@article {pmid40369317,
year = {2025},
author = {Gao, YQ and Tan, YJ and Fang, JY},
title = {Roles of the gut microbiota in immune-related adverse events: mechanisms and therapeutic intervention.},
journal = {Nature reviews. Clinical oncology},
volume = {},
number = {},
pages = {},
pmid = {40369317},
issn = {1759-4782},
abstract = {Immune checkpoint inhibitors (ICIs) constitute a major breakthrough in the field of cancer therapy; their use has resulted in improved outcomes across various tumour types. However, ICIs can cause a diverse range of immune-related adverse events (irAEs) that present a considerable challenge to the efficacy and safety of these treatments. The gut microbiota has been demonstrated to have a crucial role in modulating the tumour immune microenvironment and thus influences the effectiveness of ICIs. Accumulating evidence indicates that alterations in the composition and function of the gut microbiota are also associated with an increased risk of irAEs, particularly ICI-induced colitis. Indeed, these changes in the gut microbiota can contribute to the pathogenesis of irAEs. In this Review, we first summarize the current clinical challenges posed by irAEs. We then focus on reported correlations between alterations in the gut microbiota and irAEs, especially ICI-induced colitis, and postulate mechanisms by which these microbial changes influence the occurrence of irAEs. Finally, we highlight the potential value of gut microbial changes as biomarkers for predicting irAEs and discuss gut microbial interventions that might serve as new strategies for the management of irAEs, including faecal microbiota transplantation, probiotic, prebiotic and/or postbiotic supplements, and dietary modulations.},
}

@article {pmid40368261,
year = {2025},
author = {Murayama, R and Cai, Y and Nakamura, H and Hashimoto, K},
title = {Demyelination in Psychiatric and Neurological Disorders: Mechanisms, Clinical Impact, and Novel Therapeutic Strategies.},
journal = {Neuroscience and biobehavioral reviews},
volume = {},
number = {},
pages = {106209},
doi = {10.1016/j.neubiorev.2025.106209},
pmid = {40368261},
issn = {1873-7528},
abstract = {Demyelination, defined as the loss of myelin sheaths around neuronal axons, is increasingly recognized as a key factor in a broad range of psychiatric and neurological disorders, including schizophrenia, major depressive disorder, bipolar disorder, post-traumatic stress disorder, autism spectrum disorder, substance use disorders, Alzheimer's disease, Parkinson's disease, and multiple sclerosis. This review investigates the core mechanisms driving demyelination, its clinical impact, and emerging therapeutic strategies aimed at maintaining or restoring myelin integrity. Disruption of myelin impairs crucial neural communication pathways, resulting in cognitive, motor, and behavioral deficits that substantially reduce quality of life and create significant economic and social challenges. Key contributors to demyelination include genetic predisposition, environmental triggers, immune dysregulation, neuroinflammation, and alterations in the gut-brain axis mediated by the vagus nerve. Promising therapies include sphingosine 1-phosphate receptor modulators and muscarinic acetylcholine receptor antagonists, both of which diminish immune-related myelin damage and may enhance neuroprotection. In addition, the novel antidepressant arketamine appears to boost myelination through transforming growth factor-β1 signaling pathways. Approaches targeting the gut-brain axis, such as noninvasive transcutaneous auricular vagus nerve stimulation and fecal microbiota transplantation, may also help reduce inflammation and support myelin repair. Future research should center on clarifying the precise molecular mechanisms of demyelination, developing targeted therapies, and leveraging advanced neuroimaging for earlier detection and personalized treatment. By combining immunomodulatory and neuroprotective strategies, there is potential to significantly improve outcomes for individuals affected by demyelinating psychiatric and neurological disorders.},
}

@article {pmid40364844,
year = {2025},
author = {Nazir, A and Hussain, FHN and Nadeem Hussain, TH and Al Dweik, R and Raza, A},
title = {Therapeutic targeting of the host-microbiota-immune axis: implications for precision health.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1570233},
pmid = {40364844},
issn = {1664-3224},
mesh = {Humans ; *Precision Medicine/methods ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Prebiotics/administration & dosage ; *Gastrointestinal Microbiome/immunology ; Animals ; *Host Microbial Interactions/immunology ; *Microbiota/immunology ; Immunomodulation ; },
abstract = {The human body functions as a complex ecosystem, hosting trillions of microbes that collectively form the microbiome, pivotal in immune system regulation. The host-microbe immunological axis maintains homeostasis and influences key physiological processes, including metabolism, epithelial integrity, and neural function. Recent advancements in microbiome-based therapeutics, including probiotics, prebiotics and fecal microbiota transplantation, offer promising strategies for immune modulation. Microbial therapies leveraging microbial metabolites and engineered bacterial consortia are emerging as novel therapeutic strategies. However, significant challenges remain, including individual microbiome variability, the complexity of host-microbe interactions, and the need for precise mechanistic insights. This review comprehensively examines the host microbiota immunological interactions, elucidating its mechanisms, therapeutic potential, and the future directions of microbiome-based immunomodulation in human health. It will also critically evaluate challenges, limitations, and future directions for microbiome-based precision medicine.},
}

Humans
*Precision Medicine/methods
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Prebiotics/administration & dosage
*Gastrointestinal Microbiome/immunology
Animals
*Host Microbial Interactions/immunology
*Microbiota/immunology
Immunomodulation

@article {pmid40364435,
year = {2025},
author = {Zhang, Y and Wei, Y and Han, X and Shi, L and Yu, H and Ji, X and Gao, Y and Gao, Q and Zhang, L and Duan, Y and Li, W and Yuan, Y and Shi, J and Cheng, L and Li, Y},
title = {Faecalibacterium prausnitzii prevents age-related heart failure by suppressing ferroptosis in cardiomyocytes through butyrate-mediated LCN2 regulation.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2505119},
doi = {10.1080/19490976.2025.2505119},
pmid = {40364435},
issn = {1949-0984},
mesh = {Animals ; *Myocytes, Cardiac/metabolism/drug effects/microbiology ; *Ferroptosis/drug effects ; *Heart Failure/prevention & control/microbiology/metabolism ; Rats ; Gastrointestinal Microbiome ; Humans ; *Butyrates/metabolism ; Fecal Microbiota Transplantation ; Male ; *Faecalibacterium prausnitzii/physiology/genetics ; *Lipocalin-2/metabolism/genetics ; Aged ; Aging ; Dysbiosis/microbiology ; Female ; Rats, Sprague-Dawley ; },
abstract = {Aging is a primary driver of the escalating prevalence of heart failure (HF). Age-associated gut microbiota dysbiosis has been implicated in various age-related diseases, yet its role in age-related HF remains largely unexplored. In this study, we sought to explore the potential link between age-related gut microbiota alterations and HF in the elderly. We analyzed a publicly available single-cell sequencing dataset, which revealed markedly increased ferroptosis activity in cardiac myocytes of elderly individuals compared to their younger counterparts. Notably, treatment with the ferroptosis inhibitor, ferrostatin-1, mitigated cardiac ferroptosis and prevented cardiac dysfunction in aging rats. Furthermore, fecal microbiota transplantation from elderly HF patients significantly increased cardiac ferroptosis activity and induced cardiac dysfunction in healthy recipient rats. Integrated 16S rRNA sequencing and PCR quantification revealed a marked depletion of Faecalibacterium prausnitzii (F. prausnitzii) in elderly individuals, with a more pronounced decline in elderly patients with HF. Oral administration of F. prausnitzii or its metabolite butyrate effectively attenuated age-related HF through inhibiting ferroptosis. Additionally, gene-editing techniques were employed to generate F. prausnitzii BCoAT mutant deficient in butyrate production. Intriguingly, the protective effect was lost in the butyrate-deficient F. prausnitzii strain. Mechanistically, butyrate reduced intracellular iron accumulation and suppressed ferroptosis by downregulating LCN2 expression in senescent cardiomyocytes. Our findings highlight the critical role of aged microbiota-induced ferroptosis in HF and propose F. prausnitzii or butyrate may serve as potential targets for the prevention and treatment of age-related HF.},
}

Animals
*Myocytes, Cardiac/metabolism/drug effects/microbiology
*Ferroptosis/drug effects
*Heart Failure/prevention & control/microbiology/metabolism
Rats
Gastrointestinal Microbiome
Humans
*Butyrates/metabolism
Fecal Microbiota Transplantation
Male
*Faecalibacterium prausnitzii/physiology/genetics
*Lipocalin-2/metabolism/genetics
Aged
Aging
Dysbiosis/microbiology
Female
Rats, Sprague-Dawley

@article {pmid40361641,
year = {2025},
author = {Mafe, AN and Büsselberg, D},
title = {Could a Mediterranean Diet Modulate Alzheimer's Disease Progression? The Role of Gut Microbiota and Metabolite Signatures in Neurodegeneration.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {9},
pages = {},
doi = {10.3390/foods14091559},
pmid = {40361641},
issn = {2304-8158},
support = {NPRP 14S0311-210033//Qatar National Research Fund/ ; },
abstract = {Neurodegenerative disorders such as Alzheimer's disease (AD), the most common form of dementia, represent a growing global health crisis, yet current treatment strategies remain primarily palliative. Recent studies have shown that neurodegeneration through complex interactions within the gut-brain axis largely depends on the gut microbiota and its metabolites. This review explores the intricate molecular mechanisms linking gut microbiota dysbiosis to cognitive decline, emphasizing the impact of microbial metabolites, including short-chain fatty acids (SCFAs), bile acids, and tryptophan metabolites, on neuroinflammation, blood-brain barrier (BBB) integrity, and amyloid-β and tau pathology. The paper highlights major microbiome signatures associated with Alzheimer's disease, detailing their metabolic pathways and inflammatory crosstalk. Dietary interventions have shown promise in modulating gut microbiota composition, potentially mitigating neurodegenerative processes. This review critically examines the influence of dietary patterns, such as the Mediterranean and Western diets, on microbiota-mediated neuroprotection. Bioactive compounds like prebiotics, omega-3 fatty acids, and polyphenols exhibit neuroprotective effects by modulating gut microbiota and reducing neuroinflammation. Furthermore, it discusses emerging microbiome-based therapeutic strategies, including probiotics, prebiotics, postbiotics, and fecal microbiota transplantation (FMT), as potential interventions for slowing Alzheimer's progression. Despite these advances, several knowledge gaps remain, including interindividual variability in microbiome responses to dietary interventions and the need for large-scale, longitudinal studies. The study proposes an integrative, precision medicine approach, incorporating microbiome science into Alzheimer's treatment paradigms. Ultimately, cognizance of the gut-brain axis at a mechanistic level could unlock novel therapeutic avenues, offering a non-invasive, diet-based strategy for managing neurodegeneration and improving cognitive health.},
}

@article {pmid40361238,
year = {2025},
author = {Maschek, S and Østergaard, TH and Krych, L and Zachariassen, LF and Sørensen, DB and Junker Mentzel, CM and Hansen, AK and Sjögren, JM and Barfod, KK},
title = {Investigating fecal microbiota transplants from individuals with anorexia nervosa in antibiotic-treated mice using a cross-over study design.},
journal = {Journal of eating disorders},
volume = {13},
number = {1},
pages = {82},
pmid = {40361238},
issn = {2050-2974},
abstract = {Anorexia nervosa (AN) is a complex and serious mental disorder, which may affect individuals of all ages and sex, but primarily affecting young women. The disease is characterized by a disturbed body image, restrictive eating behavior, and a lack of acknowledgment of low body weight. The underlying causes of AN remain largely unknown, and current treatment options are limited to psychotherapy and nutritional support. This paper investigates the impact of Fecal Microbiota Transplants (FMT) from patients with AN on food intake, body weight, behavior, and gut microbiota into antibiotic-treated mice. Two rounds of FMT were performed using AN and control (CO) donors. During the second round of FMT, a subset of mice received gut microbiota (GM) from a different donor type. This split-group cross-over design was chosen to demonstrate any recovery effect of FMT from a non-eating disorder state donor. The first FMT, from donors with AN, resulted in lower food intake in mice without affecting body weight. Analysis of GM showed significant differences between AN and CO mice after FMT1, before cross-over. Specific bacterial genera and families Ruminococcaceae, Lachnospiraceae, and Faecalibacterium showed different abundances in AN and CO receiving mice. Behavioral tests showed decreased locomotor activity in AN mice after FMT1. After FMT2, serum analysis revealed higher levels of appetite-influencing hormones (PYY and leptin) in mice receiving AN-GM. Overall, the results suggest that AN-GM may contribute to altered food intake and appetite regulation, which can be ameliorated with FMT from a non-eating disorder state donor potentially offering FMT as a supportive treatment for AN.},
}

@article {pmid40359452,
year = {2025},
author = {Yang, G and Li, M and Zheng, X and Chen, X and Peng, Y and Li, J and Yang, S and Chen, H and Wang, Y and Zhang, H and Gong, C and Hu, F and Wan, J and Zhu, Z and Zhang, L and Li, R},
title = {Trehalose Acts as a Mediator: Imbalance in Brain Proteostasis Induced by Polystyrene Nanoplastics via Gut Microbiota Dysbiosis during Early Life.},
journal = {ACS nano},
volume = {},
number = {},
pages = {},
doi = {10.1021/acsnano.5c01639},
pmid = {40359452},
issn = {1936-086X},
abstract = {As an emerging contaminant, nanoplastics have evolved into a global ecological issue. Studies have shown that nanoplastics induce neurotoxicity across species, however, the causal mechanism remains unknown. This study aimed to explore the mechanism underlying the neurotoxicity caused by polystyrene nanoplastics (PS-NPs) via microbiota-gut-brain axis in immature mice, which serve as a model of infants and young children who are at higher exposure risk to NPs. The results indicated that while only a minority of PS-NPs reached the brain after exposure, they still had significant neurotoxic effects, as reflected by abnormalities in behavior, biochemical marker levels and histopathology. Proteomics and quantification analyses revealed that a proteostasis imbalance mediated by lysosomal and proteasome dysfunction in the brain is the key reason for the induced neurotoxicity. Further, we confirmed the indirect role of gut microbiota in the neurotoxicity induced by PS-NPs through 16S rDNA analyses and fecal microbiota transplantation. Crucial bacterial species such as Eubacterium coprostanoligenes potentially act as indicators for gut dysbiosis after PS-NPs exposure. Notably, we first estimated the indirect effect of gut microbiota on neurotoxicity attributed to PS-NPs in immature mice as 39.20% by high-dimensional mediation analysis. Trehalose was identified as a mediator connecting the gut microbiota and the brain, and the crucial role of trehalose supplementation was highlighted in remodeling the brain proteostasis to alleviate the neurotoxicity in immature mice. These findings are expected to contribute to a deeper understanding of the risk assessment and health protection of the nervous system from exposure to PS-NPs early in life.},
}

@article {pmid40359297,
year = {2025},
author = {Pakuwal, E and Tan, JL and Page, AJ and Stringer, AM and Woodman, RJ and Chinnaratha, MA},
title = {A systematic review and meta-analysis on the efficacy of fecal microbiome transplantation in patients with severe alcohol-associated hepatitis.},
journal = {European journal of gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1097/MEG.0000000000003003},
pmid = {40359297},
issn = {1473-5687},
abstract = {BACKGROUND: Severe alcohol-associated hepatitis (sAH) has a high short-term mortality, with limited treatment options. Fecal microbiota transplantation (FMT) has shown benefits in small, uncontrolled studies.

AIM: Perform a systematic review and meta-analysis to provide updated evidence on the efficacy and safety of FMT in sAH patients.

METHOD: Electronic databases were searched till 4 December 2023 for studies comparing FMT with standard of care (SOC) in sAH patients. Sensitivity analysis (leave-one-out method) and subgroup analyses were performed. Pooled risk ratio (RR) was used to compare the survival outcomes.

