pmid = {40846688},
issn = {2040-4603},
support = {81972322//National Natural Science Foundation of China/ ; JYTMS20230108//Scientific Study Project for Institutes of Higher Learning, Ministry of Education, Liaoning Province/ ; RXXM202302//Young Backbone Talents of China Medical University/ ; 2023-MS-163//Liaoning Provincial Natural Science Foundation/ ; },
mesh = {*Ferroptosis/physiology ; Humans ; *Gastrointestinal Microbiome/physiology ; Animals ; Iron/metabolism ; Dysbiosis/metabolism ; Reactive Oxygen Species/metabolism ; *Microbiota/physiology ; Lipid Peroxidation ; },
abstract = {The human microbiome is a unique organ and maintains host immunomodulation and nutrient metabolism. Structural and functional microbiome alterations are commonly known as dysbiosis, which is strongly associated with disease progression. Ferroptosis is a novel iron-dependent cell death mode characterized by intracellular iron accumulation, increased reactive oxygen species (ROS), and lipid peroxidation (LPO). Importantly, the complex crosstalk between the microbiome and ferroptosis in disease has attracted considerable research attention. The microbiome influences ferroptosis by regulating host iron homeostasis, mitochondrial metabolism, and LPO, among many other pathways. Thus, the in-depth analysis of microbiome-ferroptosis crosstalk and associated mechanisms could provide new strategies to treat human diseases. Therefore, understanding this crosstalk is critical. Here, we systematically explore the associations between gut microbiome and ferroptosis across multiple diseases. We show that the oral microbiome also influences disease progression by regulating ferroptosis. Furthermore, we provide a potential for certain disease therapies by targeting the crosstalk between the microbiome and ferroptosis.},
}

*Ferroptosis/physiology
Humans
*Gastrointestinal Microbiome/physiology
Animals
Iron/metabolism
Dysbiosis/metabolism
Reactive Oxygen Species/metabolism
*Microbiota/physiology
Lipid Peroxidation

@article {pmid40842975,
year = {2025},
author = {Tu, J and Yu, L and Zou, R and He, J and Qu, C},
title = {Influence of the gut microbiome on lymphoma treatment: current evidence and future therapeutic directions.},
journal = {Therapeutic advances in medical oncology},
volume = {17},
number = {},
pages = {17588359251363207},
pmid = {40842975},
issn = {1758-8340},
abstract = {The heterogeneity of lymphoma responses to various treatments remains a significant challenge in clinical practice. Emerging evidence implicates the potential role of the gut microbiome in lymphoma pathogenesis and progression. Advances in high-throughput sequencing and metabolomics have significantly enhanced our understanding of the complex interaction between the gut microbiome and lymphoma. Although causality requires further elucidation, the gut microbiome critically shapes host responses to traditional combined chemotherapy, hematopoietic stem cell transplantation, and targeted therapies, including chimeric antigen receptor T-cell therapy. Notably, the use of antibiotics, particularly broad-spectrum antibiotics, can alter the gut microbiome, thereby impacting treatment efficacy. Prudent antibiotic management should balance infection control with microbiome-dependent immune homeostasis. Strategies to restore gut microbial balance through a high-fiber diet, probiotics, prebiotics, fecal microbiota transplantation, and butyrate supplementation are critically important. Integrating microbiome-based therapies into lymphoma treatment could establish low-toxicity therapeutic paradigms for lymphoma patients.},
}

@article {pmid40842134,
year = {2025},
author = {Korten, NM and Thelen, AC and Voelz, C and Beyer, C and Seitz, J and Trinh, S and Blischke, L},
title = {Exploring the Link Between the Gut Microbiota and Epigenetic Factors in Anorexia Nervosa.},
journal = {Brain and behavior},
volume = {15},
number = {8},
pages = {e70733},
doi = {10.1002/brb3.70733},
pmid = {40842134},
issn = {2162-3279},
mesh = {*Anorexia Nervosa/microbiology/genetics/metabolism ; Humans ; *Gastrointestinal Microbiome/physiology ; *Epigenesis, Genetic/physiology ; Brain/metabolism ; Dysbiosis ; },
abstract = {OBJECTIVE: Anorexia nervosa (AN) is an often chronic eating disorder that involves genetic, neurohormonal, and epigenetic factors along with key contributions from the microbiota-gut-brain axis. However, interactions between these factors are poorly understood. Recent studies have emphasized the microbiota-gut-brain axis and epigenetic changes as potentially important contributors to AN. Exploring these interactions may improve understanding of the etiology and persistence of AN.

METHODS: Studies specifically addressing microbial-epigenetic interactions in AN remain limited. However, similar associations have been documented in related disorders such as obesity and depression, providing potential models for AN research.

RESULTS: Research in obesity has shown that dietary factors influence the composition of the gut microbiota and subsequent epigenetic modifications, affecting metabolic parameters and disease progression. Similarly, in depression, microbially produced metabolites influence brain function and epigenetic processes, contributing to neuropsychiatric symptoms. In AN, altered microbial composition may affect weight regulation and epigenetic patterns. Therapies targeting the microbiome, such as fecal microbiota transplantation, are under investigation for AN, highlighting the potential therapeutic utility of ameliorating microbial dysbiosis.

DISCUSSION: This article highlights the importance of investigating microbial-epigenetic interactions in AN. By drawing parallels with obesity and depression, we aim to deepen our understanding of AN mechanisms and ultimately improve patient outcomes.},
}

*Anorexia Nervosa/microbiology/genetics/metabolism
Humans
*Gastrointestinal Microbiome/physiology
*Epigenesis, Genetic/physiology
Brain/metabolism
Dysbiosis

@article {pmid40744276,
year = {2025},
author = {Cassir, N and Ghani, R and Biehl, LM and Graells, T and Kuijper, EJ and Mullish, BH and Marchesi, JR and Benech, N and , },
title = {Nonantimicrobial therapies for recurrent urinary tract infection in women: is there a place for faecal microbiota transfer?.},
journal = {Clinical microbiology and infection : the official publication of the European Society of Clinical Microbiology and Infectious Diseases},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cmi.2025.07.022},
pmid = {40744276},
issn = {1469-0691},
abstract = {BACKGROUND: Recurrent urinary tract infection (rUTI) is a common condition, affecting approximately one-third of women after an initial UTI. It significantly impacts health care costs and patients' quality of life. The relationship between the pathophysiology of UTI and the gut and vaginal microbiota is recognized as a contributing factor to rUTI in women. As antibiotic resistance among uropathogens continues to increase, there is a clear need to develop novel therapeutic interventions. Faecal microbiota transfer (FMT) is a potent nonantimicrobial strategy for modulating the gut microbiota; however, its clinical relevance in the context of rUTI is unclear.

OBJECTIVES: This narrative review aimed to summarize the current evidence on the use of FMT for the treatment of rUTI, focusing on women, excluding those with mechanical dysfunctions such as urinary incontinence, neurogenic bladder, and bladder cancer, compared with other nonantimicrobial interventions. We also discussed the pathophysiology and epidemiology of rUTI to identify patients for whom microbiota-targeting therapies may be the most effective.

CONTENT: Periurethral colonization and migration to the bladder of uropathogens that inhabit the gut and vagina have been linked to the aetiology of UTI in women, particularly in patients with multidrug-resistant organisms. FMT appears to be a promising approach for preventing the clinical development of rUTI, although prospective data remain limited. In contrast, other reported nonantimicrobial strategies targeting the gut and urogenital microbiota have shown variable significant clinical efficacy. Prospective randomized controlled clinical trials are then needed to further confirm a potential therapeutic benefit, optimize the FMT procedure, and better assess its cost-effectiveness.},
}

@article {pmid40695592,
year = {2025},
author = {Welsch, EC and Barron, MR and Storage, KM and Kazen, AB and Aboulalazm, FA and Kirby, JR and Kindel, TL},
title = {Gut microbiome and bile acid changes after male rodent sleeve gastrectomy: what comes first?.},
journal = {American journal of physiology. Regulatory, integrative and comparative physiology},
volume = {329},
number = {3},
pages = {R410-R421},
doi = {10.1152/ajpregu.00297.2024},
pmid = {40695592},
issn = {1522-1490},
support = {R01HL158900//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; HL072483//HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI)/ ; Clowes Career Development Award//American College of Surgeons (ACS)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Bile Acids and Salts/metabolism ; *Gastrectomy/methods ; Male ; Mice, Inbred C57BL ; *Liver/metabolism ; Mice ; Fecal Microbiota Transplantation ; },
abstract = {Understanding how a sleeve gastrectomy (SG) achieves metabolic improvement is challenging due to the complex relationship between the liver, bile acid (BA) pool, and gut microbiome. We hypothesized that SG alters the gut microbiome, which then increases the BA pool, leading to metabolic efficacy. We performed fecal material transfer (FMT) from SG or sham mice to surgically naïve mice with an intact microbiome. We evaluated the effect of surgery and FMT on BA-related liver enzymes, BA concentrations, and gut microbiome composition via 16S and metagenomic analysis. SG significantly deflected weight gain compared with sham surgery, 5 ± 2 g versus 10 ± 3 g, respectively (P = 0.004). SG significantly increased the BA pool and decreased liver transcription of slc10a1 (P = 0.04) and cyp8b1 (P = 0.03). Random forest analysis identified several features with significantly increased relative abundance in SG compared with sham mice, including Lactobacillus. Examination of metabolic profiles with metagenomic analysis revealed a BA salt hydrolase produced by the Ligilactobacillus species. FMT of SG stool to surgically naïve mice significantly decreased the BA pool compared with sham FMT (P = 0.034). Unlike SG surgery, we found no effect of SG or sham FMT on bile acid-related enzymes in the liver after 14 wk of treatment. Overall, we propose that the metabolic benefits of SG surgery are related to decreased liver transcription of cyp8b1 and slc10a1 with subsequent increases in the systemic and enterohepatic BA pool, including lithocholic acid. The gut microbiome adapts to the altered BA pool with associated increases in Ligilactobacillus and bile salt hydrolase production.NEW & NOTEWORTHY We propose that the metabolic benefits of sleeve gastrectomy are initiated by decreased liver transcription of cyp8b1 and slc10a1. A notable downstream effect includes changes in systemic bile acid composition and circulation, including increased LCA. An altered gut microbiome after surgery includes increases in Ligilactobacillus that was shown to express a bile salt hydrolase, which could be a contributor to the post-sleeve gastrectomy gut microbiome changes.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Bile Acids and Salts/metabolism
*Gastrectomy/methods
Male
Mice, Inbred C57BL
*Liver/metabolism
Mice
Fecal Microbiota Transplantation

@article {pmid40838552,
year = {2025},
author = {Szegedi, I and Bomberák, D and Éles, Z and Lóczi, L and Bagoly, Z},
title = {Cardiovascular disease and microbiome: focus on ischemic stroke.},
journal = {Polish archives of internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.20452/pamw.17088},
pmid = {40838552},
issn = {1897-9483},
abstract = {Cardiovascular and cerebrovascular diseases, encompassing conditions such as ischemic heart disease and ischemic stroke (IS), remain the leading global cause of death and disability. While traditional cardiovascular risk factors (eg, hypertension, diabetes, and atherosclerosis) are well established, emerging research underscores the critical role of gut microbiota in the development and progression of both cardiac and cerebrovascular events. The microbiota-gut-brain axis is a bidirectional communication system involving neural, immune, and metabolic pathways that link gut microbial activity to vascular and brain function. Dysbiosis, marked by reduced microbial diversity and an imbalance between beneficial and pathogenic taxa, has been associated with systemic inflammation, endothelial dysfunction, increased intestinal permeability, and thrombosis. Microbial metabolites, such as trimethylamine N‑oxide (TMAO), short‑chain fatty acids, and bile acid derivatives modulate blood-brain barrier integrity, vascular tone, and neuroinflammatory responses. Both cardiovascular and cerebrovascular diseases share key microbiota‑related mechanisms, including TMAO‑mediated platelet activation and low‑grade endotoxemia, although IS is more acutely affected by gut barrier disruption and neuroinflammation. In IS, gut dysbiosis also contributes to poststroke complications, such as hemorrhagic transformation, neuropsychiatric issues, and epilepsy. Advances in sequencing and metabolomics enabled identification of microbial signatures associated with the risk for an acute ischemic event and patient prognosis. Therapeutic strategies targeting the gut microbiota-including dietary interventions, probiotics, prebiotics, and synbiotics, fecal microbiota transplantation, and intestinal epithelial stem cell therapy-show promise in mitigating vascular injury and improving recovery. This narrative review highlights current insights into microbiota‑related cardiovascular and cerebrovascular events, with a focus on IS.},
}

@article {pmid40838009,
year = {2025},
author = {Yuan, S and Jia, W and Liu, X and Liu, R and Cao, M and Wu, Y and Li, Y and Xu, W and Xiao, C and Hong, Z and Zhang, B},
title = {Therapeutic effect of fecal microbiota transplantation on hyperuricemia mice by improving gut microbiota.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1599107},
pmid = {40838009},
issn = {1664-302X},
abstract = {OBJECTIVE: The primary objective of this study was to assess the impact of fecal microbiota transplantation (FMT) on serum biochemical parameters, renal injury, and gut microbiota in hyperuricemia (HUA) mice.

METHODS: Six-week-old male C57BL/6 J mice were given a high-purine diet and potassium oxonate injections to induce HUA, followed by a two-week FMT treatment. Regular body weight checks, serum biochemical analyses, and fecal sampling for 16S rRNA gene sequencing were conducted to evaluate the treatment's impact on gut microbiota.

RESULTS: The model group showed significant increases in uric acid (UA), creatinine (Cr), blood urea nitrogen (BUN) levels, and increased xanthine oxidase (XOD) activity compared to controls (p < 0.05). FMT treatment effectively reduced these levels and XOD activity (p < 0.05). At the genus level, specific taxa like Muribaculaceae and Prevotellaceae_UCG-001 were less abundant, while Blautia and Ruminiclostridium_9 were more abundant in the model group. Following FMT, gut microbiota composition returned to near-normal levels, with significant differences from the model group (p < 0.05).

CONCLUSION: This study demonstrates that FMT holds therapeutic potential for HUA mice by reducing UA levels, alleviating renal damage, and restoring gut microbiota balance.},
}

@article {pmid40836410,
year = {2025},
author = {Quan, J and Liu, X and Liang, S and Nie, L and Zhang, L and Hong, X and He, M and Lei, S and Duan, L and Zhang, Y and Zhuang, L},
title = {Electroacupuncture suppresses motor impairments via microbiota-metabolized LPS/NLRP3 signaling in 6-OHDA induced Parkinson's disease rats.},
journal = {International immunopharmacology},
volume = {162},
number = {},
pages = {115089},
doi = {10.1016/j.intimp.2025.115089},
pmid = {40836410},
issn = {1878-1705},
mesh = {Animals ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; *Electroacupuncture ; *Gastrointestinal Microbiome ; Lipopolysaccharides/metabolism ; Male ; Rats ; Oxidopamine ; Signal Transduction ; Rats, Sprague-Dawley ; Dopaminergic Neurons ; *Parkinson Disease/therapy ; Disease Models, Animal ; Fecal Microbiota Transplantation ; },
abstract = {Emerging evidence indicates that electroacupuncture (EA) exerts significant therapeutic effects on Parkinson's disease (PD)-related symptoms, with the immune mechanisms of the gut-brain axis playing a pivotal role in PD pathophysiology. This study aimed to explore whether EA mitigated PD-related symptoms and conferred neuroprotection to dopaminergic neurons in a 6-hydroxydopamine (6-OHDA) rat model by modulating the microbiota-metabolized lipopolysaccharide (LPS)/NLRP3 pathway. EA treatment ameliorated motor and anxiety symptoms in 6-OHDA rats and elevated the levels of TH. Metabolomic analysis indicated that the therapeutic effects of EA are associated with the gut microbiota and the NOD-like receptor signaling pathway. 16S rRNA sequencing demonstrated that EA significantly modified the composition of the gut microbiota, evidenced by alterations in the relative abundance of 16 genera, and led to the downregulation of the LPS and NOD-like receptor signaling pathways. Additionally, EA was found to attenuate intestinal inflammation, decrease serum inflammatory markers, reduce neuroinflammation, and suppress the overexpression of microglia and astrocytes, while concurrently preserving the integrity of the intestinal and blood-brain barriers. Fecal microbiota transplantation experiments further substantiated the pivotal role of gut microbiota in mediating the anti-PD effects of EA. In summary, EA has the potential to alleviate PD-related symptoms and safeguard dopaminergic neurons by rectifying gut microbiota dysbiosis and downregulating the LPS/NLRP3 immune pathway along the gut-brain axis in PD rat models.},
}