RESULTS: Eight studies with 444 patients (FMT: 218; SOC: 226) met the eligibility criteria and were included in this meta-analysis. The 28- and 90-day survival range was higher in the FMT group (75-100% and 53-87%) compared to the SOC group (48-80% and 25-56%). The random-effects model showed a statistically significant increase in survival in the FMT arm at 28 days [RR (95% confidence interval) 2.30 (1.24-4.28), P = 0.01] and 90 days [2.53 (1.34-4.77), P < 0.001]. However, there was no statistically significant change in survival at the 6-month [1.89 (0.89-4.05), P = 0.10] and the 12-month time [1.86 (0.68-5.08), P = 0.23]. Sensitivity analysis showed no major changes in the overall effect sizes, and subgroup analysis showed that the survival benefit was restricted only to the retrospective studies. No serious treatment-related adverse events were reported.

CONCLUSION: FMT is a safe and efficacious treatment option that improves short-term survival in sAH patients, without major adverse events. A multicentre randomized controlled trial with an adequate sample size is required to confirm these findings.},
}

@article {pmid40357397,
year = {2025},
author = {Xing, G and Cui, Y and Guo, Z and Han, B and Zhao, G},
title = {Progress on the mechanism of intestinal microbiota against colorectal cancer.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1565103},
pmid = {40357397},
issn = {2235-2988},
mesh = {*Colorectal Neoplasms/therapy/microbiology/prevention & control/immunology ; Humans ; *Gastrointestinal Microbiome/physiology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Animals ; Immunotherapy ; Signal Transduction ; },
abstract = {The intestinal microbiota plays a crucial role in the occurrence and development of colorectal cancer, and its anti - colorectal cancer mechanism has become a research hotspot. This article comprehensively expounds on the molecular mechanisms of the intestinal microbiota in anti - colorectal cancer, including aspects such as immune regulation, activation of carcinogenic signaling pathways (it should be noted that it is more reasonable to be "inhibition of carcinogenic signaling pathways"), metabolite - mediated effects, and maintenance of intestinal barrier function. At the same time, it explores the roles and potential mechanisms of intervention methods such as probiotic supplementation therapy, immunotherapy, and fecal microbiota transplantation. In addition, it analyzes the impact of the intestinal flora on the therapeutic efficacy of colorectal cancer. The existing research results are summarized, and the future research directions are prospected, with the aim of providing new theoretical bases and treatment ideas for the prevention and treatment of colorectal cancer.},
}

*Colorectal Neoplasms/therapy/microbiology/prevention & control/immunology
Humans
*Gastrointestinal Microbiome/physiology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Animals
Immunotherapy
Signal Transduction

@article {pmid40108157,
year = {2025},
author = {Huang, R and Shen, ZY and Huang, D and Zhao, SH and Dan, LX and Wu, P and Tang, QZ and Ma, ZG},
title = {Microbiota-indole-3-propionic acid-heart axis mediates the protection of leflunomide against αPD1-induced cardiotoxicity in mice.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {2651},
pmid = {40108157},
issn = {2041-1723},
support = {82070410; 82270248//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Animals ; *Leflunomide/pharmacology/therapeutic use ; Mice ; *Cardiotoxicity/prevention & control/etiology/metabolism ; *Gastrointestinal Microbiome/drug effects ; *Indoles/pharmacology/metabolism ; Myocytes, Cardiac/drug effects/metabolism ; *Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Mice, Inbred C57BL ; *Heart/drug effects ; *Propionates/metabolism/pharmacology ; Male ; Receptors, Aryl Hydrocarbon/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Fecal Microbiota Transplantation ; Immune Checkpoint Inhibitors/adverse effects ; },
abstract = {Anti-programmed death 1 (αPD1) immune checkpoint blockade is used in combination for cancer treatment but associated with cardiovascular toxicity. Leflunomide (Lef) can suppress the growth of several tumor and mitigate cardiac remodeling in mice. However, the role of Lef in αPD1-induced cardiotoxicity remains unclear. Here, we report that Lef treatment inhibits αPD1-related cardiotoxicity without compromising the efficacy of αPD1-mediated immunotherapy. Lef changes community structure of gut microbiota in αPD1-treated melanoma-bearing mice. Moreover, mice receiving microbiota transplants from Lef+αPD1-treated melanoma-bearing mice have better cardiac function compared to mice receiving transplants from αPD1-treated mice. Mechanistically, we analyze metabolomics and identify indole-3-propionic acid (IPA), which protects cardiac dysfunction in αPD1-treated mice. IPA can directly bind to the aryl hydrocarbon receptor and promote phosphoinositide 3-kinase expression, thus curtailing the cardiomyocyte response to immune injury. Our findings reveal that Lef mitigates αPD1-induced cardiac toxicity in melanoma-bearing mice through modulation of the microbiota-IPA-heart axis.},
}

Animals
*Leflunomide/pharmacology/therapeutic use
Mice
*Cardiotoxicity/prevention & control/etiology/metabolism
*Gastrointestinal Microbiome/drug effects
*Indoles/pharmacology/metabolism
Myocytes, Cardiac/drug effects/metabolism
*Programmed Cell Death 1 Receptor/antagonists & inhibitors
Mice, Inbred C57BL
*Heart/drug effects
*Propionates/metabolism/pharmacology
Male
Receptors, Aryl Hydrocarbon/metabolism
Phosphatidylinositol 3-Kinases/metabolism
Fecal Microbiota Transplantation
Immune Checkpoint Inhibitors/adverse effects

@article {pmid40356099,
year = {2025},
author = {Zhang, Y and Ni, P and Chen, H and Tang, L and Song, H and Wen, H and Miao, Y and Li, W and Li, X},
title = {Vitamin D3 ameliorates hyperglycemia by modulating gut microbiota and metabolites in prediabetic KKay mice.},
journal = {Food research international (Ottawa, Ont.)},
volume = {211},
number = {},
pages = {116369},
doi = {10.1016/j.foodres.2025.116369},
pmid = {40356099},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Prediabetic State/metabolism/drug therapy/microbiology ; *Hyperglycemia/drug therapy/metabolism ; *Cholecalciferol/pharmacology ; Male ; Blood Glucose/metabolism/drug effects ; Diet, High-Fat/adverse effects ; Toll-Like Receptor 4/metabolism ; Glucose Tolerance Test ; Signal Transduction/drug effects ; Mice, Inbred C57BL ; Fecal Microbiota Transplantation ; Feces/microbiology ; Proto-Oncogene Proteins c-akt/metabolism ; },
abstract = {Prediabetes represents a pivotal stage in the development and pathogenesis of diabetes, during which notable alterations in the gut microbiota can be observed. Vitamin D (VD) showed anti-diabetic properties, but it is unknown whether the improvement of VD on hyperglycemia is associated with gut microbiota. Thus, our objective was to investigate and verify the effects of VD3 on glucose metabolism in prediabetes, as well as to elucidate the underlying mechanisms. In this study, different concentrations of VD3 were intraperitoneally administered to prediabetic mice induced by high fat diet for 16 weeks. Biochemical analyses, oral glucose tolerance test, 16S rRNA and untargeted metabolomics were used, the mechanism was explored. Then, fecal suspensions collected from the above donors were transplanted into KKay mice for 6 weeks, and the relevant indicators were measured. The results showed that VD3 intervention alleviated glucose metabolism in KKay mice. It increased the protein expression of colon tight junction proteins, alleviated metabolic endotoxemia and inflammation, so that reduced tumor necrosis factor alpha (TNFα) induced toll-like receptor 4/nuclear factor kappa-B (TLR4/NFκB) and improvement of phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) insulin signaling pathway. VD3 affected the structure of gut microbiota and metabolites, and functional prediction analysis suggested that VD3 may affect carbohydrate. Besides, the effect of VD3 could be delivered by fecal microbiota transplantation (FMT). Consequently, VD3 ameliorate glucose metabolism by modulating gut microbiota and metabolites in KKay mice, and this ability could be transferred by FMT.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Prediabetic State/metabolism/drug therapy/microbiology
*Hyperglycemia/drug therapy/metabolism
*Cholecalciferol/pharmacology
Male
Blood Glucose/metabolism/drug effects
Diet, High-Fat/adverse effects
Toll-Like Receptor 4/metabolism
Glucose Tolerance Test
Signal Transduction/drug effects
Mice, Inbred C57BL
Fecal Microbiota Transplantation
Feces/microbiology
Proto-Oncogene Proteins c-akt/metabolism

@article {pmid40355758,
year = {2025},
author = {Saeedi Saravi, SS and Pugin, B and Constancias, F and Shabanian, K and Spalinger, M and Thomas, A and Le Gludic, S and Shabanian, T and Karsai, G and Colucci, M and Menni, C and Attaye, I and Zhang, X and Allemann, MS and Lee, P and Visconti, A and Falchi, M and Alimonti, A and Ruschitzka, F and Paneni, F and Beer, JH},
title = {Gut microbiota-dependent increase in phenylacetic acid induces endothelial cell senescence during aging.},
journal = {Nature aging},
volume = {},
number = {},
pages = {},
pmid = {40355758},
issn = {2662-8465},
support = {#310030_21A053//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; #CRSK-3_229134//Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation)/ ; #21A053//Novartis Stiftung für Medizinisch-Biologische Forschung (Novartis Foundation for Medical-Biological Research)/ ; },
abstract = {Endothelial cell senescence is a key driver of cardiovascular aging, yet little is known about the mechanisms by which it is induced in vivo. Here we show that the gut bacterial metabolite phenylacetic acid (PAA) and its byproduct, phenylacetylglutamine (PAGln), are elevated in aged humans and mice. Metagenomic analyses reveal an age-related increase in PAA-producing microbial pathways, positively linked to the bacterium Clostridium sp. ASF356 (Clos). We demonstrate that colonization of young mice with Clos increases blood PAA levels and induces endothelial senescence and angiogenic incompetence. Mechanistically, we find that PAA triggers senescence through mitochondrial H2O2 production, exacerbating the senescence-associated secretory phenotype. By contrast, we demonstrate that fecal acetate levels are reduced with age, compromising its function as a Sirt1-dependent senomorphic, regulating proinflammatory secretion and redox homeostasis. These findings define PAA as a mediator of gut-vascular crosstalk in aging and identify sodium acetate as a potential microbiome-based senotherapy to promote healthy aging.},
}

@article {pmid40354906,
year = {2025},
author = {Zain, NMM and Merrick, B and Martin-Lilley, T and Edwards, LA and Ter Linden, D and Tsoka, S and Mason, AJ and Hatton, GB and Allen, E and Royall, PG and Lilley, AK and Bruce, KD and Shawcross, DL and Goldenberg, SD and Forbes, B},
title = {Bacterial diversity, viability and stability in lyophilised faecal microbiota capsules support ongoing clinical use.},
journal = {International journal of pharmaceutics},
volume = {},
number = {},
pages = {125703},
doi = {10.1016/j.ijpharm.2025.125703},
pmid = {40354906},
issn = {1873-3476},
abstract = {Lyophilised encapsulated faecal microbiota provides a practical and cost-effective treatment option to patients with recurrent Clostridioides difficile infection. This study focused on quality assurance of an enteric-coated capsule formulation of FMT as a medicinal product by evaluating bacterial composition, diversity and viability through manufacturing steps and upon product storage at a range of temperatures. Faecal donations from pre-screened healthy individuals (n = 5) were processed according to a published protocol into one or more treatments; 5 capsules = 1 treatment dose/patient. Culture-independent next-generation 16S rRNA gene sequencing was used to speciate and quantify bacteria using a live-dead cell separation method to discriminate the viable cell load. Species diversity in donor stools aligned with other healthy gut microbiome and remained unchanged through the manufacturing process and after storage at -80 °C for 36 weeks. While diversity indices were consistent, a notable difference was observed between viable and total microbiome, particularly in species richness, which decreased when non-viable or compromised cells were excluded from analysis. Anaerobic species exhibited minimal viability loss despite processing in an aerobic environment. Furthermore, capsules were stable with storage at -20 °C and 2-8 °C, with no significant reduction of total live bacterial load after 24 weeks. In summary, 'live-dead' culture-independent analysis was used to characterise the viable faecal microbiome, which retained a diversity of bacterial species, including anaerobes, through manufacture and after storage in capsules for up to 36 weeks. These data support the comparable effectiveness of lyophilised encapsulated FMT to other formulations and delivery methods.},
}

@article {pmid40354842,
year = {2025},
author = {Zhang, S and Mao, X and Chang, L and Li, M and Wei, C and Li, H and Shen, X and Niu, K and Zhang, R and Jiang, Y and Lu, X and Song, Y and Zhou, L and Gao, L and Zhao, Z and Niu, L and Yang, Q and Hou, Y and Wu, Y},
title = {Bazi Bushen Capsule Modulates Akkermansia muciniphila and Spermidine Metabolism to Attenuate Brain Aging in SAMP8 Mice.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {119944},
doi = {10.1016/j.jep.2025.119944},
pmid = {40354842},
issn = {1872-7573},
abstract = {Bazi Bushen Capsule (BZBS), a traditional Chinese medicine formulation composed of multiple bioactive herbal components, has been validated in multicenter randomized double-blind controlled trials for its potent anti-aging properties. Previous studies from our group have demonstrated that BZBS effectively restores gut microbiota homeostasis and attenuates the impairment of intestinal barrier function, thereby ameliorating age-related cognitive decline. However, the specific molecular mechanisms by which BZBS modulates key microbial-metabolite networks to delay brain aging remain poorly understood and warrant further investigation.

AIM OF THE STUDY: This study aims to elucidate the key microbiota-metabolite networks through which BZBS improves cognitive function and delays brain aging in senescence-accelerated mouse-prone 8 (SAMP8) mice.

MATERIALS AND METHODS: Eight-week-old male SAMP8 mice were used as experimental models, randomly divided into Model, BZ-low (0.5 g/kg/d BZBS), BZ-high (1 g/kg/d BZBS), and RAPA (2 mg/kg/d rapamycin) groups. Senescence-accelerated mouse resistant 1 (SAMR1) mice served as the control group. Cognitive function was assessed using the Barnes Maze test and the three-chamber social test. The structural damage and pathological changes in the brain tissue were evaluated through transcranial Doppler, micro-computed tomography, Nissl staining, and Western blot analysis. Next, the intestinal barrier function was detected by hematoxylin-eosin (HE) staining, periodic acid-Schiff (PAS) staining, and immunofluorescence (IF) staining. Characteristic bacteria were identified by 16S rRNA sequencing, and metabolomic profiling was performed using non-targeted metabolomics. Akkermansia muciniphila (Akk) was cultured, and fecal microbiota transplantation (FMT) was employed to evaluate its contribution to intestinal barrier function.

RESULTS: The study revealed that BZBS therapy not only enhances cognitive capabilities but also restores the intestinal barrier function. Akk was identified as a key regulatory agent mediating the therapeutic effects of BZBS. BZBS administration significantly increased the abundance of Akk and modulated its metabolite profile, particularly components associated with spermidine, thereby reinforcing the intestinal barrier and mitigating age-related cognitive decline. Furthermore, this study demonstrated that Akk, administered via fecal microbiota transplantation, alleviated dextran sulfate sodium (DSS)-induced colitis..

CONCLUSION: The results showed that BZBS capsule, a traditional Chinese medicine, may delay brain aging in SAMP8 mice by modulating Akk and its spermidine production.},
}

@article {pmid40354071,
year = {2025},
author = {Fernandez, E and Wargo, JA and Helmink, BA},
title = {The Microbiome and Cancer: A Translational Science Review.},
journal = {JAMA},
volume = {},
number = {},
pages = {},
doi = {10.1001/jama.2025.2191},
pmid = {40354071},
issn = {1538-3598},
abstract = {IMPORTANCE: Growing evidence suggests that microbes located within the gastrointestinal tract and other anatomical locations influence the development and progression of diseases such as cancer.