Animals
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
*Electroacupuncture
*Gastrointestinal Microbiome
Lipopolysaccharides/metabolism
Male
Rats
Oxidopamine
Signal Transduction
Rats, Sprague-Dawley
Dopaminergic Neurons
*Parkinson Disease/therapy
Disease Models, Animal
Fecal Microbiota Transplantation

@article {pmid40836368,
year = {2025},
author = {Guo, P and Zeng, M and Liu, M and Zhang, Y and Jia, J and Zhang, Z and Liang, S and Zheng, X and Feng, W},
title = {Zingibroside R1 Isolated From Achyranthes bidentata Blume Ameliorates LPS/D-GalN-Induced Liver Injury by Regulating Succinic Acid Metabolism via the Gut Microbiota.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.70067},
pmid = {40836368},
issn = {1099-1573},
support = {22A360004//Key scientific research plan of colleges in Henan Province/ ; 2019YFC1708802//National Key Research and Development Project/ ; 2017YFC1702800//National Key Research and Development Project/ ; ZYQR201810080//Henan province high-level personnel special support "Zhong Yuan One Thousand People Plan," Zhong Yuan Leading Talent/ ; 171100310500//The Major Science and Technology Projects in Henan Province: Study on the key technology for quality control and the key characteristics of Rehmannia glutinosa, Dioscorea opposita Thunb and Achyranthes bidentata Blume from Henan Province/ ; 2023KYCX059//Henan University of Traditional Chinese Medicine 2023 Graduate Student Research and Innovation Ability Enhancement Program/ ; },
abstract = {Achyranthes bidentata Blume is a traditional Chinese medicine used to treat liver and kidney protection and improve liver injury; however, its active components and mechanism of action remain unclear. This study focused on the monomer compound zingibroside R1 (R1) from Achyranthes bidentata Blume, specifically studying its effects on liver injury through the modulation of succinic acid-mediated immunity and inflammation via the gut microbiota. We isolated R1 and investigated its therapeutic effects in a lipopolysaccharide (LPS)- and D-galactosamine-induced acute liver injury mouse model. Liver tissue pathology, serum biomarkers, oxidative stress parameters, immune inflammation, and the gut microbiota composition were assessed. Metabolic profiling was performed via UPLC-Q-TOF-MS, and faecal microbiota transplantation experiments were conducted to validate the role of the gut microbiota in the hepatoprotective effects of R1. R1 treatment significantly alleviated LPS/GalN-induced liver injury, reducing liver haemorrhaging, hepatocyte necrosis, nuclear shrinkage, and inflammatory infiltration. R1 treatment also decreased the serum ALT and AST levels and mitigated oxidative stress. The levels of inflammation and immunity were markedly reduced following R1 treatment. Gut microbiota analysis revealed that R1 treatment restored Lactobacillus levels. Metabolomic analysis indicated that R1 influenced key metabolic pathways, including purine metabolism and glycerophospholipid metabolism pathways, and succinic acid was identified as a critical metabolite in the gut-liver interaction. Faecal microbiota transplantation (FMT) results confirmed that the therapeutic effect of R1 on liver injury is exerted by the gut microbiota, which affects the inflammation mediated by succinic acid metabolism. R1 from Achyranthes bidentata Blume provides hepatoprotective protection against LPS/GalN-induced liver injury by modulating the gut microbiota and succinic acid metabolism. These findings underscore the potential of R1 as a therapeutic agent for treating liver diseases, highlighting the importance of the gut microbiota in mediating liver health.},
}

@article {pmid40832881,
year = {2025},
author = {Cai, J and He, Y and Qu, L and Liu, J and Xie, X and Cao, Y},
title = {Liberation of galactose from lactose by gut microbial β-galactosidase prevents uterine bacterial infection.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wraf185},
pmid = {40832881},
issn = {1751-7370},
abstract = {Reproductive infection is closely associated with adverse reproductive outcomes, contributing to a reduced live birth rate per pregnancy and an elevated infertility rate. Nutrition is widely acknowledged as a fundamental determinant of human and animal health, as well as the etiopathogenesis of various diseases, with the gut microbiota playing an integral part in this process. Lactose, a disaccharide present in mammalian milk, has been identified as a potential prebiotic. Here, we found that lactose was able to mitigate the inflammatory response elicited by uterine bacterial infection, preserve the integrity of the endometrial epithelial barrier, and reduce the bacterial load in the uterus. The protective effects of lactose were found to be gut microbiota-dependent and fecal microbiota transplantation from lactose-treated mice to recipient mice also ameliorated E. coli-induced metritis. 16S rRNA gene amplicon sequencing revealed that lactose supplementation changed the gut microbiota, specifically increasing the abundance of Lactobacillus intestinalis (L. intestinalis). Whole-genome sequencing identified that L. intestinalis expressed β-galactosidase, a lactose-metabolizing enzyme. Inhibition or exogenous supplementation of β-galactosidase confirmed its essential role in mediating lactose's protective effects against E. coli uterine infection. Furthermore, intragastric administration of [1-13Cgal]-lactose confirmed that galactose, a lactose metabolite, could translocate from the gut to the uterus. Mechanistically, galactose upregulated the CEBPB-dependent S100a8 expression after E. coli infection, and the protective effect could be blunted by S100a8 inhibition. Collectively, these findings highlight a nutrition-microbiota-host interaction that is stimulated by lactose supplementation, providing potential benefits for reproductive infection.},
}

@article {pmid40832481,
year = {2025},
author = {Kim, J and Kim, Y and Lee, YJ and Lee, HJ and Sim, I and Koh, S and Suh, DH and Jung, ES and Jo, JC},
title = {Gut Microbiome and Metabolome Dynamics as Predictors of Clinical Outcomes in Hematopoietic Stem Cell Transplantation.},
journal = {MedComm},
volume = {6},
number = {9},
pages = {e70334},
pmid = {40832481},
issn = {2688-2663},
abstract = {Hematopoietic stem cell transplantation (HSCT) profoundly disrupts the gut microbiome and metabolome, which in turn influence immune-related complications and patient outcomes. To systematically characterize these perturbations, we performed a longitudinal analysis of fecal microbiota composition and metabolite profiles in HSCT recipients at three critical timepoints: pre-transplant (T1), peri-transplant (T2), and post-transplant (T3). We observed that reduced microbial diversity at T1 and T3 was strongly associated with increased incidence of graft-versus-host disease (GVHD), progressive disease (PD), and decreased overall survival (OS). Metabolomic profiling revealed a significant decline in short-chain fatty acids (SCFAs), particularly acetate, from T1 to T2, which correlated with adverse clinical outcomes including GVHD, diarrhea, PD, and lower OS. Elevated levels of uric acid at T2 were predictive of GVHD onset, while decreased 1-phenylethylamine was linked to transplant-associated diarrhea. Furthermore, enrichment of beneficial bacterial taxa such as Lachnospiraceae and Ruminococcaceae was associated with improved survival. Together, these findings highlight the gut microbiome-metabolome axis as a dynamic biomarker for HSCT prognosis. This integrated insight offers potential avenues for microbiota-targeted diagnostics and interventions aimed at mitigating transplant-related complications and improving patient survival.},
}

@article {pmid40832205,
year = {2025},
author = {Fan, Y and Ni, M and Aggarwala, V and Mead, EA and Ksiezarek, M and Cao, L and Kamm, MA and Borody, T and Paramsothy, S and Kaakoush, NO and Grinspan, A and Faith, JJ and Fang, G},
title = {Long read metagenomics-based precise tracking of bacterial strains and genomic changes after fecal microbiota transplantation.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2024.09.30.615906},
pmid = {40832205},
issn = {2692-8205},
abstract = {Fecal microbiota transplantation (FMT) has revolutionized the treatment of recurrent Clostridioides difficile infection (rCDI) and is being evaluated across other diseases. Accurate tracking of bacterial strains that stably engraft in recipients is critical for understanding the determinants of strain engraftment, evaluating their correlation with clinical outcomes, and guiding the development of therapeutic bacterial consortia. While short-read sequencing has advanced FMT research, it faces challenges in strain-level de novo metagenomic assembly. In this study, we described a novel framework, LongTrack, which uses long-read metagenomic assemblies and rigorous informatics tailored for FMT strain tracking. We highlighted LongTrack advantage over short-read approaches especially when multiple strains co-exist in the same sample. We showed LongTrack uncovered hundreds of engrafted strains across six FMT cases of rCDI and inflammatory bowel disease patients. Furthermore, long reads also allowed us to assess the genomic and epigenomic stability of engrafted strains during the 5-year follow-ups, revealing structural variations that may be associated with strain adaptation in a new host environment. Combined, our study advocates the use of long-read metagenomics and LongTrack to enhance strain tracking in future FMT studies, paving the way for the development of more effective defined biotherapeutic as an alternative to FMT.},
}

@article {pmid40832058,
year = {2025},
author = {Zhao, Y and Wang, B and Wei, X and Liu, D and Wang, R and Ma, H and Qiao, Z and Kong, N and Feng, J and Cui, D and Hou, S and Zhang, H},
title = {Gut Microbiota Dysbiosis in Preeclampsia: Mechanisms, Biomarkers, and Probiotic-Based Interventions.},
journal = {Mediators of inflammation},
volume = {2025},
number = {},
pages = {3010379},
pmid = {40832058},
issn = {1466-1861},
mesh = {Female ; Animals ; *Pre-Eclampsia/microbiology/blood/metabolism ; Pregnancy ; *Gastrointestinal Microbiome/physiology ; *Dysbiosis/microbiology ; Mice ; Mice, Inbred C57BL ; *Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Humans ; Tumor Necrosis Factor-alpha/blood ; Biomarkers/blood/metabolism ; Feces/microbiology ; Interleukin-6/blood ; RNA, Ribosomal, 16S/genetics ; Anti-Bacterial Agents/therapeutic use ; Lipopolysaccharides/blood ; },
abstract = {Background: This study aimed to investigate the impact of fecal microbiota transplantation (FMT) on gut microbiota composition and serum inflammatory factors in a murine model. Methods: Female C57BL/6J mice (n = 60) were divided into four groups: control (Con), negative (Neg), normal transplantation (NT), and preeclampsia transplantation (PET). The Con group received no treatment, while the Neg, NT, and PET groups were administered a triple antibiotic regimen (ampicillin, neomycin sulfate, and metronidazole) for 14 days to deplete gut microbiota. Following antibiotic treatment, FMT was performed: the NT group received fecal microbiota from healthy pregnant women and the PET group received microbiota from severe preeclampsia patients. Fecal samples and serum were collected for 16S rRNA sequencing and inflammatory factor analysis, respectively. Results: Significant differences in gut microbial composition were observed between the PET group and other groups, with enriched taxa such as Coprococcus, Bacillales, and Staphylococcus in the PET group. Conversely, taxa such as Helicobacter and Klebsiella were more abundant in the fecal microbiota of mice in the NT group. Furthermore, serum levels of lipopolysaccharide (LPS), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6) were markedly elevated in the PET group compared to the control, negative, and NT groups. Transplantation with fecal bacteria from preeclampsia patients leads to significant alterations in gut microbiota composition and increased serum inflammatory factors levels in mice. Conclusion: These findings provide insights into the relationship between gut microbiota and inflammatory processes in preeclampsia and underscore the potential therapeutic implications of FMT in modulating gut microbiota dysbiosis and inflammatory responses.},
}

Female
Animals
*Pre-Eclampsia/microbiology/blood/metabolism
Pregnancy
*Gastrointestinal Microbiome/physiology
*Dysbiosis/microbiology
Mice
Mice, Inbred C57BL
*Probiotics/therapeutic use
Fecal Microbiota Transplantation
Humans
Tumor Necrosis Factor-alpha/blood
Biomarkers/blood/metabolism
Feces/microbiology
Interleukin-6/blood
RNA, Ribosomal, 16S/genetics
Anti-Bacterial Agents/therapeutic use
Lipopolysaccharides/blood

@article {pmid40831851,
year = {2025},
author = {Hamad, S and Mubarak Jan, B and Al-Mohammed, A},
title = {Recurrent Clostridioides difficile Infection in a Patient With Chronic Colitis: A Successful Response to Fecal Microbiota Transplantation.},
journal = {Cureus},
volume = {17},
number = {7},
pages = {e88285},
pmid = {40831851},
issn = {2168-8184},
abstract = {Recurrent Clostridioides difficile infection (rCDI) remains a significant treatment challenge, particularly in patients with underlying gastrointestinal conditions. We present the case of a 72-year-old woman with multiple sclerosis and sarcoidosis, who experienced four separate episodes of rCDI despite treatment with vancomycin, fidaxomicin, and intravenous metronidazole. Colonoscopy revealed patchy inflammation with aphthous ulcerations, and histology confirmed chronic colitis without dysplasia or cytomegalovirus infection. Following a structured vancomycin taper, the patient underwent fecal microbiota transplantation (FMT), with complete resolution of symptoms. This case supports the early use of FMT in rCDI and highlights the need for individualized treatment strategies in patients with co-existing colonic inflammation.},
}

@article {pmid40831218,
year = {2025},
author = {Zhou, L and Wang, C and Gao, J and Wu, X and Li, G and Jiang, X and Xia, Y and Zhang, J and Lv, B and Zhao, F and Zhang, H and Pi, H and Qiu, J and Xu, S and Zou, Z and Chen, C},
title = {Novel Role of Gut-Derived Roseburia Intestinalis in Safeguarding Intestinal Barrier Integrity and Microenvironment Homeostasis During Arsenic Exposure.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e11895},
doi = {10.1002/advs.202511895},
pmid = {40831218},
issn = {2198-3844},
support = {82473594//National Natural Science Foundation of China/ ; KJQN 202200448//Science and Technology Research Program of Chongqing Municipal Education Commission/ ; W0043//Future Medical Youth Innovation Team of Chongqing Medical University/ ; 2023DBXM006//Chongqing Medical Scientific Research Project, Joint project of Chongqing Health Commission and Science and Technology Bureau/ ; CSTB2023NSCQ-LZX0059//Natural Science Foundation of Chongqing/ ; },
abstract = {As a well-known metalloid, arsenic usually causes human intestinal disorders via contaminated drinking water. However, the mechanisms underlying how arsenic induces intestinal injury remain unresolved, and the effective means of intervention are very limited. By establishing an acute arsenic exposure animal model, this work shows that arsenic disrupts the mechanical, chemical, immunological, and biological barriers of the intestine, and thereby changes the microenvironment in the gut. We further verify that the administration of fecal microbiota transplantation with a healthy gut microbiome alleviates the intestinal damage induced by arsenic. Intriguingly, by using 16S rRNA sequencing and anaerobic culture, we identify a novel role of gut-derived strain, Roseburia intestinalis, which exhibits significant protection against arsenic-induced intestinal toxicity in mice. By applying non-targeted metabolomics after arsenic exposure, this work further establishes the beneficial effects and the potential metabolites associated with Roseburia intestinalis, including cacodylic acid, carindone, 3-hydroxymelatonin and L-galacto-2-heptulose, etc. Transcriptomic analysis reveals that the protective effects of Roseburia intestinalis against arsenic-induced intestinal injury include mainly immune-related pathways. Taken together, these findings highlight that supplementation with gut-derived Roseburia intestinalis is an alternative strategy that could be used in the prevention and treatment of arsenic-related intestinal disorders.},
}

@article {pmid37338497,
year = {2025},
author = {Wong, EYT and Lee, JWJ and Lim, JFY and Toh, HC},
title = {The East Asian gut microbiome and its role in oncology: a narrative review.},
journal = {Singapore medical journal},
volume = {66},
number = {8},
pages = {426-430},
pmid = {37338497},
issn = {2737-5935},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Neoplasms/therapy/microbiology ; Immunotherapy/methods ; Asia, Eastern ; *Medical Oncology ; Fecal Microbiota Transplantation ; Immune Checkpoint Inhibitors/therapeutic use ; East Asian People ; },
abstract = {The field of onco-microbiome is rapidly expanding. Multiple studies have shown the crucial role of gut microbiota in the regulation of nutrient metabolism, immunomodulation and protection against pathogens. Tools for manipulating the gut microbiota include dietary modification and faecal microbiota transfer. Accumulating evidence has also documented the application of specific intestinal microbiome in cancer immunotherapy, notably in enhancing the efficacy of immune checkpoint inhibitors. The aim of this review is to focus on the East Asian microbiome and to provide a current overview of microbiome science and its clinical application in cancer biology and immunotherapy.},
}