OBSERVATIONS: Clinical and preclinical evidence suggests that microbes in the gastrointestinal tract and other anatomical locations, such as the respiratory tract, may affect carcinogenesis, development of metastases, cancer treatment response, and cancer treatment-related adverse effects. Within tumors of patients with cancer, microbes may affect response to treatment, and therapies that reduce or eliminate these microbes may improve outcomes in patients with cancer. Modulating gastrointestinal tract (gut) microbes through fecal microbiota transplant and other strategies such as dietary intervention (eg, high-fiber diet intervention) has improved outcomes in small studies of patients treated with cancer immunotherapy. In contrast, disruption of the gut microbiota by receipt of broad-spectrum antibiotics prior to treatment with cancer immunotherapy has been associated with poorer overall survival and higher rates of adverse effects in patients treated with immune checkpoint blockade for solid tumors and also with chimeric antigen receptor T-cell therapy for hematologic malignancies.

CONCLUSIONS AND RELEVANCE: Microbes in the gut and other locations in the body may influence the development and progression of cancer and may affect the response to adverse effects from cancer therapy. Future therapies targeting microbes in the gut and other locations in the body could potentially improve outcomes in patients with cancer.},
}

@article {pmid40352262,
year = {2025},
author = {Bao, M and Wu, R and Li, J and Tang, R and Song, C},
title = {Research summary, possible mechanisms and perspectives of gut microbiota changes causing precocious puberty.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1596654},
doi = {10.3389/fnut.2025.1596654},
pmid = {40352262},
issn = {2296-861X},
abstract = {The increasing global incidence of precocious puberty, linked to environmental, metabolic, and genetic factors, necessitates innovative therapies beyond gonadotropin-releasing hormone (GnRH) analogs. Accumulating evidence implicates gut microbiota dysbiosis as a pivotal regulator of pubertal timing via interactions with hormone metabolism (e.g., estrogen reactivation via β-glucuronidase), neuroendocrine pathways (nitric oxide signaling), and immune-inflammatory responses. This review delineates taxonomic alterations in central precocious puberty (CPP) and obesity-related subtypes, including Streptococcus enrichment and Alistipes depletion, alongside functional shifts in microbial metabolite production. Mechanistic insights highlight microbiota-driven modulation of the hypothalamic-pituitary-gonadal (HPG) axis, leptin/insulin dynamics, and epigenetic regulation. Emerging interventions-probiotics, fecal microbiota transplantation (FMT), and dietary modifications-demonstrate efficacy in preclinical models and early clinical studies for delaying puberty onset and restoring hormonal balance. Translational efforts to validate these strategies are critical for addressing the clinical and psychosocial challenges posed by precocious puberty, positioning gut microbiota modulation as a novel therapeutic frontier in pediatric endocrinology.},
}

@article {pmid40350912,
year = {2025},
author = {Lu, CY and Yuan, XM and He, LH and Mao, JR and Chen, YG},
title = {[Mechanism of total flavone of Abelmoschus manihot in treating ulcerative colitis and depression via intestinal flora-glycerophospholipid metabolism- macrophage polarization pathway].},
journal = {Zhongguo Zhong yao za zhi = Zhongguo zhongyao zazhi = China journal of Chinese materia medica},
volume = {50},
number = {5},
pages = {1286-1297},
doi = {10.19540/j.cnki.cjcmm.20241111.701},
pmid = {40350912},
issn = {1001-5302},
mesh = {Animals ; Mice ; *Gastrointestinal Microbiome/drug effects ; *Abelmoschus/chemistry ; *Macrophages/drug effects/immunology/metabolism ; *Colitis, Ulcerative/drug therapy/metabolism/microbiology/genetics/immunology ; *Flavones/administration & dosage ; Male ; *Depression/drug therapy/metabolism/microbiology/genetics ; *Glycerophospholipids/metabolism ; Humans ; *Drugs, Chinese Herbal/administration & dosage ; Mice, Inbred C57BL ; },
abstract = {This study delves into the mechanism of total flavone of Abelmoschus manihot(TFA) in treating ulcerative colitis(UC) and depression via inhibiting M1 polarization of macrophages and reshaping intestinal flora and glycerolphospholipid metabolism. The study established a mouse model of UC and depression induced by chronic restraint stress(CRS) and dextran sulfate sodium(DSS). The fecal microbiota transplantation(FMT) experiment after TFA intervention was conducted. Mice in the FMT donor group were modeled and treated, and fecal samples were taken to prepare the bacterial solution. Mice in the FMT receptor group were treated with antibiotic intervention, and then administered bacterial solution by gavage from mice in the donor group, followed by UC depression modeling. After the experiment, behavioral tests were conducted to evaluate depressive-like behaviors by measuring the levels of 5-hydroxytryptamine(5-HT) and brain-derived neurotrophic factor(BDNF) in the hippocampus of mice. The levels of tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-1β(IL-1β)in the brain and colon tissue of mice were also measured, and the polarization status of macrophages was evaluated by measuring the mRNA levels of CD86 and CD206. 16S ribosomal RNA(16S rRNA) sequencing technology was used to analyze changes in the intestinal flora of mice. Wide target lipidomics was used to detect serum lipid metabolite levels in mice after FMT,and correlation analysis was conducted between lipids and differential intestinal flora significantly regulated by TFA. In vitro experiments, representative glycerophospholipid metabolites and glycerophospholipid inhibitors were used to intervene in Raw264.7 macrophages, and the mRNA levels of TNF-α,IL-6,IL-1β,CD86,and CD206 were detected. The results showed that TFA and FMT after intervention could significantly improve depressive-like behavior and intestinal inflammation in mice with UC and depression, significantly downregulate pro-inflammatory cytokines and CD86 mRNA expression in brain and colon tissue, inhibiting M1 polarization of macrophages, and significantly upregulate CD206 mRNA expression, promoting M2 polarization of macrophages. In addition, the high-dose group had a more significant effect. After TFA intervention, FMT significantly corrected the metabolic disorder of glycerophospholipids in mice with UC and depression, and there was a significant correlation between differential intestinal flora and glycerophospholipids. In vitro experiments showed that glycerophospholipid metabolites, especially lysophosphatidylcholine(LPC),significantly upregulated pro-inflammatory cytokines and CD86 mRNA expression, promote M1 polarization of macrophages, while glycerophospholipid inhibitors had the opposite effect. The results indicate that TFA effectively treats depression and UC by correcting intestinal flora dysbiosis and reshaping glycerophospholipid metabolism, thereby inhibiting M1 polarization of macrophages.},
}

Animals
Mice
*Gastrointestinal Microbiome/drug effects
*Abelmoschus/chemistry
*Macrophages/drug effects/immunology/metabolism
*Colitis, Ulcerative/drug therapy/metabolism/microbiology/genetics/immunology
*Flavones/administration & dosage
Male
*Depression/drug therapy/metabolism/microbiology/genetics
*Glycerophospholipids/metabolism
Humans
*Drugs, Chinese Herbal/administration & dosage
Mice, Inbred C57BL

@article {pmid40350437,
year = {2025},
author = {Hsu, CY and Ahmad, I and Maya, RW and Abass, MA and Gupta, J and Singh, A and Joshi, KK and Premkumar, J and Sahoo, S and Khosravi, M},
title = {The potential therapeutic approaches targeting gut health in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS): a narrative review.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {530},
pmid = {40350437},
issn = {1479-5876},
mesh = {Humans ; *Fatigue Syndrome, Chronic/therapy/microbiology/physiopathology ; *Gastrointestinal Microbiome ; Dysbiosis ; },
abstract = {BACKGROUND: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disorder characterized by persistent fatigue and cognitive impairments, with emerging evidence highlighting the role of gut health in its pathophysiology. The main objective of this review was to synthesize qualitative and quantitative data from research examining the gut microbiota composition, inflammatory markers, and therapeutic outcomes of interventions targeting the microbiome in the context of ME/CFS.

METHODS: The data collection involved a detailed search of peer-reviewed English literature from January 1995 to January 2025, focusing on studies related to the microbiome and ME/CFS. This comprehensive search utilized databases such as PubMed, Scopus, and Web of Science, with keywords including "ME/CFS," "Gut-Brain Axis," "Gut Health," "Intestinal Dysbiosis," "Microbiome Dysbiosis," "Pathophysiology," and "Therapeutic Approaches." Where possible, insights from clinical trials and observational studies were included to enrich the findings. A narrative synthesis method was also employed to effectively organize and present these findings.

RESULTS: The study found notable changes in the gut microbiota diversity and composition in ME/CFS patients, contributing to systemic inflammation and worsening cognitive and physical impairments. As a result, various microbiome interventions like probiotics, prebiotics, specific diets, supplements, fecal microbiota transplantation, pharmacological interventions, improved sleep, and moderate exercise training are potential therapeutic strategies that merit further exploration.

CONCLUSIONS: Interventions focusing on the gut-brain axis may help reduce neuropsychiatric symptoms in ME/CFS by utilizing the benefits of the microbiome. Therefore, identifying beneficial microbiome elements and incorporating their assessments into clinical practice can enhance patient care through personalized treatments. Due to the complexity of ME/CFS, which involves genetic, environmental, and microbial factors, a multidisciplinary approach is also necessary. Since current research lacks comprehensive insights into how gut health might aid ME/CFS treatment, standardized diagnostics and longitudinal studies could foster innovative therapies, potentially improving quality of life and symptom management for those affected.},
}

Humans
*Fatigue Syndrome, Chronic/therapy/microbiology/physiopathology
*Gastrointestinal Microbiome
Dysbiosis

@article {pmid40350306,
year = {2025},
author = {Liu, C and Gao, Y and Chen, Y and Zhu, L and Rao, F and Huang, Y and Zeng, Y and Cai, R and Wang, F and Cheng, J},
title = {Nephropathy II Decoction Attenuates Renal Fibrosis via Regulating TLR4 and Gut Microbiota Along the Gut-Kidney Axis.},
journal = {Biological & pharmaceutical bulletin},
volume = {48},
number = {5},
pages = {577-594},
doi = {10.1248/bpb.b24-00863},
pmid = {40350306},
issn = {1347-5215},
mesh = {Animals ; *Toll-Like Receptor 4/metabolism/genetics ; *Gastrointestinal Microbiome/drug effects ; Fibrosis ; *Drugs, Chinese Herbal/pharmacology/therapeutic use ; *Kidney/pathology/drug effects/metabolism ; Male ; Myeloid Differentiation Factor 88/metabolism ; Mice ; Mice, Inbred C57BL ; Reperfusion Injury/drug therapy/pathology/metabolism ; Signal Transduction/drug effects ; NF-kappa B/metabolism ; },
abstract = {Nephropathy II Decoction (NED) is a widely used Chinese medicinal formulation for managing chronic kidney disease (CKD). Despite its extensive application, the precise mechanisms underlying its therapeutic effects remain poorly understood. This study aims to elucidate the role of NED in attenuating renal fibrosis and to explore its impact on the gut-kidney axis. The principal constituents of NED were analyzed using ultra-performance LC-tandem mass spectrometry (UPLC-MS/MS). A bilateral renal ischemia-reperfusion injury (bIRI) model was employed to induce fibrosis. RT-qPCR was utilized to assess the expression of mRNA related to the toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88) and nuclear factor-κB (NF-κB) signaling pathway. Western blotting analysis was performed to identify changes in renal fibrosis markers, TLR4/MyD88/NF-κB pathway proteins, and the colon proteins ZO-1 and Occludin-1. Serum levels of uremic toxins were quantified using enzyme-linked immunosorbent assay (ELISA), and 16S ribosomal RNA (rRNA) gene sequencing was conducted to explore changes in the gut microbiome of the mice. Our study demonstrated that mice in the NED group exhibited reduced serum creatinine, blood urea nitrogen, and urinary protein levels, alongside improvements in kidney damage and a decrease in renal fibrosis markers. In the bIRI group, TLR4/MyD88/NF-κB protein and mRNA levels, as well as intestinal tight junction proteins and enterogenic uremic toxins, were significantly reduced. NED treatment reversed these changes and modified the gut microbiota. Furthermore, fecal microbial transplantation (FMT) alleviated kidney damage and fibrosis in bIRI mice. In summary, NED ameliorates kidney injury and fibrosis by modulating the gut microbiota and may further attenuate fibrosis through the inhibition of TLR4 expression, thereby influencing the gut-kidney axis.},
}

Animals
*Toll-Like Receptor 4/metabolism/genetics
*Gastrointestinal Microbiome/drug effects
Fibrosis
*Drugs, Chinese Herbal/pharmacology/therapeutic use
*Kidney/pathology/drug effects/metabolism
Male
Myeloid Differentiation Factor 88/metabolism
Mice
Mice, Inbred C57BL
Reperfusion Injury/drug therapy/pathology/metabolism
Signal Transduction/drug effects
NF-kappa B/metabolism

@article {pmid40350047,
year = {2025},
author = {Huang, H and Yang, C and Li, S and Zhan, H and Tan, J and Chen, C and Liu, J and Wang, M and Li, H},
title = {Lizhong decoction alleviates experimental ulcerative colitis via regulating gut microbiota-SCFAs-Th17/Treg axis.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {119958},
doi = {10.1016/j.jep.2025.119958},
pmid = {40350047},
issn = {1872-7573},
abstract = {Lizhong decoction (LZD), a Traditional Chinese Medicine formula, is widely utilized to treat gastrointestinal diseases, including ulcerative colitis in China for thousands of years.

AIM OF THE STUDY: To investigate whether the protective effect of LZD on ulcerative colitis is dependent on gut microbiota and T-cell immune homeostasis.

MATERIAL AND METHODS: The preventive effects of LZD on dextran sodium sulfate (DSS)-induced colitis mice were evaluated through the measurement of body weight, disease activity index, colon length and hematoxylin-eosin staining. Flow cytometry was used to detect the ratio of Th17/Treg cells. Pseudo sterile mice and fecal transplantation experiments were used to investigate whether the preventive effect of LZD was dependent on the gut microbiota. The alterations of gut microbiota were identified by the 16S rDNA sequencing. The content of intestinal short-chain fatty acids (SCFAs) was detected by LC-MS/MS analysis. The downstream signal pathways of SCFAs were detected by the immunoblotting.

RESULTS: LZD administration significantly alleviated weight loss and intestinal injury in DSS-induced colitis mice. LZD administration also promotes the balance of Th17/Treg cells. Moreover, LZD administration relies on gut microbiota to alleviate ulcerative colitis and regulate Th17/Treg cell balance. LZD administration significantly improves gut microbial composition in colitis mice, elevating the abundance of SCFAs producing bacterium such as lachnospiraceae_nk4a136_group and Akkermansia. LZD treatment further increases the abundance of SCFAs and promotes activation of free fatty acid activated receptor 2 (FFAR2).

CONCLUSION: LZD administration promotes Th17/Treg cell balance in a gut microbiota-SCFAs dependent manner, which in turn ameliorates ulcerative colitis.},
}

@article {pmid40350003,
year = {2025},
author = {Nohesara, S and Mostafavi-Abdolmaleky, H and Dickerson, F and Pinto-Tomas, AA and Jeste, DV and Thiagalingam, S},
title = {Associations of Microbiome Pathophysiology with Social Activity and Behavior are Mediated by Epigenetic Modulations: Avenues for Designing Innovative Therapeutic Strategies.},
journal = {Neuroscience and biobehavioral reviews},
volume = {},
number = {},
pages = {106208},
doi = {10.1016/j.neubiorev.2025.106208},
pmid = {40350003},
issn = {1873-7528},
abstract = {A number of investigations have shown that gut microbiome influences humans' ability to communicate with others, and impairments in social interactions are linked to alterations in gut microbiome composition and diversity, via epigenetic mechanisms. This article reviews the links among gut microbiome, social behavior, and epigenetic shifts relevant to gut microbiome-derived metabolites. First, we discuss how different social determinants of health, such as socioeconomic status, diet, environmental chemicals, migration, ecological conditions, and seasonal changes may influence gut microbiome composition, diversity, and functionality, along with epigenetic alterations and thereby affect social behavior. Next, we consider how gut microbiome-derived metabolites, diet, probiotics, and fecal microbiome transplantation may reduce impairments in social interactions through the adjustment of epigenetic aberrations (e.g., DNA methylation, histone modifications, and microRNAs expression) which may suppress or increase gene expression patterns. Finally, we present the potential benefits and unresolved challenges with the use of gut microbiome-targeted therapeutics in reducing social deficits.},
}

@article {pmid40349812,
year = {2025},
author = {Quan, T and Zhang, W and Shi, Y and Gao, T},
title = {Melatonin-mediated intestinal microbiota homeostasis improves skin barrier damage involvement of gut-skin axis dysfunction in aging mice.},
journal = {Cellular signalling},
volume = {},
number = {},
pages = {111859},
doi = {10.1016/j.cellsig.2025.111859},
pmid = {40349812},
issn = {1873-3913},
abstract = {Researches suggested a close connection between the gut microbiome homeostasis and skin health. Melatonin, as a multifunctional molecule, has the potential to regulate intestinal homeostasis and skin function. The study further explored the potential mechanism of melatonin in ameliorating skin barrier damage from the perspective of the association between intestinal microbiota and gut-skin axis in aging mice. We established a natural aging-induced skin barrier damage mouse model with or without melatonin supplementation and fecal microbiota transplantation (FMT) to clarify the crucial role of intestinal microbiota-mediated gut-skin axis in melatonin improving skin barrier damage. Furthermore, lipopolysaccharide (LPS)-treated mice and human keratinocytes cells (HaCaT) explored the modulation mechanism of melatonin. Our results suggested that aging induced skin barrier damage, including skin microbiota disorder and epidermal barrier structure disruption, and intestinal dysbiosis. Similarly, FMT from aging mice and LPS treatment rebuild the aging-like skin barrier damage. Whereas, melatonin or resatorvid (TAK242, the antagonist of LPS) supplementation restored all consequence in aging and LPS-treated mice. In vitro, melatonin restored LPS-induced skin barrier proteins deficiency in HaCaT via decreasing the expression level of TLR4 and MyD88 and increasing the content of p-ERK, p-GSK-3β and β-catenin proteins, while the improving effects was mimicked by pretreatment with a TLR4 antagonist but were blocked by GSK-3β agonists. Our study revealed that melatonin-mediated intestinal microbiota homeostasis suppresses LPS escape to restore the skin barrier function, including skin dysbiosis and epidermal structural disruption via LPS/TLR4/MyD88/ERK/GSK-3β/β-catenin loop, further improving skin aging in mice.},
}

@article {pmid40349163,
year = {2025},
author = {Huang, M and Huang, M and Liu, L and Yang, F and He, C and Sun, YC and Jiao, YR and Tang, X and Hou, J and Chen, KX and He, WZ and Wei, J and Chen, HL and Li, X and Zeng, C and Lei, GH and Li, CJ},
title = {Gut Microbiota Modulates Obesity-Associated Skeletal Deterioration Through Macrophage Aging and Grancalcin Secretion.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2502634},
doi = {10.1002/advs.202502634},
pmid = {40349163},
issn = {2198-3844},
support = {2022YFC3601900//National Key Research and Development Program of China/ ; 2022YFC2009604//National Key Research and Development Program of China/ ; 82472521//National Natural Science Foundation of China/ ; 82272560//National Natural Science Foundation of China/ ; 82261160397//National Natural Science Foundation of China/ ; 81922017//National Natural Science Foundation of China/ ; 2023QYJC011//Central South University Research Program of Advanced Interdisciplinary Studies/ ; 2022SK2023//Key Research and Development Program of Hunan Province/ ; 2023RC1027//Science and Technology Innovation Program of Hunan Province/ ; 2022RC1009//Science and Technology Innovation Program of Hunan Province/ ; 2022RC3075//Science and Technology Innovation Program of Hunan Province/ ; 2024JC0004//Major Basic Research Projects in Hunan Province/ ; 2024M763722//China Postdoctoral Science Foundation/ ; 2023JJ30896//Natural Science Foundation of Hunan/ ; 2023JJ40965//Natural Science Foundation of Hunan/ ; 2025JJ60562//Natural Science Foundation of Hunan/ ; },
abstract = {Obesity is associated with skeletal deterioration and increased fracture risk, but the underlying mechanism is unclear. Herein, it is shown that obese gut microbiota promotes skeletal deterioration by inducing bone marrow macrophages (BMMs) senescence and grancalcin (GCA) secretion. Obese mice and those receiving obese fecal microbiota transplants exhibit increased senescent macrophages and elevated GCA expression in the bone marrow. In a study of 40 participants, it is found that obese patients are associated with higher serum GCA levels. It is further revealed that obese gut-microbiota derived lipopolysaccharides (LPS) stimulate GCA expression in senescent BMMs via activating Toll-like receptor 4 pathway. Mice with depletion of the Gca gene are resistant to the negative effects of obesity and LPS on bone. Moreover, neutralizing antibody against GCA mitigates skeletal deterioration in obese mice and LPS-induced chronic inflammation mouse model. The data suggest that the interaction between gut microbiota and the immune system contributes to obesity-associated skeletal deterioration, and targeting senescent macrophages and GCA shows potential of protecting skeletal health in obese population.},
}

@article {pmid40348497,
year = {2025},
author = {Munk Lauridsen, M and Jonasson, E and Bajaj, JS},
title = {Microbial Approaches to Treat and Prevent Hepatic Encephalopathy.},
journal = {Gastroenterology clinics of North America},
volume = {54},
number = {2},
pages = {429-451},
doi = {10.1016/j.gtc.2024.12.006},
pmid = {40348497},
issn = {1558-1942},
mesh = {Humans ; *Hepatic Encephalopathy/prevention & control/therapy/microbiology ; *Gastrointestinal Microbiome ; Probiotics/therapeutic use ; *Fecal Microbiota Transplantation/methods ; Rifaximin/therapeutic use ; Lactulose/therapeutic use ; Gastrointestinal Agents/therapeutic use ; },
abstract = {This review articulates the significance of the gut-liver-brain axis in understanding hepatic encephalopathy (HE), emphasizing the role of gut microbiota in influencing liver and brain health. Key treatments like lactulose, rifaximin, probiotics, and fecal microbiota transplantation are examined for their ability to modulate the gut microbiome, thereby mitigating HE symptoms through reduced neurotoxin production and enhanced gut barrier integrity. The synopsis highlights both established and emerging microbial therapies, presenting them as crucial to the management and future strategies of HE. This comprehensive overview explores current therapeutic approaches alongside promising future interventions, suggesting that personalized microbiome-focused treatments may revolutionize HE management.},
}

Humans
*Hepatic Encephalopathy/prevention & control/therapy/microbiology
*Gastrointestinal Microbiome
Probiotics/therapeutic use
*Fecal Microbiota Transplantation/methods
Rifaximin/therapeutic use
Lactulose/therapeutic use
Gastrointestinal Agents/therapeutic use

@article {pmid40348491,
year = {2025},
author = {Sartor, RB},
title = {Beyond Random Fecal Microbial Transplants: Next Generation Personalized Approaches to Normalize Dysbiotic Microbiota for Treating IBD.},
journal = {Gastroenterology clinics of North America},
volume = {54},
number = {2},
pages = {333-350},
doi = {10.1016/j.gtc.2024.11.002},
pmid = {40348491},
issn = {1558-1942},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Precision Medicine/methods ; *Gastrointestinal Microbiome ; *Dysbiosis/therapy/microbiology ; *Inflammatory Bowel Diseases/therapy/microbiology ; *Colitis, Ulcerative/therapy/microbiology ; Crohn Disease/therapy/microbiology ; Clostridioides difficile ; Pouchitis/therapy/microbiology ; },
abstract = {This review and commentary outline the strong rationale for normalizing the abnormal microbiota of patients with ulcerative colitis, Crohn's disease, and pouchitis and focus on strategies to improve current variable outcomes of fecal microbial transplant (FMT) in ulcerative colitis. Applying lessons from successful FMT therapy of recurrent Clostridioides difficile and insights from basic scientific understanding of host/microbial interactions provide strategies to enhance clinical outcomes in IBD. We outline promising approaches to develop novel-defined consortia of live biotherapeutic products and combination treatments to improve current results and to optimize and personalize treatment approaches in individual patients and disease subsets.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Precision Medicine/methods
*Gastrointestinal Microbiome
*Dysbiosis/therapy/microbiology
*Inflammatory Bowel Diseases/therapy/microbiology
*Colitis, Ulcerative/therapy/microbiology
Crohn Disease/therapy/microbiology
Clostridioides difficile
Pouchitis/therapy/microbiology

@article {pmid40348489,
year = {2025},
author = {Silveira, MAD and Rodrigues, RR and Trinchieri, G},
title = {Intestinal Microbiome Modulation of Therapeutic Efficacy of Cancer Immunotherapy.},
journal = {Gastroenterology clinics of North America},
volume = {54},
number = {2},
pages = {295-315},
doi = {10.1016/j.gtc.2024.10.005},
pmid = {40348489},
issn = {1558-1942},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Immunotherapy/methods ; *Neoplasms/therapy/immunology/microbiology ; Fecal Microbiota Transplantation ; Immune Checkpoint Inhibitors/therapeutic use ; },
abstract = {Bacteria are associated with certain cancers and may induce genetic instability and cancer progression. The gut microbiome modulates the response to cancer therapy. Training machine learning models with response associated taxa or bacterial genes predict patients' response to immunotherapies with moderate accuracy. Clinical trials targeting the gut microbiome to improve immunotherapy efficacy have been conducted. While single bacterial strains or small consortia have not be reported yet to be successful, encouraging results have been reported in small single arm and randomized studies using transplant of fecal microbiome from cancer patients who successfully responded to therapy or from healthy volunteers.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Immunotherapy/methods
*Neoplasms/therapy/immunology/microbiology
Fecal Microbiota Transplantation
Immune Checkpoint Inhibitors/therapeutic use

@article {pmid40348488,
year = {2025},
author = {Magier, SJ and Morley, TS and Kelly, CR},
title = {Optimizing Therapeutic Potential of Fecal Transplant in Inflammatory Bowel Disease.},
journal = {Gastroenterology clinics of North America},
volume = {54},
number = {2},
pages = {277-293},
doi = {10.1016/j.gtc.2024.12.002},
pmid = {40348488},
issn = {1558-1942},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; Gastrointestinal Microbiome ; *Inflammatory Bowel Diseases/therapy/microbiology ; *Colitis, Ulcerative/therapy/microbiology ; *Crohn Disease/therapy/microbiology ; Pouchitis/therapy ; Remission Induction ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic inflammatory condition of the gastrointestinal tract influenced by genetic, environmental, immune, and microbial factors. Reduced gut microbial diversity and elevated proinflammatory bacteria levels in IBD disrupt mucosal immunity, barrier function, and inflammatory pathways. Fecal microbiota transplantation (FMT) is a potential therapy to restore microbial balance. Studies suggest that FMT may induce remission in mild-to-moderate ulcerative colitis but show limited efficacy in Crohn's disease and pouchitis. Donor microbiota colonization correlates with remission, but varied study designs challenge findings. Further research is required to standardize FMT protocols, optimize donor selection, and ensure long-term safety.},
}

Humans
*Fecal Microbiota Transplantation/methods
Gastrointestinal Microbiome
*Inflammatory Bowel Diseases/therapy/microbiology
*Colitis, Ulcerative/therapy/microbiology
*Crohn Disease/therapy/microbiology
Pouchitis/therapy
Remission Induction

@article {pmid40348487,
year = {2025},
author = {Ressler, AM and Rao, K and Young, VB},
title = {Current Approaches to Treat and Prevent Recurrence of Clostridioides difficile.},
journal = {Gastroenterology clinics of North America},
volume = {54},
number = {2},
pages = {259-275},
doi = {10.1016/j.gtc.2025.02.005},
pmid = {40348487},
issn = {1558-1942},
mesh = {Humans ; *Clostridium Infections/prevention & control/therapy/microbiology/drug therapy ; *Anti-Bacterial Agents/therapeutic use/adverse effects ; *Clostridioides difficile ; *Gastrointestinal Microbiome/drug effects ; Fecal Microbiota Transplantation ; Recurrence ; Secondary Prevention/methods ; Probiotics/therapeutic use ; },
abstract = {Clostridioides difficile infection (CDI) and recurrent CDI (rCDI) are significant causes of morbidity and mortality. The microbiome plays a significant role in the body's defense against CDI and rCDI. Antibiotics can cause significant injury to the microbiome which leads to an increased risk of CDI and rCDI. Ongoing perturbations of the microbiome perpetuate this risk. Antibiotic treatments for CDI can kill C difficile but also can impact the microbiome. Microbiome therapeutics are effective in restoring the function of the gut microbiota and re-establishing colonization resistance. The field of microbiome therapeutics is evolving with newer, more refined, modalities in development.},
}

Humans
*Clostridium Infections/prevention & control/therapy/microbiology/drug therapy
*Anti-Bacterial Agents/therapeutic use/adverse effects
*Clostridioides difficile
*Gastrointestinal Microbiome/drug effects
Fecal Microbiota Transplantation
Recurrence
Secondary Prevention/methods
Probiotics/therapeutic use

@article {pmid40348275,
year = {2025},
author = {Hassib, L and Kanashiro, A and Pedrazzi, JFC and Vercesi, BF and Higa, S and Arruda, Í and Soares, Y and de Jesus de Souza, A and Barichello, T and Guimarães, FS and Ferreira, FR},
title = {Microbiota-based therapies as novel targets for autism spectrum disorder: A systematic review and meta-analysis.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111385},
doi = {10.1016/j.pnpbp.2025.111385},
pmid = {40348275},
issn = {1878-4216},
abstract = {BACKGROUND: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental condition characterized by persistent deficits in social interaction and communication. Emerging evidence suggests that alterations in the gut-brain axis play a key role in the pathophysiology of ASD, and that microbiota-targeted interventions may offer therapeutic benefits. However, no clear consensus has been reached regarding the effectiveness of these strategies in ameliorating behavioral characteristics. This systematic review and meta-analysis (PROSPERO registration ID: CRD42023494067) aimed to evaluate the impact of microbiota-based interventions-including synbiotics, prebiotics, single-strain probiotics, probiotic blends, and fecal microbiota transplantation (FMT)-on behavioral outcomes in individuals with ASD, with particular emphasis on social functioning.

RESULTS: Of the 373 records initially identified, 20 studies met the inclusion criteria, comprising 16 randomized controlled trials and 4 open-label studies. The overall effect size indicated a statistically significant improvement in ASD-related behavioral symptoms following microbiota manipulation (Hedges' g = 0.47; 95 % CI: 0.30-0.64; p < 0.001; I[2] = 33.01 %), representing a small but clinically relevant effect. Heterogeneity was classified as moderate. Among the interventions, FMT and probiotic blends yielded the most substantial effects. All major limitations of the current studies were thoroughly addressed and discussed to guide future experimental designs. Additionally, we examined preclinical evidence supporting the involvement of neural, immune, and metabolic pathways in mediating the observed behavioral improvements.