Humans
*Gastrointestinal Microbiome
*Neoplasms/therapy/microbiology
Immunotherapy/methods
Asia, Eastern
*Medical Oncology
Fecal Microbiota Transplantation
Immune Checkpoint Inhibitors/therapeutic use
East Asian People

@article {pmid40818717,
year = {2025},
author = {Yang, S and Yang, M and Lu, X and Tan, Y and Chang, W and Yang, H and Xu, D and Li, D},
title = {Stimulator of interferon genes-targeted positron emission tomography tracks early microbiota-induced tumor immune remodeling and guides immunotherapy.},
journal = {Journal of controlled release : official journal of the Controlled Release Society},
volume = {},
number = {},
pages = {114132},
doi = {10.1016/j.jconrel.2025.114132},
pmid = {40818717},
issn = {1873-4995},
abstract = {Immune checkpoint inhibitors (ICIs) have made dramatic evolution in cancer management, yet their curative effect remains limited in most tumors characterized by "cold" immunophenotype. Immune remodeling by transforming "cold" tumor to "hot" one is essential to improve ICIs response, and gut microbiota modulation has emerged as a promising approach. Nevertheless, a significant challenge lies in the absence of reliable tools for early assessment of immune remodeling. To address this, we focused on the stimulator of interferon genes (STING), an essential molecule for launching anti-tumor immunity, and developed the STING-targeted PET tracer [[18]F]FBTA. [[18]F]FBTA-PET detected a significant increase in tumor uptake with a more homogeneous spatial distribution following Lactobacillus rhamnosus GG (LGG) treatment. This increased [[18]F]FBTA uptake was prior to changes in tumor volume, T cell infiltration, and [[18]F]FDG-PET signals, and showed a strong correlation with STING expression in tumor tissues. The immune remodeling mediated by LGG administration, as captured by [[18]F]FBTA-PET, was also successfully replicated in recipient mice through fecal microbiota transplantation. Guided by [[18]F]FBTA-PET, the combination of LGG with αPD-L1 achieved superior anti-tumor efficacy. Furthermore, [[18]F]FBTA binding radioactivity positively correlated with STING expression in patients' tumor tissues. Our results established [[18]F]FBTA-PET as a robust indicator for early assessment of immune remodeling and guiding ICI-based combination therapies, highlighting its potential for clinical translation.},
}

@article {pmid40816223,
year = {2025},
author = {Merrick, B and Prossomariti, D and Allen, E and Bisnauthsing, K and Kertanegara, M and Sergaki, C and Le Guennec, AD and Delord, M and Bell, JT and Conte, MR and Moyes, DL and Shankar-Hari, M and Douiri, A and Goodman, AL and Shawcross, DL and Goldenberg, SD},
title = {Erratum to "Faecal microbiota transplant to ERadicate gastrointestinal carriage of Antibiotic-Resistant Organisms (FERARO): A feasibility randomised controlled trial" [J Infect 91 (2025) 106504].},
journal = {The Journal of infection},
volume = {91},
number = {3},
pages = {106583},
doi = {10.1016/j.jinf.2025.106583},
pmid = {40816223},
issn = {1532-2742},
}

@article {pmid40785733,
year = {2025},
author = {Pachhain, S and Halverstadt, B and Anekwe, EC and Phuntumart, V and Sprague, JE and Ward, CS and Cromwell, HC},
title = {Data on ethanol drinking and microbiome in alcohol preferring and non-preferring rats after a fecal microbiota transplant.},
journal = {Data in brief},
volume = {62},
number = {},
pages = {111901},
pmid = {40785733},
issn = {2352-3409},
abstract = {Alcohol Use Disorders (AUDs) constitute a global health crisis with limited effective treatments. Alterations in gut microbiome have been shown to be major contributors to substance use disorder and mental illness. Fecal Microbial Transfer (FMT) is emerging as a promising method for manipulating the Brain-Gut-Microbiome Axis in diverse health and disease states including AUD and has potential as a clinical treatment. The well characterized behavioral genetics of Alcohol Preferring (P) and Non-Preferring (NP) rat model offer valuable insights into the underlying mechanisms of AUD. This data article describes the quantitative results from an experiment on ethanol drinking behaviors and gut microbiome composition in P and NP rats that were administered fecal transfer of the microbiota. The results include data on ethanol consumption and preference of the two groups of animals prior to and following the FMT. Microbiome analysis showed that P rat ethanol-induced dysbiosis involved increased relative abundance of Akkermansia muciniphila and reduced Bacteroidetes and Lactobacillus while the FMT treatment partially restored levels. Gene abundance analysis showed an increase in alcohol metabolizing genes in P rats following three weeks ethanol access, indicating that the gut favors alcohol metabolizers after ethanol intake, which significantly decreased after FMT. These data provide details of the distinct microbial communities found in P and NP rats and the first to report data on detailed composition of the microbiome prior to and following FMT.},
}

@article {pmid40770861,
year = {2025},
author = {Drobnik, J and Pobrotyn, P and Grata-Borkowska, U and Madziarska, K and Baran, M},
title = {Trends and Efficacy in Clostridioides difficile Infection Management at a Polish Clinical Hospital.},
journal = {Medical science monitor : international medical journal of experimental and clinical research},
volume = {31},
number = {},
pages = {e948254},
pmid = {40770861},
issn = {1643-3750},
mesh = {Humans ; *Clostridium Infections/drug therapy/epidemiology ; Poland/epidemiology ; Male ; Female ; Vancomycin/therapeutic use ; *Clostridioides difficile/drug effects/pathogenicity ; Middle Aged ; Fidaxomicin/therapeutic use ; Aged ; Anti-Bacterial Agents/therapeutic use ; Metronidazole/therapeutic use ; Treatment Outcome ; Adult ; Hospitalization ; Aged, 80 and over ; Retrospective Studies ; Drug Therapy, Combination ; },
abstract = {BACKGROUND Clostridioides difficile infection (CDI) is a significant clinical problem. Treatment includes fidaxomicin and vancomycin, with second and subsequent recurrences treated with decreasing doses or sequential therapy with rifaximin, as well as considering treatment with a fecal transplant. This study aimed to analyze the method of treatment of CDI among patients hospitalized at the University Clinical Hospital in Wrocław (Poland). MATERIAL AND METHODS The study was conducted by analyzing medical records from 316 patients treated between 2016 and 2018. Due to the limited number of patients treated with fidaxomicin and rifaximin per year, these cases were combined for analysis when exploring the relationship between the year of hospitalization and CDI treatment. Patients spanning the turn of the year were assigned to the year with a longer hospitalization duration for a more robust analysis. RESULTS The predominant treatments for CDI were metronidazole and vancomycin in combination (40.5%), metronidazole alone (26.9%), and vancomycin alone (20.6%). Fidaxomicin was rarely used (1.6%) despite its 100% effectiveness. Although administered to only 5 patients, fidaxomicin achieved a 100% cure rate, highlighting its therapeutic promise. Treatment patterns shifted over the study period, but no significant difference in mortality was observed between years (P=0.904). Overall mortality among CDI patients was 24.7%, compared to 1.52% in the general inpatient population. Patients who died were more likely to have received metronidazole + vancomycin (P=0.009). CONCLUSIONS The mortality rate among CDI patients was notably high. Use of metronidazole alone decreased while alternative therapies (rifaximin, fidaxomicin) increased, but without impacting year-to-year mortality differences. Given its 100% cure rate in our cohort, broader use of fidaxomicin could meaningfully improve patient outcomes.},
}

Humans
*Clostridium Infections/drug therapy/epidemiology
Poland/epidemiology
Male
Female
Vancomycin/therapeutic use
*Clostridioides difficile/drug effects/pathogenicity
Middle Aged
Fidaxomicin/therapeutic use
Aged
Anti-Bacterial Agents/therapeutic use
Metronidazole/therapeutic use
Treatment Outcome
Adult
Hospitalization
Aged, 80 and over
Retrospective Studies
Drug Therapy, Combination