CONCLUSIONS: Our findings support the potential of microbiota-based therapies as a promising and well-tolerated strategy for improving behavioral symptoms in individuals with ASD. FMT and multi-strain probiotic formulations appear particularly effective. Nevertheless, further high-quality randomized controlled trials-especially involving FMT-are urgently needed to validate these results and guide clinical implementation. Thus, these findings provide a critical foundation for future investigations seeking to refine microbiota-based interventions and uncover the underlying mechanisms through which they influence ASD-related behaviors.},
}

@article {pmid40348054,
year = {2025},
author = {Meher, R},
title = {From 'Aww to Wow': Emerging role of transfusion medicine in fecal microbiota transplantation.},
journal = {Transfusion clinique et biologique : journal de la Societe francaise de transfusion sanguine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tracli.2025.05.004},
pmid = {40348054},
issn = {1953-8022},
}

@article {pmid40341264,
year = {2025},
author = {Wang, X and Li, T and Dong, L and Li, Y and Ding, H and Wang, J and Xu, Y and Sun, W and Li, L},
title = {Exploring the lipid-lowering effects of cinnamic acid and cinnamaldehyde from the perspective of the gut microbiota and metabolites.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo00384a},
pmid = {40341264},
issn = {2042-650X},
abstract = {The increasing incidence and associated metabolic complications pose major challenges in the treatment of hyperlipidaemia. Cinnamon is a food and medicinal resource associated with lipid metabolism, but the mechanism by which its active components, cinnamic acid (CA) and cinnamaldehyde (CM), alleviate hyperlipidaemia remains unclear. Biochemical, pathological, gut microbiota, and metabolomic analyses were performed to investigate the effects of CA and CM on HFD-fed mice and the underlying mechanisms involved. Supplementation with CA and CM reduced body weight, liver, and adipose tissue accumulation in HFD-induced mice; improved glucose and lipid metabolism; and decreased inflammation and oxidative stress levels, with CM showing superior efficacy. Faecal microbiota transplantation confirmed that the therapeutic effect was closely related to core gut bacteria and metabolites. Specifically, CA and CM inhibited the growth of lipid metabolism-related genera (e.g., Turicibacter and Romboutsia) and metabolites (e.g., PC, LysoPCs, prostaglandin E2, and arachidonic acid) while promoting the growth of beneficial genera (e.g., Oscillospiraceae and Colidextribacter) and metabolites (e.g., linoleic acid, phytosphingosine, and stercobilin). Additionally, Spearman's correlation analysis revealed that serum and hepatic lipids, as well as inflammatory factors, were positively correlated with Erysipelatoclostridium, Turicibacter, Eubacterium fissicatena, Enterorhabdus, cervonoyl ethanolamide, and acetoxystachybotrydial acetate, whereas they were negatively correlated with Lachnospiraceae NK4A136, stercobilin, LysoPE (15:0/0:0), and phytosphingosine. In contrast, hepatic oxidative stress markers exhibited the opposite correlation pattern. In conclusion, CA and CM have the potential to regulate the core gut microbiota and metabolites to improve lipid metabolism and decrease related inflammation and oxidative stress levels.},
}

@article {pmid40337926,
year = {2025},
author = {Shu, Y and Jiang, H and Gao, X and Hong, P and Wang, Q and Ruan, Y and Wu, H and He, J},
title = {Microcystin-LR Induces Lipid Metabolism Disorder in Pelophylax nigromaculatus Tadpoles via the Gut-Liver Axis.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.4c12957},
pmid = {40337926},
issn = {1520-5851},
abstract = {Disruption of lipid homeostasis in aquatic animals poses serious health risks, including tissue damage and systemic metabolic dysfunction. The precise mechanisms by which microcystin-LR, a potent cyanotoxin, disrupts lipid metabolism in amphibian tadpoles remain unclear. In this study, tadpoles (Pelophylax nigromaculatus) were exposed to MC-LR and fecal microbiota transplantation (FMT) experiments were performed to investigate whether or how MC-LR at environmental concentrations interfered with tadpole lipid metabolism from the perspective of the gut microbiota-gut-liver axis. Following exposure, the liver exhibited significant inflammation, hypertrophy, and fibrosis, accompanied by elevated serum lipid levels. Furthermore, the expression levels of the farnesoid X receptor (FXR), a nuclear receptor, were significantly downregulated. Molecular docking and molecular dynamics simulations indicated a strong and stable binding between FXR and MC-LR. Moreover, MC-LR suppressed liver FXR expression or activity, triggering: (1) upregulation of sterol regulatory element-binding protein 1 (SREBP1)-mediated triglyceride (TG) synthesis, (2) inhibition of free fatty acid (FFA) β-oxidation, and (3) activation of SREBP2-dependent bile acid biosynthesis. Moreover, MC-LR altered the composition of gut microbiota and specific bile acid levels (e.g., taurocholic acid and glycochenodeoxycholic acid) in the gut, thereby interfering with hepatic lipid metabolism, as evidenced by FMT-induced hepatic lipid accumulation in recipient tadpoles. These findings identify FXR as a potentially key molecular target for MC-LR and suggest that changes in bile acid levels of intestinal microbiota metabolism also may be an important pathway driving hepatic lipid dysregulation in amphibians exposed to environmental concentrations of MC-LR.},
}

@article {pmid40336226,
year = {2025},
author = {Cui, C and Gao, S and Shi, J and Wang, K},
title = {Gut-Liver Axis: The Role of Intestinal Microbiota and Their Metabolites in the Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.},
journal = {Gut and liver},
volume = {},
number = {},
pages = {},
doi = {10.5009/gnl240539},
pmid = {40336226},
issn = {2005-1212},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as one of the most prevalent chronic liver diseases globally, and its pathogenesis is closely linked to the imbalance of intestinal microbiota and their metabolites. This article reviews the mechanisms through which intestinal microbiota influence the progression of MASLD via the gut-liver axis, elaborating on the complex roles of immune cell hyperactivation, impaired intestinal barrier function, and intestinal microbial metabolites such as short-chain fatty acids and bile acids. The imbalance of intestinal microbiota not only directly promotes the development of MASLD but also further exacerbates disease progression through abnormalities in their metabolites. Various novel therapeutic strategies are being actively developed on the basis of gut-liver axis theory, including probiotic/prebiotic/synbiotic treatment, fecal microbiota transplantation, and targeted drug therapy. These strategies aim to precisely regulate microbial homeostasis and improve glucose and lipid metabolism, thereby alleviating hepatic inflammation and fibrosis and optimizing the therapeutic outcomes of patients with MASLD. In the future, as research progresses, we will further uncover the interaction mechanisms between intestinal microbiota and MASLD and continuously explore more effective treatment methods, with the goal of improving the prognosis and quality of life for MASLD patients.},
}

@article {pmid40335640,
year = {2025},
author = {Kellermayer, R and Nagy-Szakal, D and Ihekweazu, FD and Luna, RA and Versalovic, J},
title = {Mucosal disease activity may predict response to fecal microbiota transplantation in patients with ulcerative colitis.},
journal = {Pediatric research},
volume = {},
number = {},
pages = {},
pmid = {40335640},
issn = {1530-0447},
}

@article {pmid40335161,
year = {2025},
author = {Mela, V and Heras, V and Iesmantaite, M and García-Martín, ML and Bernal, M and Posligua-García, JD and Subiri-Verdugo, A and Martínez-Montoro, JI and Gómez-Pérez, AM and Banderas, B and Moreno Indias, I and Tinahones, FJ},
title = {Microbiota fasting-related changes ameliorate cognitive decline in obesity and boost ex vivo microglial function through the gut-brain axis.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-335353},
pmid = {40335161},
issn = {1468-3288},
abstract = {BACKGROUND: Obesity-related cognitive decline is linked to gut microbiota dysbiosis, with emerging evidence suggesting that dietary interventions may ameliorate cognitive impairment via gut-brain axis modulation. The role of microglial cells in this process remains underexplored.

OBJECTIVE: To investigate how diet-induced changes in gut microbiota influence cognitive function in individuals with obesity and their microglial activity, and to determine the impact of specific dietary interventions.

DESIGN: This study included 96 participants with obesity who were randomised into three dietary intervention groups: Mediterranean diet (Med), alternate-day fasting (ADF) and ketogenic diet (Keto). Cognitive performance and microbiota composition were assessed pre-intervention and post-intervention. The effects of microbiota-related changes on microglial function were further evaluated in mice models through faecal transplantation and in vitro model with microbiota exosome treatment.

RESULTS: Both the Keto and ADF groups demonstrated significant weight loss, but cognitive performance improved most notably in the ADF group, in association with reduced inflammation. Diet-related microbiota composition was correlated with the cognitive outcomes in the human study. Mice models confirmed that the cognitive benefits of ADF were microbiota-dependent and linked to enhanced microglial phagocytic capacity and reduced inflammation, accompanied by changes in microglia morphology.

CONCLUSION: Fasting-induced modifications in gut microbiota contribute to cognitive improvement in individuals with obesity, with microglial cells playing a crucial mediatory role. Among the interventions, ADF most effectively enhanced microglial function and cognitive performance, suggesting its potential as a therapeutic strategy for obesity-related cognitive decline. Further studies are required to fully elucidate the underlying mechanisms.

TRIAL REGISTRATION NUMBER: NCT04453150.},
}

@article {pmid40334428,
year = {2025},
author = {Gu, S and Chen, C and Wang, J and Wang, Y and Zhao, L and Xiong, Z and Zhang, H and Deng, T and Pan, Q and Zheng, Y and Li, Y},
title = {Camellia Japonica Radix modulates gut microbiota and 9(S)-HpODE-mediated ferroptosis to alleviate oxidative stress against MASLD.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {143},
number = {},
pages = {156806},
doi = {10.1016/j.phymed.2025.156806},
pmid = {40334428},
issn = {1618-095X},
abstract = {BACKGROUND: Camellia japonica radix (CJR), derived from the root of Camellia japonica L., has the potential to function as an herbal tea substitute for the prevention and intervention of metabolic dysfunction-associated steatotic liver disease (MASLD). It can provide systemic therapeutic benefits, boast a favorable safety profile, facilitate convenient consumption, and support long-term applicability. Despite its potential, research on CJR remains limited.

PURPOSE: The aim of this study aims is to elucidate the therapeutic mechanisms of CJR in MASLD, thereby providing evidence to support its clinical application.

METHODS: The therapeutic effects of CJR were evaluated using a water-supplementation model in MASLD mice. Integrated microbiome, transcriptome, proteome, and metabolome analyses were employed to comprehensively explore the mechanisms involved. A drug-target pull-down assay was performed to identify specific protein targets of small molecule metabolites in vitro. Fecal microbiota transplantation in antibiotic-treated ABX mice was conducted to confirm the critical role of gut microbiota and its metabolites. Furthermore, customized medicated feed supplemented with linoleic acid was used to explore the intervention effect of its metabolite, 9(S)-HpODE, as well as to evaluate its dietary intervention potential.

RESULTS: This present study explicitly elucidates the efficacy of CJR extract in alleviating hepatic inflammation and steatosis in a MASLD model mice, with its pharmacological mechanism associated with gut microbiota, linoleic acid metabolism, and GPX4-mediated ferroptosis. Notably, 9(S)-HpODE was discovered to be a key metabolite of linoleic acid, which could target both KEAP1 and SLC7A11, bidirectionally regulating GPX4-mediated ferroptosis, while acting as a signaling molecule at low doses to induce redox adaptation via oxidative preconditioning, thus ameliorating oxidative stress in MASLD.

CONCLUSION: Our findings indicate that both CJR and linoleic acid exhibit significant potential as dietary interventions for the management of MASLD, offering promising avenues for future research and clinical application.},
}

@article {pmid40333159,
year = {2025},
author = {Gao, Y and Lou, Y and Hui, Y and Chen, H and Sang, H and Liu, F},
title = {Characterization of the Gut Microbiota in Patients with Psoriasis: A Systematic Review.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {4},
pages = {},
pmid = {40333159},
issn = {2076-0817},
support = {22LCYY-QH10//Jinling Hospital/ ; },
mesh = {Humans ; *Dysbiosis/microbiology/therapy ; Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome ; Probiotics/administration & dosage ; *Psoriasis/microbiology/therapy ; RNA, Ribosomal, 16S/genetics ; },
abstract = {Background: Psoriasis is a prevalent and persistent inflammatory disorder with systemic manifestations. Emerging evidence implicates the gut microbiota in regulating inflammatory responses, metabolic pathways, and immune homeostasis. This review synthesizes current evidence on gut microbiota dysbiosis in psoriasis and evaluates the therapeutic potential of probiotics and fecal microbiota transplantation (FMT) in disease management. Method: Following PRISMA guidelines, we systematically reviewed studies investigating gut microbiome profiles in psoriasis through the MEDLINE, EMBASE, and Web of Science databases (January 2015-December 2024). Included studies utilized 16S rRNA gene sequencing or metagenomic analyses for microbial characterization. Results: Comparative analyses revealed distinct gut microbiota patterns in psoriasis patients compared with healthy controls, although specific microbial signatures exhibited inconsistencies across studies. Notably, interventions modulating gut microbiota composition-particularly probiotic supplementation-demonstrated measurable improvements in psoriasis severity scores and inflammatory markers. Conclusions: Gut microbiome modulation represents a promising therapeutic strategy for psoriasis; however, current evidence highlights the need for standardized microbial analysis methodologies and larger longitudinal studies to establish causality. Future research should prioritize the functional characterization of microbiota-host interactions to optimize therapeutic applications.},
}

Humans
*Dysbiosis/microbiology/therapy
Fecal Microbiota Transplantation
*Gastrointestinal Microbiome
Probiotics/administration & dosage
*Psoriasis/microbiology/therapy
RNA, Ribosomal, 16S/genetics

@article {pmid40332367,
year = {2025},
author = {Ionescu, VA and Diaconu, CC and Gheorghe, G and Mihai, MM and Diaconu, CC and Bostan, M and Bleotu, C},
title = {Gut Microbiota and Colorectal Cancer: A Balance Between Risk and Protection.},
journal = {International journal of molecular sciences},
volume = {26},
number = {8},
pages = {},
pmid = {40332367},
issn = {1422-0067},
mesh = {Humans ; *Colorectal Neoplasms/microbiology/prevention & control/immunology/etiology ; *Gastrointestinal Microbiome ; Animals ; Risk Factors ; Probiotics ; },
abstract = {The gut microbiome, a complex community of microorganisms residing in the intestinal tract, plays a dual role in colorectal cancer (CRC) development, acting both as a contributing risk factor and as a protective element. This review explores the mechanisms by which gut microbiota contribute to CRC, emphasizing inflammation, oxidative stress, immune evasion, and the production of genotoxins and microbial metabolites. Fusobacterium nucleatum, Escherichia coli (pks+), and Bacteroides fragilis promote tumorigenesis by inducing chronic inflammation, generating reactive oxygen species, and producing virulence factors that damage host DNA. These microorganisms can also evade the antitumor immune response by suppressing cytotoxic T cell activity and increasing regulatory T cell populations. Additionally, microbial-derived metabolites such as secondary bile acids and trimethylamine-N-oxide (TMAO) have been linked to carcinogenic processes. Conversely, protective microbiota, including Lactobacillus, Bifidobacterium, and Faecalibacterium prausnitzii, contribute to intestinal homeostasis by producing short-chain fatty acids (SCFAs) like butyrate, which exhibit anti-inflammatory and anti-carcinogenic properties. These beneficial microbes enhance gut barrier integrity, modulate immune responses, and inhibit tumor cell proliferation. Understanding the dynamic interplay between pathogenic and protective microbiota is essential for developing microbiome-based interventions, such as probiotics, prebiotics, and fecal microbiota transplantation, to prevent or treat CRC. Future research should focus on identifying microbial biomarkers for early CRC detection and exploring personalized microbiome-targeted therapies. A deeper understanding of host-microbiota interactions may lead to innovative strategies for CRC management and improved patient outcomes.},
}

Humans
*Colorectal Neoplasms/microbiology/prevention & control/immunology/etiology
*Gastrointestinal Microbiome
Animals
Risk Factors
Probiotics

@article {pmid40329424,
year = {2025},
author = {Ni, Q and Xia, L and Huang, Y and Yuan, X and Gu, W and Chen, Y and Wang, Y and Nian, M and Wu, S and Cai, H and Huang, J},
title = {Gut microbiota dysbiosis orchestrates vitiligo-related oxidative stress through the metabolite hippuric acid.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {112},
pmid = {40329424},
issn = {2049-2618},
support = {82203909//National Natural Science Foundation of China grant/ ; 82100513//National Natural Science Foundation of China grant/ ; GZC20233592//Postdoctoral Fellowship Program of CPSF/ ; 22BJQN003//Youth Talent Support Program of Air Force Medical Center/ ; 21ZT10//Boost Program for Young Doctor of Air Force Medical Center/ ; 2023JH6/100100034//Science and Technology Foundation of Liaoning Province guided by the central government in 2023/ ; },
mesh = {*Vitiligo/microbiology/metabolism/pathology ; *Oxidative Stress ; *Gastrointestinal Microbiome/physiology ; Animals ; *Dysbiosis/microbiology/metabolism ; Mice ; Humans ; *Hippurates/metabolism/blood ; Reactive Oxygen Species/metabolism ; Disease Models, Animal ; Male ; Skin/metabolism/pathology ; Fecal Microbiota Transplantation ; Female ; Melanocytes/metabolism ; Probiotics/administration & dosage ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Vitiligo, a depigmenting autoimmune skin disease characterized by melanocyte dysfunction or death, is known to be associated with an imbalance in gut microbiota. Oxidative stress plays a critical role in the pathogenesis of vitiligo. However, the complex promising interaction between abnormal accumulation of reactive oxygen species (ROS) in the skin and gut microbiota has remained unclear.

RESULTS: Here, we compared transcriptome data of vitiligo lesions and normal skin and identified a high expression of oxidative stress-related genes in vitiligo lesions. We also established a vitiligo mouse model and found that the presence of gut microbiota influenced the expression of ROS-related genes. Depletion of gut microbiota reduced abnormal ROS accumulation and mitochondrial abnormalities in melanocytes, significantly improving depigmentation. Our findings from manipulating gut microbiota through cohousing, fecal microbiota transplantation (FMT), and probiotic supplementation showed that transferring gut microbiota from mice with severe vitiligo-like phenotypes exacerbated skin depigmentation while probiotics inhibited its progression. Targeted metabolomics of fecal, serum, and skin tissues revealed gut microbiota-dependent accumulation of hippuric acid, mediating excessive ROS in the skin. Elevated serum hippuric acid levels were also confirmed in vitiligo patients. Additionally, a microbiota-dependent increase in intestinal permeability in vitiligo mice mediated elevated hippuric acid levels, and we found that hippuric acid could directly bind to ROS-related proteins (NOS2 and MAPK14).

CONCLUSIONS: Our results suggested the important role of gut microbiota in regulating vitiligo phenotypes and oxidative stress. We identified hippuric acid, a gut microbiota-host co-metabolite, as a critical mediator of oxidative stress in vitiligo skin and its binding targets (NOS2 and MAPK14), resulting in oxidative stress. Validation in a small human cohort suggested that hippuric acid could serve as a novel diagnostic biomarker and therapeutic target for vitiligo. These findings provided new insights into how gut microbiota regulates skin oxidative stress in vitiligo and suggested potential treatment strategies for the disease. Video Abstract.},
}

*Vitiligo/microbiology/metabolism/pathology
*Oxidative Stress
*Gastrointestinal Microbiome/physiology
Animals
*Dysbiosis/microbiology/metabolism
Mice
Humans
*Hippurates/metabolism/blood
Reactive Oxygen Species/metabolism
Disease Models, Animal
Male
Skin/metabolism/pathology
Fecal Microbiota Transplantation
Female
Melanocytes/metabolism
Probiotics/administration & dosage
Mice, Inbred C57BL

@article {pmid40329327,
year = {2025},
author = {Ding, L and Qi, K and Zhou, Y and Li, Q and Liu, M and Hu, N and Wang, J and Qiu, J and Deng, X and Xu, L},
title = {Ingestion of Artemisia argyit essential oil combats Salmonella pullorum infections by altering gut microbiota composition in chicks.},
journal = {Veterinary research},
volume = {56},
number = {1},
pages = {98},
pmid = {40329327},
issn = {1297-9716},
support = {2023YFD1800903//National Key Research and Development Program of China/ ; U22A20523//National Natural Science Foundation of China/ ; JJKH20250155KJ//Scientific Research Project of the Education Department of Jilin Province/ ; 2023-JCXK-01//Fundamental Research Funds for the Central Universities/ ; 2024T170330//China Postdoctoral Science Foundation/ ; 2024M751096//China Postdoctoral Science Foundation/ ; GZB20240268//postdoctoral Fellowship Program (Grade B) of China Postdoctoral Science Foundation/ ; },
mesh = {Animals ; *Artemisia/chemistry ; *Gastrointestinal Microbiome/drug effects ; *Chickens ; *Oils, Volatile/pharmacology/administration & dosage ; *Poultry Diseases/microbiology/prevention & control/drug therapy ; *Salmonella Infections, Animal/microbiology/prevention & control/drug therapy ; Fecal Microbiota Transplantation/veterinary ; Animal Feed/analysis ; *Salmonella/drug effects/physiology ; Dietary Supplements/analysis ; *Plant Oils/pharmacology ; Diet/veterinary ; },
abstract = {Pullorum disease, caused by Salmonella pullorum (S. pullorum), is a highly contagious illness affecting the poultry industry. Emerging evidence suggests that Artemisia argyit essential oil can influence the composition of gut microbes in the host, thereby promoting overall health. However, the specific mechanisms by which Artemisia argyit essential oil modulates gut microbiota to combat S. pullorum infection remains unclear. This study explored the effectiveness of various doses of Artemisia argyit essential oil in preventing S. pullorum infection in chicks. Our findings indicate that consuming this essential oil can mitigate the intestinal mucosal barrier damage and excessive inflammatory response caused by S. pullorum, as well as reverse the weight loss seen in infected chicks. Additionally, chicks that received faecal microbiota transplantation (FMT) from the gut microbiota of Artemisia argyit essential oil donors exhibited notable recovery from S. pullorum infections. This suggests that the observed protection may be linked to the modulation of gut microbiota. Furthermore, 16S rRNA sequencing revealed an increased abundance of Lactobacillus reuteri (L. reuteri), which along with the activation of Wnt/β-catenin pathways, played critical roles in the enhanced health of S. pullorum-infected chicks treated with Artemisia argyit essential oil. In summary, these findings highlight that the dietary inclusion of Artemisia argyit essential oil promotes the intestinal enrichment of L. reuteri, offering a promising strategy for the treatment and prevention of pullorum disease in chicks.},
}

Animals
*Artemisia/chemistry
*Gastrointestinal Microbiome/drug effects
*Chickens
*Oils, Volatile/pharmacology/administration & dosage
*Poultry Diseases/microbiology/prevention & control/drug therapy
*Salmonella Infections, Animal/microbiology/prevention & control/drug therapy
Fecal Microbiota Transplantation/veterinary
Animal Feed/analysis
*Salmonella/drug effects/physiology
Dietary Supplements/analysis
*Plant Oils/pharmacology
Diet/veterinary

@article {pmid40329009,
year = {2025},
author = {Nobels, A and van Marcke, C and Jordan, BF and Van Hul, M and Cani, PD},
title = {The gut microbiome and cancer: from tumorigenesis to therapy.},
journal = {Nature metabolism},
volume = {},
number = {},
pages = {},
pmid = {40329009},
issn = {2522-5812},
support = {T.0032.25//Fonds De La Recherche Scientifique - FNRS (Belgian National Fund for Scientific Research)/ ; EOS: program no. 40007505//Fonds De La Recherche Scientifique - FNRS (Belgian National Fund for Scientific Research)/ ; WELBIO-CR-2022A-02//Fonds De La Recherche Scientifique - FNRS (Belgian National Fund for Scientific Research)/ ; },
abstract = {The gut microbiome has a crucial role in cancer development and therapy through its interactions with the immune system and tumour microenvironment. Although evidence links gut microbiota composition to cancer progression, its precise role in modulating treatment responses remains unclear. In this Review, we summarize current knowledge on the gut microbiome's involvement in cancer, covering its role in tumour initiation and progression, interactions with chemotherapy, radiotherapy and targeted therapies, and its influence on cancer immunotherapy. We discuss the impact of microbial metabolites on immune responses, the relationship between specific bacterial species and treatment outcomes, and potential microbiota-based therapeutic strategies, including dietary interventions, probiotics and faecal microbiota transplantation. Understanding these complex microbiota-immune interactions is critical for optimizing cancer therapies. Future research should focus on defining microbial signatures associated with treatment success and developing targeted microbiome modulation strategies to enhance patient outcomes.},
}

@article {pmid40328737,
year = {2025},
author = {Hitch, TCA and Masson, JM and Pauvert, C and Bosch, J and Nüchtern, S and Treichel, NS and Baloh, M and Razavi, S and Afrizal, A and Kousetzi, N and Aguirre, AM and Wylensek, D and Coates, AC and Jennings, SAV and Panyot, A and Viehof, A and Schmitz, MA and Stuhrmann, M and Deis, EC and Bisdorf, K and Chiotelli, MD and Lissin, A and Schober, I and Witte, J and Cramer, T and Riedel, T and Wende, M and Winter, KA and Amend, L and Riva, A and Trinh, S and Mitchell, L and Hartman, J and Berry, D and Seitz, J and Bossert, LC and Grognot, M and Allers, T and Strowig, T and Pester, M and Abt, B and Reimer, LC and Overmann, J and Clavel, T},
title = {HiBC: a publicly available collection of bacterial strains isolated from the human gut.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {4203},
pmid = {40328737},
issn = {2041-1723},
support = {513892404//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 445552570//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 395357507//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 403224013//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 460129525//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/genetics ; Plasmids/genetics ; *Bacteria/isolation & purification/classification/genetics ; Phylogeny ; Feces/microbiology ; },
abstract = {Numerous bacteria in the human gut microbiome remain unknown and/or have yet to be cultured. While collections of human gut bacteria have been published, few strains are accessible to the scientific community. We have therefore created a publicly available collection of bacterial strains isolated from the human gut. The Human intestinal Bacteria Collection (HiBC) (https://www.hibc.rwth-aachen.de) contains 340 strains representing 198 species within 29 families and 7 phyla, of which 29 previously unknown species are taxonomically described and named. These included two butyrate-producing species of Faecalibacterium and new dominant species associated with health and inflammatory bowel disease, Ruminococcoides intestinale and Blautia intestinihominis, respectively. Plasmids were prolific within the HiBC isolates, with almost half (46%) of strains containing plasmids, with a maximum of six within a strain. This included a broadly occurring plasmid (pBAC) that exists in three diverse forms across Bacteroidales species. Megaplasmids were identified within two strains, the pMMCAT megaplasmid is globally present within multiple Bacteroidales species. This collection of easily searchable and publicly available gut bacterial isolates will facilitate functional studies of the gut microbiome.},
}

Humans
*Gastrointestinal Microbiome/genetics
Plasmids/genetics
*Bacteria/isolation & purification/classification/genetics
Phylogeny
Feces/microbiology

@article {pmid40328388,
year = {2025},
author = {Wang, J and Yang, L and Liu, L and Ren, J and Jiang, Z and Zhao, X and Jiao, L and Gao, Y and Guo, Y and Yu, T and Li, B and Li, Y and Tong, H},
title = {Pectin from Fructus Mori relieve oxidative stress and regulates gut microbiota in POF mice.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {143941},
doi = {10.1016/j.ijbiomac.2025.143941},
pmid = {40328388},
issn = {1879-0003},
abstract = {Pectin, a complex acidic heteropolysaccharide with diverse biological activities, is widely unilized in cosmetics and food industry. Fructus Mori (F. Mori), an important cultivated fruit, contains abundant pectin. In this study, a pectic polysaccharide (FPA1-1) was extracted from F. Mori through hot-water extraction, ethanol precipitation, and chromatographic purification. Structural analysis revealed that FPA1-1 was a rhamnogalacturonan-I (RG-I)-rich mixed pectin with a branching degree of 48.42 %. In vivo experiments, FPA1-1 (400 mg/kg) effectively shortened the oestrous cycle, reduced follicle stimulating hormone (FSH) level, promoted synthesis and secretion of estradiol hormone (E2) and luteinizing hormone (LH), suppressed serum interleukin-1β (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels and improved antioxidant capacity in premature ovarian failure (POF) mice. Moreover, FPA1-1 modulated gut dysbiosis of POF mice by decreasing Firmicutes/ Bacteroidetes ratio and Desulfobacterota abundance at phylum level, enriching Bacteroides, Prevotellaceae, Parabacteroides, Alloprevotella, and Muribaculaceae abundance and inhibiting Desulfovibrionaceae proliferation. FPA1-1 treatment increased short-chain fatty acids (SCFAs) level. Antibiotic cocktail treatment and fecal microbiota transplantation (FMT) experiments confirmed that FPA1-1 ameliorates the ovarian function through altering the gut microbiota composition. These findings provided an experimental basis for further research and applications of F. mori pectin in female ovarian health.},
}

@article {pmid40326772,
year = {2025},
author = {Chen, Z and Chai, S and Ding, Y and Pang, K and Dong, T and Dai, D and Wang, J and Wang, S and Liu, S},
title = {Gut microbiota modulates lung gene expression and metabolism to aid SD rats in adapting to low-pressure hypoxia.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0004525},
doi = {10.1128/spectrum.00045-25},
pmid = {40326772},
issn = {2165-0497},
abstract = {UNLABELLED: Hypoxia has long posed a serious threat to the health of both animals and humans, causing respiratory acidosis, metabolic disorders, systemic inflammation, oxidative stress damage, and other issues, thereby endangering life and limiting development in high-altitude areas. Gut microbiota plays a crucial role in life activities and hypoxia adaptation. We transplanted the gut microbiota from small mammals, plateau zokors (Myospalax baileyi), from the Qinghai-Tibetan plateau (3,500 m) to Sprague-Dawley (SD) rats housed in a hypobaric chamber (equivalent to 6,000 m altitude) for 30 days. The results showed that microbiota transplantation significantly reshaped the gut microbiota structure of the rats, notably increasing the abundance of short-chain fatty acid-producing bacteria Lachnospiraceae and Prevotellaceae, alleviating hypoxia and acidosis, reducing pulmonary hypertension and right ventricular hypertrophy, increasing the production of anti-inflammatory substances like indole-3-lactic acid, and reducing the generation of pro-inflammatory substances, such as histamine and uric acid. It also decreased the expression of inflammatory genes like lgE, TNFα, and IFN-γ in the lung. Fecal microbiota transplantation from plateau-specific species to low-altitude SD rats effectively altered metabolism, changed gene expression, decreased pulmonary artery pressure, and enhanced plateau adaptability. This study demonstrates the potential effectiveness of treating hypoxic pulmonary hypertension through microbiota transplantation and offers insights into improving hypoxia adaptation.