@article {pmid40770084,
year = {2025},
author = {Xie, M and Li, X and Lau, HC and Yu, J},
title = {The gut microbiota in cancer immunity and immunotherapy.},
journal = {Cellular & molecular immunology},
volume = {},
number = {},
pages = {},
pmid = {40770084},
issn = {2042-0226},
abstract = {The human gastrointestinal tract harbors trillions of microorganisms, including bacteria, fungi, and viruses, to form the gut microbiota. Cumulative evidence has demonstrated the critical impact of gut microbes on cancer immunity. In cancer, an altered gut microbiota enriched with pathogenic bacteria can actively promote immune evasion and disrupt antitumor immunity, thereby supporting tumor growth and survival. Conversely, beneficial commensal bacteria (e.g., Lactobacillus and Bifidobacterium) have emerged as therapeutic probiotics for cancer prevention and as adjuvants for cancer therapy. The gut microbiota is also closely linked to the efficacy of immunotherapy. This review summarizes the effects of pathogenic bacteria and beneficial commensals, including T cells, B cells, natural killer cells, innate lymphoid cells, and myeloid-derived suppress cells, on various innate and adaptive immune cell populations in cancer. It also explores the mechanisms by which the gut microbiota influences immunotherapy efficacy, such as the modulation of innate immune cells and CD8[+] T cells. Given its importance, an increasing number of studies have developed approaches to target the gut microbiota to improve immunotherapy outcomes and reduce immune-related adverse events. These strategies include antimicrobial intervention, probiotics, prebiotics/dietary modifications, microbial metabolites, phage therapy, and fecal microbiota transplantation. This review also evaluates clinical applications that use the gut microbiota to predict immunotherapy outcomes. Overall, the current understanding of host‒microbe interactions within the tumor microenvironment has laid a critical foundation for the translation of microbiota research into clinical practice, ultimately benefiting patients.},
}

@article {pmid38109364,
year = {2024},
author = {Pun, CK and Huang, HC and Chang, CC and Hsu, SJ and Huang, YH and Hou, MC and Lee, FY},
title = {Hepatic encephalopathy: From novel pathogenesis mechanism to emerging treatments.},
journal = {Journal of the Chinese Medical Association : JCMA},
volume = {87},
number = {3},
pages = {245-251},
doi = {10.1097/JCMA.0000000000001041},
pmid = {38109364},
issn = {1728-7731},
mesh = {Humans ; *Hepatic Encephalopathy/therapy/drug therapy ; Quality of Life ; Gastrointestinal Agents ; Lactulose/therapeutic use ; Rifaximin/therapeutic use ; },
abstract = {Hepatic encephalopathy (HE) is one of the major complications of liver disease and significantly affects the quality of life (QOL) of patients. HE is common and frequently relapses in cirrhotic patients. The management of HE is supportive, and precipitating conditions should be eliminated. Most drugs used to treat HE are conventional and include nonabsorbable disaccharides such as lactulose, and antibiotics such as rifaximin. However, their therapeutic efficacy is still suboptimal, and novel therapeutic agents are urgently needed. In addition, the optimal management and diagnosis of minimal HE/covert HE are under debate. In this review, we focus on novel pathogenetic mechanisms such as central nervous system clearance, and emerging therapeutic targets of HE, such as fecal material transplantation. We also discuss different classifications and etiologies of HE.},
}

Humans
*Hepatic Encephalopathy/therapy/drug therapy
Quality of Life
Gastrointestinal Agents
Lactulose/therapeutic use
Rifaximin/therapeutic use

@article {pmid35068600,
year = {2022},
author = {Zhu, J and Su, J},
title = {Alterations of the Gut Microbiome in Recurrent Malignant Gliomas Patients Received Bevacizumab and Temozolomide Combination Treatment and Temozolomide Monotherapy.},
journal = {Indian journal of microbiology},
volume = {62},
number = {1},
pages = {23-31},
pmid = {35068600},
issn = {0046-8991},
abstract = {UNLABELLED: This case-control study explored compositions of gut microbiome in recurrent malignant gliomas patients who had received bevacizumab and Temozolomide combination treatment and Temozolomide monotherapy. We investigated gut microbiota communities in feces of 29 recurrent malignant gliomas patients received combination treatment with bevacizumab and Temozolomide (Group 1) and monotherapy with Temozolomide alone (Group 2). We took advantage of the high-throughput Illumina Miseq sequencing technology by targeting the third and fourth hypervariable (V3-V4) regions of the 16S ribosomal RNA (rRNA) gene. We found that the structures and richness of the fecal microbiota in Group 1 were different from Group 2 with LEfSe analysis. The fecal microbiota in both Group 1 and Group 2 were mainly composed by Firmicutes, Proteobacteria, Bacteroidetes and Actinobacteria. However, Group 1 patients had higher relative abundance of Firmicutes, Bacteroidetes, Actinobacteria and lower relative abundance of Bacteroidetes and Cyanobacteria in their fecal microbiota than that in Group 2 patients. To evaluate bevacizumab involved post-treatment state of the fecal microbiota profile, we used random forest predictive model and ensembled decision trees with an AUC of 0.54. This study confirmed that the gut microbiota was different in recurrent malignant gliomas patients received the combination therapy of bevacizumab and Temozolomide compared with Temozolomide monotherapy. Our discover can help better understand the influence of bevacizumab related treatment on recurrent malignant gliomas patients. Therefore, this finding may also support the potentially therapeutic options for recurrent malignant gliomas patients such as fecal microbiota transplant.

SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s12088-021-00962-2.},
}

@article {pmid40825820,
year = {2025},
author = {Ahn, JS and Kim, HM and Han, EJ and Hong, ST and Chung, HJ},
title = {Discovery of intestinal microorganisms that affect the improvement of muscle strength.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {30179},
pmid = {40825820},
issn = {2045-2322},
support = {RS-2023-00224099//the National Research Foundation (NRF)/ ; },
abstract = {This study provides the first evidence related to the identification of microbial strains closely associated with muscle strength enhancement, independent of the host's genetic background. Fecal transplants from humans into mice revealed a significant impact of gut bacteria on muscle strength, with some mice experiencing increases, while others showed no change or decreases. Interestingly, analysis of the fecal and gastrointestinal tract bacteria from each mouse classified by the degree of muscle strength revealed significant differences based on muscle strength. Furthermore, a more diverse microbial community was observed in the gastrointestinal tract compared to the feces. Further investigation identified two bacterial species, Lactobacillus johnsonii (L. johnsonii) and Limosilactobacillus reuteri (L. reuteri), that are related to improved muscle strength. Indeed, we confirmed that the supplementation with these bacteria in aged mice significantly enhanced their muscle strength by increasing the mRNA expression levels of follistatin (FST) and insulin-like growth factor-1 (IGF1) in muscle tissue. Overall, this study provides the first evidence that specific gut bacteria can directly improve muscle strength and introduces a novel approach to studying the gut microbiome's influence on complex traits.},
}

@article {pmid40825448,
year = {2025},
author = {Qi, XY and Liu, MX and Jiang, XJ and Gao, T and Xu, GQ and Zhang, HY and Su, QY and Du, Y and Luo, J and Zhang, SX},
title = {Gut microbiota in rheumatoid arthritis: Mechanistic insights, clinical biomarkers, and translational perspectives.},
journal = {Autoimmunity reviews},
volume = {},
number = {},
pages = {103912},
doi = {10.1016/j.autrev.2025.103912},
pmid = {40825448},
issn = {1873-0183},
abstract = {Rheumatoid arthritis (RA) is a systemic autoimmune disease shaped by complex interactions between genetics and environmental factors, among which gut microbiota has emerged as a critical modulator. Recent advances have implicated gut microbiota dysbiosis in RA pathophysiology, with evidence spanning mechanistic, diagnostic, and therapeutic dimensions. This review summarizes current knowledge of the gut-joint axis and outlines microbiota-based strategies for RA management. Numerous studies have demonstrated consistent alterations in gut microbial communities in patients with RA, with enrichment of Prevotella copri observed in 75% of patients with new-onset RA compared to 21.4% of healthy controls, suggesting a potential association with disease initiation. Mechanistically, we detail how microbial dysbiosis, including that of bacteria, fungi, and viruses, disrupts intestinal barrier integrity, skews T helper 17/T regulatory and T follicular helper/T follicular regulatory immune axes, induces molecular mimicry, and alters the profiles of microbial metabolites such as short-chain fatty acids. Diagnostically, microbial taxa and metabolites serve as promising biomarkers. Machine learning models based on microbiota profiles have achieved area under the curve (AUC) values exceeding 0.88, with discriminatory taxa such as Ruminococcus gnavus and Fusicatenibacter. Therapeutically, we reviewed microbiota-targeted interventions, such as probiotics, prebiotics, antibiotics, fecal microbiota transplantation, diet, and herbal medicines, highlighting the emerging field of pharmacomicrobiomics. Gut microbial signatures have shown promise in predicting treatment responses, including methotrexate efficacy via the enterotype-based gut microbial human index model (AUC = 0.945). This review proposes an integrated framework linking microbial alterations with RA onset and progression and presents gut microbiota as a promising frontier for biomarker discovery, personalized intervention, and precision medicine.},
}

@article {pmid40825385,
year = {2025},
author = {Du, Y and He, C and An, Y and Zhao, Y and Zhang, H and Shan, Z and Yang, Y and Wang, M and Xie, J and Huang, Y and Fu, W and Yuan, Y and Zhao, B},
title = {Gut microbiota modified by mulberry leaf water extract improves T2DM through browning of WAT/BAT activation mediated by SCFAs-AMPK/SIRT1/PGC-1α signaling pathway.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {120408},
doi = {10.1016/j.jep.2025.120408},
pmid = {40825385},
issn = {1872-7573},
abstract = {Mulberry leaf (Morus alba L.), traditionally recorded in "Compendium of Materia Medica" for diabetes treatment. Mulberry leaf water extract (MLE) has also been shown in modern studies to improve blood glucose levels while restoring gut microbiota homeostasis and increasing short-chain fatty acids (SCFAs) levels. However, the causal relationship between MLE-promoted SCFAs elevation and improvements in glucose/lipid metabolism as well as the exact mechanism, remain unclear.