IMPORTANCE: We report the beneficial effects of FMT on respiratory capacity, lung metabolism, and lung gene expression in SD rats under hypoxic conditions. We revealed the inhibitory effects of gut microbiota on lung mast cells and histamine expression under hypoxic conditions. The study demonstrated the potential effectiveness of treating HPH through FMT and offers insights into improving hypoxia adaptation.},
}

@article {pmid40323507,
year = {2025},
author = {Wadan, AS and El-Aziz, MKA and Ellakwa, DE},
title = {The microbiota-gut-brain-axis theory: role of gut microbiota modulators (GMMs) in gastrointestinal, neurological, and mental health disorders.},
journal = {Naunyn-Schmiedeberg's archives of pharmacology},
volume = {},
number = {},
pages = {},
pmid = {40323507},
issn = {1432-1912},
abstract = {The modulation of gut microbiota presents promising therapeutic possibilities for various health conditions, ranging from gastrointestinal infections to neurodegenerative and mental health disorders. Among the available interventions, gut microbiota modulators (GMMs) such as probiotics and prebiotics have demonstrated significant potential in infection prevention and neuroprotection. Despite these encouraging findings, the clinical application of GMMs remains challenging due to safety concerns and inconsistent effectiveness across diverse patient populations. These factors create substantial barriers to the widespread adoption of microbiota-based therapies in clinical practice. To overcome these challenges and fully leverage the therapeutic potential of microbiota modulation, this review explores the feasibility of repurposing GMMs for managing multiple health disorders. A broad spectrum of microbiota-targeted strategies is examined, including dietary modifications, fecal microbiota transplantation, bacteriophage therapy, microbiome engineering, and immune system modulation. A particularly innovative approach involves integrating GMMs with pharmaceutical delivery systems to enhance therapeutic efficacy while mitigating potential adverse effects. This integrative strategy underscores the pivotal role of the gut microbiome in health and disease, supporting the development of precision medicine tailored to individual patient needs. By combining GMMs with targeted delivery mechanisms, this approach not only improves treatment effectiveness but also addresses critical concerns regarding safety and patient variability. Furthermore, this review outlines future research directions within the rapidly evolving field of microbiota modulation, emphasizing the necessity of comprehensive clinical trials and long-term safety evaluations. By critically assessing both the challenges and opportunities associated with microbiota-based interventions, this study provides a strategic framework for translating experimental research into viable clinical applications. A holistic approach to gut microbiota modulation has the potential to redefine treatment paradigms, offering personalized therapeutic strategies for a wide range of disorders and advancing the broader field of precision medicine.},
}

@article {pmid40321610,
year = {2025},
author = {Dong, Z and Zhang, R and Shen, L and Ji, HF and He, H and Ji, X and Zhao, L},
title = {Gut Microbiota and Immunoglobulin A Nephropathy: Exploration of Dietary Intervention and Treatment Strategies.},
journal = {Food science & nutrition},
volume = {13},
number = {5},
pages = {e70218},
pmid = {40321610},
issn = {2048-7177},
abstract = {Immunoglobulin A nephropathy (IgAN) is a primary glomerular disease characterized by the deposition of IgA. The pathogenesis of it is related to the dysbiosis of gut microbiota. Dysbiosis of gut microbiota influences mucosal immune response and systemic immune system, leading to glycosylation-deficient IgA1 (Gd-IgA1) increasing, which promotes the development of IgAN. Diet plays an important role in regulating gut microbiota and treating IgAN. In this review, we summarize the interplay between gut microbiota and IgAN, and their underlying mechanisms. We also describe the effects of dietary intake on IgAN, as well as the composition of gut microbiota. The progress on IgAN treatment mainly focuses on inhibiting or regulating the immune system. Moreover, therapeutic strategies related to gut microbiota such as dietary intervention, supplement of probiotics and prebiotics, as well as fecal microbiota transplantation (FMT) have shown the possibility of improving IgAN prognosis. Thus, exploration of the gut-kidney axis, the long-term effects of diet and microbiome is necessary to develop more effective treatment strategies.},
}

@article {pmid40321299,
year = {2025},
author = {Pan, L and Xie, L and Yang, W and Feng, S and Mao, W and Ye, L and Cheng, H and Wu, X and Mao, X},
title = {The role of brain-liver-gut Axis in neurological disorders.},
journal = {Burns & trauma},
volume = {13},
number = {},
pages = {tkaf011},
pmid = {40321299},
issn = {2321-3868},
abstract = {In recent years, with the increasing volume of related research, it has become apparent that the liver and gut play important roles in the pathogenesis of neurological disorders. Considering the interactions among the brain, liver, and gut, the brain-liver-gut axis has been proposed and gradually recognized. In this article, we summarized the complex network of interactions within the brain-liver-gut axis, encompassing the vagus nerve, barrier permeability, immunity and inflammation, the blood-brain barrier, gut microbial metabolites, the gut barrier, neurotoxic metabolites, and beta-amyloid (Aβ) metabolism. We also elaborated on the impact of the brain-liver-gut axis on various neurological disorders. Furthermore, we outline several therapies aimed at modulating the brain-liver-gut axis, including antibiotics, probiotics and prebiotics, fecal microbiota transplantation (FMT), vagus nerve stimulation (VNS), and dietary interventions. The focus is on elucidating possible mechanisms underlying neurological disorders pathogenesis and identifying effective treatments that are based on our understanding of the brain-liver-gut axis.},
}

@article {pmid40320851,
year = {2025},
author = {Kim, KS and Yang, SY and Jeong, H and Hong, M and Noh, J and Koh, H and Lee, DW},
title = {Development of a Korean Nutrition Model for In Silico Gut Microbiome Analyses Integrated With Nutrigenomics.},
journal = {Molecular nutrition & food research},
volume = {},
number = {},
pages = {e70090},
doi = {10.1002/mnfr.70090},
pmid = {40320851},
issn = {1613-4133},
support = {RS-2021-NR056579//Bio & Medical Technology Development Program of the National Research Foundation (NRF) of Korea/ ; //Ministry of Science and ICT (MSIT)/ ; 20018770//Bioindustrial Technology Development Program of Korea/ ; //Ministry of Trade, Industry and Energy/ ; 2025-12-0026//Yonsei University Research Fund/ ; },
abstract = {The gut microbiome plays a crucial role in human health and disease, with diet serving as a critical determinant of microbial composition and metabolic function. However, most existing nutrition databases are Western-centric, lacking comprehensive dietary information for non-Western populations, including Koreans. This limitation hinders the accuracy of in silico gut microbiome analyses and microbiome-disease associations. We developed the Korean Nutrition Model (KNM) to enhance in silico microbiome analyses by incorporating detailed macronutrient and micronutrient compositions reflective of Korean dietary patterns. KNM was constructed using a decision algorithm that integrates data from the Ministry of Food and Drug Safety and FooDB. Comparative analysis with the European Nutrition Model revealed significant differences in carbohydrate and vitamin compositions, which in turn influenced microbial growth rates and metabolic fluxes in in silico simulations. We further evaluated gut microbiota differences between Korean and European cohorts, including healthy individuals and inflammatory bowel disease patients. Our findings demonstrate that using an appropriate, population-specific nutrition model significantly improves microbiome analyses, reducing the risk of false associations. This study underscores the importance of regionally tailored dietary models and provides a framework for enhancing global dietary models to facilitate precision nutrition and microbiome-based disease interventions.},
}

@article {pmid40317768,
year = {2025},
author = {Kooij, KL and Andreani, NA and Keller, L and Trinh, S and van der Gun, L and Hak, J and Garner, K and Luijendijk, M and Drost, L and Danner, U and van Elburg, A and Dempfle, A and Seitz, J and Herpertz-Dahlmann, B and Baines, JF and Adan, RAH},
title = {Antibiotic-Induced Microbial Dysbiosis Worsened Outcomes in the Activity-Based Anorexia Model.},
journal = {The International journal of eating disorders},
volume = {},
number = {},
pages = {},
doi = {10.1002/eat.24452},
pmid = {40317768},
issn = {1098-108X},
support = {MIGBAN FKZ: 01EW1906A//ERA_Net/ ; 509492174//Deutsche Forschungsgemeinschaft/ ; },
abstract = {OBJECTIVE: Anorexia nervosa (AN) is a complex psychiatric disorder characterized by persistent dieting and reduced food intake, leading to significantly low body weight. Dysbiosis in the gut microbiome of patients with AN has been suggested to contribute to the pathogenesis. Here, we used fecal microbiota transplantation (FMT) in the activity-based anorexia (ABA) rat model to investigate the impact of AN-associated gut microbiota on disease-related outcomes.

METHOD: We validated the FMT in 12 Wistar rats by depleting the gut microbiome with antibiotics and transplanting two donors' fecal samples. We then transplanted fecal samples from four patients with AN or four healthy controls in 48 rats just before the ABA model exposure and included an antibiotic-only control group. During ABA, the rats had access to a running wheel and only 1.5 h access to chow for 7 days. We monitored body weight, body temperature, food intake, wheel revolutions, and gut microbiome biodiversity and composition.

RESULTS: The antibiotic treatment significantly depleted the rats' gut microbiome and subsequent transplantation made the rats' microbiome more similar to the donors' microbiome. The antibiotic-only group showed reduced survival, as well as lower body weight and temperature during ABA. Transplanted microbiota from patients with AN and healthy controls improved outcomes in the ABA model.

DISCUSSION: We do not find evidence that the microbiome of patients with AN differentially contributes to anorexia-like phenotypes based upon partial microbiome transplantation. However, the presence of a microbiome impacts the outcome of the ABA model.},
}

@article {pmid40316878,
year = {2025},
author = {Shirzadi, P and Farokh, P and Osouli Meinagh, S and Izadi-Jorshari, G and Hajikarimloo, B and Mohammadi, G and Parvardeh, S and Nassiri-Asl, M},
title = {The Influence of the Probiotics, Ketogenic Diets, and Gut Microbiota on Epilepsy and Epileptic Models: A Comprehensive Review.},
journal = {Molecular neurobiology},
volume = {},
number = {},
pages = {},
pmid = {40316878},
issn = {1559-1182},
support = {01-33153//Shahid Beheshti University of Medical Sciences/ ; },
abstract = {About one-third of epilepsies are resistant to antiepileptic drugs; thus, uncovering new pathways in the pathophysiology of epilepsy can reduce the global disease burden. Probiotics are live, non-pathogenic microorganisms that benefit the host by regulating the gut microbiome. This review aims to study the effect of probiotics and ketogenic diets on gut microbiota and their potential as a therapy for epilepsy. We conducted a systematic search of the databases PubMed, Scopus, Embase, and the Web of Science for pertinent studies that have been published. Our search methodology was meticulously structured to be exhaustive, integrating targeted keywords and Boolean operators to guarantee the acquisition of all potentially pertinent articles. Probiotics interact with the gut microbiome, balance its composition, and influence the gut-brain axis. Moreover, they reduce neuroinflammation and oxidative stress. The ketogenic diet (KD) affects gut bacteria, influencing neurotransmitter levels and short-chain fatty acids (SCFAs), which play a role in the gut-brain axis. Studies have shown the positive effects of various probiotics in animal models of epilepsy. They demonstrate improvements in seizure activity, anxiety, and neuroinflammation. In human studies, probiotics reduced seizure frequency and enhanced quality of life in patients with drug-resistant epilepsy. We believe using probiotics or dietary interventions like KD could be a promising therapeutic strategy for managing epilepsy. This could reduce seizure frequency and make life better for patients with epilepsy.},
}

@article {pmid40316655,
year = {2025},
author = {Neyrinck, AM and Ahmed, H and Leyrolle, Q and Leclercq, S and Amadieu, C and Meuronen, T and Layé, S and Cani, PD and Kärkkäinen, O and Bindels, LB and Hanhineva, K and Delzenne, NM},
title = {Fecal transplantation from humans with obesity to mice drives a selective microbial signature without impacting behavioral and metabolic health.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {15455},
pmid = {40316655},
issn = {2045-2322},
support = {ANR-19-NEUR-0003-03//Agence Nationale de la Recherche/ ; PDR T.0068.19 and PINT-MULTI R.8013.19//FNRS/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; *Obesity/microbiology/therapy/metabolism ; Humans ; *Gastrointestinal Microbiome ; Mice ; Male ; *Behavior, Animal ; Feces/microbiology ; Mice, Inbred C57BL ; Female ; Metabolomics ; Metabolome ; },
abstract = {Obesity is associated with alterations in the gut microbiome that may contribute to metabolic and mental health disturbances. Fecal microbiota transplantation (FMT) from humans to mice is a model proposed to study human microbiota-associated disorders. In this study, we investigated whether gut microbiota from human donors with obesity could affect behavior and metabolomic profiles of mice. Stools from donors with obesity and from lean donors were inoculated to antibiotic-pretreated mice fed a standard low-fat diet throughout the experiment. Obese-recipient mice exhibited a lower bacterial alpha-diversity and limited changes in specific taxa (e.g., an increase in Eubacterium) but were similar to lean-recipient mice in terms of dietary intake, body weight, fat mass, anxiety/depression-like behavior and glucose homeostasis. Non-targeted LC-MS metabolomic analysis revealed no change in the portal and cava serum samples. However, 1-methylnicotinamide, indole-3-acetic acid (I3A) and methyllysine were increased in the cecal content of obese-recipient compared to lean-recipient mice. Microbial metabolites derived from amino acids were positively correlated with Eubacterium. These results indicate that FMT from donors with obesity to mice fed chow diet (low in lipids) leads to minor but persistent change in intestinal microbial-derived metabolites, without recapitulating the metabolic and behavioral alterations of obesity.},
}

Animals
*Fecal Microbiota Transplantation/methods
*Obesity/microbiology/therapy/metabolism
Humans
*Gastrointestinal Microbiome
Mice
Male
*Behavior, Animal
Feces/microbiology
Mice, Inbred C57BL
Female
Metabolomics
Metabolome

@article {pmid40316371,
year = {2025},
author = {Werner, M and Vigani, A},
title = {The Microbiome in Critical Illness.},
journal = {The Veterinary clinics of North America. Small animal practice},
volume = {55},
number = {3},
pages = {443-458},
doi = {10.1016/j.cvsm.2025.01.008},
pmid = {40316371},
issn = {1878-1306},
mesh = {Animals ; *Critical Illness/therapy ; Dogs ; *Dog Diseases/microbiology/therapy ; *Gastrointestinal Microbiome/physiology ; Probiotics/therapeutic use ; *Cat Diseases/microbiology/therapy ; Cats ; Fecal Microbiota Transplantation/veterinary ; *Gastrointestinal Diseases/veterinary/microbiology/therapy ; },
abstract = {Evidence suggests that the intestinal microbiome may play an important role in the pathogenesis and progression of acute critical illness in humans and other mammals, although evidence in small animal medicine is sparse. Moreover, the intestinal microbiota plays many important metabolic roles (production of short-chain fatty acids, trimethylamine-N-oxide, and normal bile acid metabolism) and is crucial for immunity as well as defense against enteropathogens. The use of probiotics and fecal microbiota transplantation as instruments to modulate the intestinal microbiota seems to be safe and effective in studies on critically ill dogs with acute gastrointestinal diseases.},
}

Animals
*Critical Illness/therapy
Dogs
*Dog Diseases/microbiology/therapy
*Gastrointestinal Microbiome/physiology
Probiotics/therapeutic use
*Cat Diseases/microbiology/therapy
Cats
Fecal Microbiota Transplantation/veterinary
*Gastrointestinal Diseases/veterinary/microbiology/therapy

@article {pmid40316177,
year = {2025},
author = {Yin, Y and Guan, M and Wu, S and Cui, C and Wang, R and Zhao, X and Yang, X and Qiao, L and Li, Y and Zhang, C},
title = {Young fecal microbiota transplantation improves working memory in aged recipient rats by increasing interleukin-4 and interleukin-17 levels.},
journal = {Neuroscience research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neures.2025.04.005},
pmid = {40316177},
issn = {1872-8111},
abstract = {While transplanting the fecal microbiota from young to aged rodents has been extensively studied (that is, young FMT [yFMT]), its mechanism of alleviating working memory decline has not been fully elucidated. In this report, we aimed to investigate the effect of yFMT on the working memory of aged recipient rats performing delayed match-to-position (DMTP) tasks and the associated cellular and molecular mechanisms. The results revealed that yFMT mitigated the decline in DMTP task performance of aged recipients. This improvement was associated with a reshaped gut microbiota and increased levels of brain-derived neurotrophic factor, N-methyl-D-aspartate receptor subunit 1, and synaptophysin, enhancing synaptic formation and transmission. The remodeling of the gut microbiome influenced peripheral circulation and the hippocampus and medial prefrontal cortex by regulating the Th17/Treg ratio and microglial polarization. Ultimately, interleukin-4 and interleukin-17 emerged as potential key molecules driving the beneficial effects of FMT. These observations provide new insights into the gutbrain axis, emphasizing the connection between the gut and brain through the circulation system, and suggest an immunological mechanism that may help reverse age-related declines in the gut microbiota.},
}

@article {pmid40316082,
year = {2025},
author = {Qiu, MT and Zhou, L and Wang, XY and Li, ZP and Wei, MX and Zeng, ZH and Cheng, J and Xu, GH and Zhu, JX and Yi, LT},
title = {Anti-colitis comparison of polysaccharides and anthocyanins extracted from black wolfberry based on microbiomics, immunofluorescence and multi-cytokines profile analysis.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {143700},
doi = {10.1016/j.ijbiomac.2025.143700},
pmid = {40316082},
issn = {1879-0003},
abstract = {Black wolfberry (Lycium ruthenicum) is a widely consumed food known for its pharmacological properties, particularly its anti-inflammatory and antioxidant effects. This study investigates the therapeutic potential of black wolfberry polysaccharides (LRP) and anthocyanins (LRA) in treating ulcerative colitis, a chronic inflammatory bowel disease. Using a DSS-induced mouse model of colitis, we administered varying doses of LRP and LRA and evaluated their effects on disease activity, inflammation, gut barrier function, and microbiota composition. LRP demonstrated dose-dependent efficacy, with the 200 mg/kg dose showing the most significant reduction in the disease activity index (DAI), improvement in histopathology, and restoration of tight junction protein expression. In contrast, LRA exhibited an inverted U-shaped response, with the 100 mg/kg dose being the most effective. Additionally, LRP treatment modulated cytokine levels, promoting an anti-inflammatory response, and significantly restored gut microbiota balance by increasing Muribaculaceae and Limosilactobacillus while reducing Bacteroides and Helicobacter. Fecal microbiota transplantation (FMT) experiments further confirmed that the therapeutic effects of LRP are microbiota-dependent. These findings suggest that LRP, a polysaccharide derived from black wolfberry, offers a dietary intervention for colitis through immune modulation and gut microbiota restoration.},
}

@article {pmid40315641,
year = {2025},
author = {Wei, FH and Xie, WY and Zhao, PS and Ji, ZH and Gao, F and Chen, CZ and Zhang, Z and Gao, W and Yuan, B},
title = {Crataegus pinnatifida polysaccharide alleviates DSS-induced colitis in mice by regulating the intestinal microbiota and enhancing arginine biosynthesis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {142},
number = {},
pages = {156794},
doi = {10.1016/j.phymed.2025.156794},
pmid = {40315641},
issn = {1618-095X},
abstract = {BACKGROUND: The development of effective and safe dietary supplements is essential for both the prevention and management of ulcerative colitis (UC), as its pathogenesis is intricate and difficult to completely resolve. Crataegus pinnatifida, a medicinal food with a long history of use, has broad medicinal value. Recent research has revealed promising insights into the role of polysaccharide derived from Crataegus pinnatifida on modulating short-chain fatty acids (SCFAs) to alleviate UC inflammation. However, the mechanisms by which CPP regulates the intestinal microbiota and key metabolites during the antagonistic phase of UC have yet to be elucidated.