AIM OF THE STUDY: This study aimed to clarify the causal relationship between MLE-promoted SCFAs elevation and improvements in glucose/lipid metabolism as well as the exact mechanism.

MATERIALS AND METHODS: db/db mice received antibiotic-induced microbiota depletion to generate pseudo-germ-free model, followed by parallel interventions: fecal microbiota transplantation (FMT) from MLE (4 g crude drug/kg)-treated or untreated donors, and direct SCFAs supplementation. Glucose and lipid metabolism in brown adipose tissue (BAT) and inguinal white adipose tissue (IWAT), and hepatic steatosis/inflammation were evaluated through biochemical assays, qRT-PCR and histology. Protein expressions in adipose tissues were assessed by Western blotting and immunohistochemistry. Gut microbiota composition was analyzed by 16S rRNA sequencing and fecal SCFAs levels were detected by targeted metabolomics.

RESULTS: Both FMT-MLE and SCFAs treatments demonstrated marked metabolic benefits, including enhanced glucose/lipid homeostasis, improved lipid metabolism, alleviated hepatic steatosis and inflammation, restored microbial balance, and elevated SCFAs concentrations. Mechanistically, mice treated with FMT-MLE and SCFAs showed increased BAT activity and exhibited increased energy expenditure, and browning of WAT. Additionally, FMT-MLE and SCFAs upregulated the protein expression of phosphorylated-AMP-activated protein kinase (p-AMPK), p-AMPK/adenosine monophosphate-activated protein kinase (AMPK), sirtuin 1 (SIRT1) and peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) in BAT and IWAT.

CONCLUSION: MLE-modulated gut microbiota ameliorates T2DM via SCFAs-activated AMPK/SIRT1/PGC-1α signaling, promoting WAT browning and BAT activation.},
}

@article {pmid40823499,
year = {2025},
author = {Mikulska, M and Robin, C and Neofytos, D and Oltolini, C and Piekarska, A and Reigadas, E and Gil, L and Chemaly, RF and Groll, AH and Muñoz, P and Teh, BW},
title = {Management of Clostridioides difficile infection in patients with haematological malignancies and after cellular therapy: guidelines from 10th European Conference on Infections in Leukaemia (ECIL-10).},
journal = {EClinicalMedicine},
volume = {87},
number = {},
pages = {103371},
doi = {10.1016/j.eclinm.2025.103371},
pmid = {40823499},
issn = {2589-5370},
abstract = {Clostridioides difficile infection (CDI) poses a significant challenge in patients with haematological malignancies (HM) and those undergoing cellular therapy such as haematopoietic cell transplantation (HCT) or CAR T-cell therapy. These patients have high rates of both colonization with Clostridioides difficile and diarrhoea due to non-infectious causes, leading to challenges with establishing diagnosis and optimal management of CDI, especially in the setting of molecular detection of toxin genes alone. Current severity criteria are of limited usefulness since underlying haematological disease and its treatment impact white blood count and inflammatory manifestations of severe CDI. Extensive exposure to antibiotics, profound microbiota damage and bidirectional relationship with gastro-intestinal graft-versus-host disease after transplant further complicate clinical management. Therefore, the 10th European Conference on Infections in Leukemia (ECIL-10) group comprehensively reviewed the literature (published 01/01/2010-15/09/2024) on the epidemiology, treatment and prevention of CDI, and formulated consensus recommendations for the management of CDI specific to this population. New definitions of proven, probable and possible CDI in this population were developed and proposed for use in clinical research to standardise reporting.},
}

@article {pmid40822487,
year = {2025},
author = {Han, M and Zhou, Y and Gao, X and Cheng, X and Deng, L and Ji, S and Li, Z and Cai, Y and Yan, C and Chen, Y},
title = {Modulation of gut microbiota by Gardeniae Fructus oil exerts TLR4/NF-κB/NLRP3 pathway-mediated antidepressant effects based on transcriptomics and fecal transplantation.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1635897},
doi = {10.3389/fphar.2025.1635897},
pmid = {40822487},
issn = {1663-9812},
abstract = {BACKGROUND: Although our team has demonstrated the antidepressant effect of Gardeniae Fructus oil (OGF) in the early stages, the mechanism of whether OGF works by regulating the gut microbiota is not clear. This study aims to elucidate OGF's gut-brain axis mechanism in depression.

METHODS: Chronic unpredictable mild stress (CUMS) was used to establish a depressed mouse model, and the depression-like behavior of mice was observed by behavioral tests after antibiotic pretreatment and fecal microbiota transplantation (FMT). HE staining was used to observe the pathological changes in the hippocampus and colon; ELISA was used to detect the content of neurotransmitters and pro-inflammatory factors; Western blot was used to detect the expression of colonic tight junction proteins. The signaling pathways regulating the antidepressant properties of OGF were obtained by transcriptome sequencing analysis and validated at the protein level.

RESULTS: Compared with the CON group, mice in the CUMS group showed significant depressive-like behavior, pathological damage to the hippocampus and colon tissues, significant decrease in levels of 5-HT, DA, and BDNF in the hippocampus, significant increase in levels of IL-1β, IL-6, TNF-α, DAO, and LPS in serum, significant decrease in colonic tight junction protein expression, and significant increase in protein expression of TLR4, p-NF-κB, NLRP3, ASC, and IL-1β in the hippocampus (P < 0.01); Compared with the CUMS group, the FMT group could effectively improve the above situation (P < 0.05, P < 0.01), whose therapeutic effect was second only to the OGF group (P < 0.01), while ABX + OGF group did not show obvious therapeutic effect.

CONCLUSION: OGF might exert antidepressant effects by modulating gut microbiota and mediating the hippocampal TLR4/NF-κB/NLRP3 pathway.},
}

@article {pmid40822485,
year = {2025},
author = {Hu, P and Zhang, L and Hu, H and Wang, D and Chen, J and Xiao, J and Wu, H and Qi, L and Qin, K and Zuo, X and Li, J},
title = {Red yeast rice extract improves lipid metabolism by modulating gut microbiota in high-fat diet mice.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1608582},
doi = {10.3389/fphar.2025.1608582},
pmid = {40822485},
issn = {1663-9812},
abstract = {As a traditional food-medicine dual-purpose substance, red yeast rice (RYR) has gained wide attention for its lipid-lowering activity. However, existing studies mainly focus on the liver-targeted effects of statin-like components, with limited systematic insights into its lipid metabolism regulation via gut microbiota. This study combines high-fat diet (HFD)-induced hyperlipidemia mouse models, 16S rRNA gene sequencing, untargeted metabolomics, and fecal microbiota transplantation (FMT) to investigate the potential of RYR extract in improving lipid metabolism through gut microbiota modulation. The results showed that RYR extract significantly improved body weight, serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C) levels, and hepatic lipid deposition in HFD-fed mice. Additionally, RYR extract effectively restored the intestinal structural damage and enhanced intestinal barrier function. 16S rRNA revealed that RYR extract significantly modulated the gut microbiota, increasing the abundance of beneficial bacteria such as Bifidobacterium and restoring the ratio of Firmicutes to Bacteroidota. Metabolomics analysis revealed that RYR extract significantly modulated the gut microbiota-derived metabolites, particularly in the tryptophan metabolism and phenylalanine metabolism. FMT experiments showed that the fecal microbiota from RYR-treated group obviously improved the blood lipid levels, liver pathology, and intestinal function in HFD-fed mice. These results suggest that RYR extract improves lipid metabolism through the modulation of gut microbiota and related metabolic pathways, which provides new insights into the mechanism research of RYR's lipid-lowering effect.},
}

@article {pmid40822387,
year = {2025},
author = {Wang, K and Gao, C and Zhu, L and Chen, M and Tong, YX and Zhang, S},
title = {Fecal microbiota transplantation for chronic constipation: a systematic review and meta-analysis of clinical efficacy, safety, and microbial dynamics.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1604571},
doi = {10.3389/fmicb.2025.1604571},
pmid = {40822387},
issn = {1664-302X},
abstract = {BACKGROUND: Chronic constipation, a prevalent gastrointestinal disorder with limited treatment efficacy in refractory cases, has prompted exploration of fecal microbiota transplantation (FMT) as a novel therapeutic strategy. This systematic review and meta-analysis evaluate the efficacy, safety, and gut microbial dynamics of FMT in adults with chronic constipation.

METHODS: We systematically searched PubMed, Embase, Web of Science, and Cochrane Library up to January 2025, identifying 1,072 records. Nine studies (n = 245 patients) met inclusion criteria for qualitative synthesis, with eight contributing to meta-analysis. Outcomes included constipation remission and improvement, stool metrics, quality of life, and microbiota changes. Random-effects models analyzed pooled remission rates, mean differences (MDs), and heterogeneity (I[2] statistics).

RESULTS: Fecal microbiota transplantation achieved a 50.7% pooled remission rate (95% CI: 38.7%-62.7%) and 64.8% improvement rate (95% CI: 51.4%-76.3%). Significant improvements were observed in stool consistency (MD = 1.32, 95% CI: 1.05-1.35), quality of life (GIQLI MD = 32.19, 95% CI: 17.15-47.23), and symptom severity (Wexner MD = -4.83, 95% CI: -7.15-2.51). Post-FMT microbiota analyses revealed enrichment of beneficial taxa (Bifidobacterium, Prevotella; Firmicutesacteroidetes) and suppression of pro-inflammatory Enterobacteriaceae. Transient gastrointestinal adverse events (e.g., bloating: 17.3%) resolved spontaneously, with no severe complications reported.

CONCLUSION: Fecal microbiota transplantation demonstrates clinically meaningful symptom relief and gut microbiota remodeling in chronic constipation, supported by favorable short-term safety. While heterogeneity in protocols and limited RCT data warrant caution, these findings advocate standardized FMT frameworks and confirmatory trials to optimize therapeutics for refractory constipation.

https://www.crd.york.ac.uk/prospero/, identifier CRD42025643634.},
}

@article {pmid40821820,
year = {2025},
author = {Dai, Z and Cheng, W and Peng, H and Qiu, X and Sun, J and Liu, X and Sun, X and Cai, J and Wang, J and Li, G and Lv, Y and Chen, S and Zhong, Z},
title = {Microbiota composition-based donor selection affects FMT efficacy in a murine colitis model.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1635244},
doi = {10.3389/fimmu.2025.1635244},
pmid = {40821820},
issn = {1664-3224},
abstract = {BACKGROUND: Growing evidence links gut microbial dysbiosis to inflammatory bowel disease (IBD) pathogenesis, establishing fecal microbiota transplantation (FMT) as a microbiota-targeted therapy; however, variable outcomes in randomized trials highlight the need to identify compositional features of donor microbiota associated with FMT efficacy.

OBJECTIVE: This study aimed to investigate how the composition of the donor gut microbiota influences the therapeutic efficacy of FMT in IBD.

METHOD: Fecal DNA from 39 IBD patients and 42 healthy donors was analyzed via 16S rRNA sequencing. Donor-enriched genera (identified through differential analysis and median abundance thresholds) guided FMT selection. Dextran sulfate sodium (DSS)-induced colitis mice received donor microbiota transplants; disease activity and microbiota dynamics were evaluated through longitudinal sequencing.

RESULTS: IBD patients showed reduced microbial diversity and increased Proteobacteria phylum versus healthy donors, as well as the genera Escherichia-Shigella, Megamonas, and Klebsiella. Linear discriminant analysis effect size (LEfSe) analysis identified 50 differentially abundant genera, with 36 beneficial taxa enriched in donors. Based on median abundance of these health-associated genera, four high- and low-abundance donors were selected. FMT from high-abundance donors outperformed low-abundance donors and 5-ASA in colitis mice, restoring microbial diversity to healthy levels. Recipient mice showed increased Firmicutes and Bacteroidota and decreased Verrucomicrobiota, with Lactobacillus and Dubosiella enrichment and normalization of Lachnospiraceae NK4A136 group, Akkermansia, Turicibacter, and Parabacteroides. LEfSe identified 24 genera distinguishing IBD and control mice; post-FMT microbiota of high-abundance donor recipients more closely resembled controls, correlating with therapeutic success.

CONCLUSION: FMT ameliorated IBD symptoms in murine models, with therapeutic efficacy associated with the relative abundance of health-associated microbial genera in donor microbiota.},
}

@article {pmid40821112,
year = {2025},
author = {Zhao, S and Dan, L and Huang, R and Shen, Z and Huang, D and Wu, P and Ma, Z},
title = {Decoding the impact of gut microbiota on heart failure.},
journal = {Genes & diseases},
volume = {12},
number = {6},
pages = {101592},
doi = {10.1016/j.gendis.2025.101592},
pmid = {40821112},
issn = {2352-3042},
abstract = {Decreased cardiac output in heart failure leads to intestinal ischemia and increased permeability. Substantial changes occur in the gut microbiota, characterized by a decline in beneficial bacteria and an overgrowth of potentially harmful bacteria. The gut microbiota is intricately linked to prevalent risk factors for heart failure, including hypertension, diabetes, obesity, and renal insufficiency. Furthermore, imbalanced microbiota-derived metabolites enter the bloodstream and may contribute to the progression of heart failure. Ongoing research explores gut microbiota manipulation to alleviate heart failure with probiotics, targeted antibiotics, fecal microbiota transplantation, and dietary adjustments. This review summarizes how gut microbiota participates in heart failure and highlights the emerging promise of modulating gut dysbiosis as a therapeutic approach for managing heart failure.},
}

@article {pmid40819131,
year = {2025},
author = {Tang, B and Li, S and Li, X and He, J and Zhou, A and Wu, L and Xiao, X and Wang, S and Jiang, H and Jian, J and Hou, Z and Ge, Y and Lei, Y and Zhou, J and Tu, D and Lu, C and Yang, M and Yang, S},
title = {Cholecystectomy-related gut microbiota dysbiosis exacerbates colorectal tumorigenesis.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {7638},
pmid = {40819131},
issn = {2041-1723},
support = {82030020//National Natural Science Foundation of China (National Science Foundation of China)/ ; 82172958//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
abstract = {Cholecystectomy represents the most prevalent biliary surgical procedure for gallbladder abnormalities. Growing evidence suggests that cholecystectomy is associated with an elevated risk of colorectal cancer. However, the underlying mechanism remains elusive. Here we show that cholecystectomy exacerbates colorectal tumorigenesis in both AOM/DSS and APC[min/+] mice models. Metagenomic sequencing and targeted metabolomics show that cholecystectomy leads to a decrease of Bifidobacterium breve (B. breve) and an increase of Ruminococcus gnavus (R. gnavus), along with increased levels of glycoursodeoxycholic acid (GUDCA) in human and tauroursodeoxycholic acid (TUDCA) in mice. Fecal microbiota transplantation, single bacterial colonization and bile acid supplementation demonstrate that cholecystectomy-related gut microbiota perturbations promote the production of TUDCA and facilitate colorectal tumorigenesis. RNA-sequencing and co-immunoprecipitation reveal that the compromised bile acid metabolism inhibits farnesoid X receptor (FXR) signaling, disrupts the FXR/β-catenin interaction, and ultimately exacerbates colorectal tumorigenesis. Significantly, FXR agonist obeticholic acid (OCA) averts cholecystectomy-related colorectal tumorigenesis. The gut microbiota holds a crucial position in cholecystectomy-induced colorectal tumorigenesis, and modulation of the gut microbiota-bile acid-FXR axis represents a promising preventive strategy.},
}