OBJECTIVE: This research elucidated the protective role of CPP in relation to UC, highlighted the mechanisms through which CPP operates, particularly regarding gut microbiota and metabolism, and offered a theoretical foundation for the potential use of CPP as a dietary supplement aimed at preventing UC.

METHODS: The impact of CPP on acute UC induced by 3 % DSS in mice was examined through the evaluation of the disease activity index, measurement of colon length, and observation of body weight changes. Enzyme-linked immunosorbent assay (ELISA) was used to measure inflammatory factor levels in both serum and colon, as well as to assess oxidative stress mediators. The intestinal histological damage, mucus layer damage and the level of tight junction protein were analyzed by histopathological staining and western blot (WB). The impact of gut microbiota on CPP in colitis was evaluated using 16S rRNA sequencing, microbiota depletion experiments, and fecal microbiota transplantation (FMT) studies. The key metabolic pathways and key metabolites affected by CPP in the treatment of UC were analyzed through untargeted metabolomics sequencing, ELISA, and WB assays.

RESULTS: Prophylactic dietary supplementation with Crataegus pinnatifida polysaccharide (CPP) notably reduced the fundamental clinical manifestations of UC induced by DSS, including DAI score, reduced colon length, and weight loss, as well as inflammation and oxidative stress. CPP promoted the expression of Claudin-1, ZO-1 and Occludin and promoted mucin secretion, which contributed to the mitigation of intestinal barrier damage caused by DSS. 16S sequencing results and metabolomics results revealed that CPP intervention upregulated the relative abundance of Lactobacillus, thereby reshaping the intestinal microbiota and activate the arginine biosynthesis pathway. The results of fecal microbiota transplantation and antibiotic clearance experiments indicated that the alleviating effect of CPP on UC was dependent on the intestinal microbiota and this alleviating effect was transferred through fecal microbiota transplantation. Mechanistically, CPP indirectly promoted the expression of the rate-limiting enzyme argininosuccinate synthase 1 (ASS1) in the intestinal Arginine biosynthesis pathway by reshaping the intestinal microbiota, thereby increasing intestinal Arginine level and alleviating the inflammatory response and oxidative stress induced by DSS and intestinal barrier damage.

CONCLUSION: Our research findings demonstrate that CPP is a plant-derived polysaccharide that alleviates UC by modulating the gut microbiota and enhancing arginine biosynthesis.},
}

@article {pmid40314722,
year = {2025},
author = {Castagnoli, R and Pala, F and Subramanian, P and Oguz, C and Schwarz, B and Lim, AI and Burns, AS and Fontana, E and Bosticardo, M and Corsino, C and Angelova, A and Delmonte, OM and Kenney, H and Riley, D and Smith, G and Ott de Bruin, L and Oikonomou, V and Dos Santos Dias, L and Fink, D and Bohrnsen, E and Kimzey, CD and Marseglia, GL and Alva-Lozada, G and Bergerson, JRE and Brett, A and Brigatti, KW and Dimitrova, D and Dutmer, CM and Freeman, AF and Ale, H and Holland, SM and Licciardi, F and Pasic, S and Poskitt, LE and Potts, DE and Dasso, JF and Sharapova, SO and Strauss, KA and Ward, BR and Yilmaz, M and Kuhns, DB and Lionakis, MS and Daley, SR and Kong, HH and Segre, JA and Villa, A and Pittaluga, S and Walter, JE and Vujkovic-Cvijin, I and Belkaid, Y and Notarangelo, LD},
title = {Immunopathological and microbial signatures of inflammatory bowel disease in partial RAG deficiency.},
journal = {The Journal of experimental medicine},
volume = {222},
number = {8},
pages = {},
pmid = {40314722},
issn = {1540-9538},
support = {U01 DK062413/DK/NIDDK NIH HHS/United States ; HHSN316201300006W/75N93022F00001/HH/HHS/United States ; //National Institute of Allergy and Infectious Diseases/ ; U01DK062413/DK/NIDDK NIH HHS/United States ; DP1HL174182/HL/NHLBI NIH HHS/United States ; 831262//Crohn's & Colitis Foundation Career Development/ ; AI001222/NH/NIH HHS/United States ; DP1 HL174182/HL/NHLBI NIH HHS/United States ; //Fondazione Ghislieri/ ; //Cedars-Sinai Medical Center/ ; },
mesh = {Animals ; *Inflammatory Bowel Diseases/immunology/microbiology/pathology/genetics ; *Homeodomain Proteins/genetics ; Humans ; Mice ; Female ; Male ; Disease Models, Animal ; Gastrointestinal Microbiome ; Bone Marrow Transplantation ; T-Lymphocytes, Regulatory/immunology ; Th17 Cells/immunology ; Mice, Inbred C57BL ; },
abstract = {Partial RAG deficiency (pRD) can manifest with systemic and tissue-specific immune dysregulation, with inflammatory bowel disease (IBD) in 15% of the patients. We aimed at identifying the immunopathological and microbial signatures associated with IBD in patients with pRD and in a mouse model of pRD (Rag1w/w) with spontaneous development of colitis. pRD patients with IBD and Rag1w/w mice showed a systemic and colonic Th1/Th17 inflammatory signature. Restriction of fecal microbial diversity, abundance of pathogenic bacteria, and depletion of microbial species producing short-chain fatty acid were observed, which were associated with impaired induction of lamina propria peripheral Treg cells in Rag1w/w mice. The use of vedolizumab in Rag1w/w mice and of ustekinumab in a pRD patient were ineffective. Antibiotics ameliorated gut inflammation in Rag1w/w mice, but only bone marrow transplantation (BMT) rescued the immunopathological and microbial signatures. Our findings shed new light in the pathophysiology of gut inflammation in pRD and establish a curative role for BMT to resolve the disease phenotype.},
}

Animals
*Inflammatory Bowel Diseases/immunology/microbiology/pathology/genetics
*Homeodomain Proteins/genetics
Humans
Mice
Female
Male
Disease Models, Animal
Gastrointestinal Microbiome
Bone Marrow Transplantation
T-Lymphocytes, Regulatory/immunology
Th17 Cells/immunology
Mice, Inbred C57BL

@article {pmid40314681,
year = {2025},
author = {Li, X and Su, K and He, Y and Shao, S and Lan, L and Zhang, Q and Li, L},
title = {Knowledge Mapping of International Microbiota Research: Analyzing Thirty-Year Citation Classics and Exploring Future Expectations.},
journal = {The new microbiologica},
volume = {48},
number = {1},
pages = {46-59},
pmid = {40314681},
issn = {1121-7138},
mesh = {Humans ; *Bibliometrics ; *Biomedical Research ; Gastrointestinal Microbiome ; *Microbiota ; },
abstract = {Microbiota research has rapidly emerged as a pivotal field, with over 250,000 publications and more than ten million citations recorded in the Web of Science Core Collection database by 2024. There were 1682 original microbiota citation classics (each receiving 400 citations or more) identified over the past three decades, totaling 1,559,594 citations and averaging 927 citations per paper. Collaborative efforts in the production of these citation classics involved 87 out of 89 participating countries and 2107 out of 2142 institutions. The USA, various European countries, and China emerged as the leading contributors to this burgeoning research area. Jeffrey I. Gordon, Rob Knight, and Curtis Huttenhower were the prominent figures in microbiota research. Author keywords were analyzed, which revealed a notable shift in research focus from environmental microorganisms to human gut microbiota. Advances such as high-throughput 16S rRNA sequencing and metagenomics expanded the scope of investigations into host-microbiota interactions. Current research interests encompass exploring mechanisms underlying gut-X-axis conditions, including inflammatory bowel disease, obesity, diabetes, colorectal cancer, liver diseases, and neurological disorders. Moreover, environmental exposures have been evidenced to alter gut microbiota and metabolites, contributing a novel research direction. Future research direction is also anticipated to delve further into biosynthetic gene engineering technologies aimed at microbial interventions, including probiotics and fecal microbiota transplantation. This study outlines the evolving landscape of microbiota research and provides valuable insights to inform future investigations within the field.},
}

Humans
*Bibliometrics
*Biomedical Research
Gastrointestinal Microbiome
*Microbiota

@article {pmid40314129,
year = {2025},
author = {Xiao, K and Li, K and Xiao, K and Yang, J and Zhou, L},
title = {Gut Microbiota and Hepatocellular Carcinoma: Metabolic Products and Immunotherapy Modulation.},
journal = {Cancer medicine},
volume = {14},
number = {9},
pages = {e70914},
pmid = {40314129},
issn = {2045-7634},
support = {21MC1930500//Shanghai Clinical Research Center of Traditional Chinese Medicine Oncology, Science and Technology Commission of Shanghai Municipality/ ; ZYYZDXK-2023063//High-Level Traditional Chinese Medicine Key Discipline Construction Project of the National Administration of Traditional Chinese Medicine/ ; //Youth Talent Project of Longhua Hospital, affiliated with Shanghai University of Traditional Chinese Medicine/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/drug effects ; *Carcinoma, Hepatocellular/therapy/immunology/microbiology/metabolism/pathology ; *Liver Neoplasms/therapy/immunology/microbiology/metabolism/pathology ; *Immunotherapy/methods ; Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Animals ; },
abstract = {BACKGROUND: The relationship between hepatocellular carcinoma (HCC) and gut microbiota has gained attention for its impact on HCC immunotherapy.

METHODS: Key gut microbial metabolites, including bile acids, toll-like receptor 4, short-chain fatty acids, and bacterial toxins, contribute to HCC progression and influence immune responses through the gut-liver axis. As immune checkpoint inhibitors (ICIs) become common in HCC treatment, modulating the gut microbiota offers new strategies to enhance ICIs efficacy. However, individual differences in microbial composition introduce challenges, with some HCC patients showing resistance to ICIs.

RESULTS: This review summarizes the latest findings on the role of gut microbiota in HCC and explores emerging therapeutic approaches, including fecal microbiota transplantation, probiotics, antibiotics, and natural compounds.

CONCLUSIONS: The focus is on translating these insights into personalized medicine to optimize ICIs responses and improve HCC treatment outcomes.},
}

Humans
*Gastrointestinal Microbiome/immunology/drug effects
*Carcinoma, Hepatocellular/therapy/immunology/microbiology/metabolism/pathology
*Liver Neoplasms/therapy/immunology/microbiology/metabolism/pathology
*Immunotherapy/methods
Immune Checkpoint Inhibitors/therapeutic use/pharmacology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Animals

@article {pmid40313405,
year = {2025},
author = {Zhao, H and Qiu, X and Wang, S and Wang, Y and Xie, L and Xia, X and Li, W},
title = {Multiple pathways through which the gut microbiota regulates neuronal mitochondria constitute another possible direction for depression.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1578155},
pmid = {40313405},
issn = {1664-302X},
abstract = {As a significant mental health disorder worldwide, the treatment of depression has long faced the challenges of a low treatment rate, significant drug side effects and a high relapse rate. Recent studies have revealed that the gut microbiota and neuronal mitochondrial dysfunction play central roles in the pathogenesis of depression: the gut microbiota influences the course of depression through multiple pathways, including immune regulation, HPA axis modulation and neurotransmitter metabolism. Mitochondrial function serves as a key hub that mediates mood disorders through mechanisms such as defective energy metabolism, impaired neuroplasticity and amplified neuroinflammation. Notably, a bidirectional regulatory network exists between the gut microbiota and mitochondria: the flora metabolite butyrate enhances mitochondrial biosynthesis through activation of the AMPK-PGC1α pathway, whereas reactive oxygen species produced by mitochondria counteract the flora composition by altering the intestinal epithelial microenvironment. In this study, we systematically revealed the potential pathways by which the gut microbiota improves neuronal mitochondrial function by regulating neurotransmitter synthesis, mitochondrial autophagy, and oxidative stress homeostasis and proposed the integration of probiotic supplementation, dietary fiber intervention, and fecal microbial transplantation to remodel the flora-mitochondrial axis, which provides a theoretical basis for the development of novel antidepressant therapies targeting gut-brain interactions.},
}

@article {pmid40312419,
year = {2025},
author = {Cao, M and Deng, Y and Hao, Q and Yan, H and Wang, QL and Dong, C and Wu, J and He, Y and Huang, LB and Xia, X and Gao, Y and Chen, HN and Zhang, WH and Zhang, YJ and Zhuo, X and Dai, L and Hu, H and Peng, Y and Zhang, F and Liu, Z and Huang, W and Zhang, H and Yang, L and Shu, Y and Zhang, W and Zhang, Y and Xu, H},
title = {Single-cell transcriptomic analysis reveals gut microbiota-immunotherapy synergy through modulating tumor microenvironment.},
journal = {Signal transduction and targeted therapy},
volume = {10},
number = {1},
pages = {140},
pmid = {40312419},
issn = {2059-3635},
support = {82273445//National Natural Science Foundation of China (National Science Foundation of China)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/immunology/genetics/drug effects ; *Tumor Microenvironment/immunology/genetics/drug effects ; Mice ; *Single-Cell Analysis ; *Immunotherapy ; CD8-Positive T-Lymphocytes/immunology ; Humans ; Gene Expression Profiling ; Transcriptome ; *Neoplasms/immunology/genetics/therapy/microbiology ; *Immune Checkpoint Inhibitors/pharmacology ; Mice, Knockout ; Macrophages/immunology ; },
abstract = {The gut microbiota crucially regulates the efficacy of immune checkpoint inhibitor (ICI) based immunotherapy, but the underlying mechanisms remain unclear at the single-cell resolution. Using single-cell RNA sequencing and subsequent validations, we investigate gut microbiota-ICI synergy by profiling the tumor microenvironment (TME) and elucidating critical cellular interactions in mouse models. Our findings reveal that intact gut microbiota combined with ICIs may synergistically increase the proportions of CD8[+], CD4[+], and γδ T cells, reduce glycolysis metabolism, and reverse exhausted CD8[+] T cells into memory/effector CD8[+] T cells, enhancing antitumor response. This synergistic effect also induces macrophage reprogramming from M2 protumor Spp1[+] tumor-associated macrophages (TAMs) to Cd74[+] TAMs, which act as antigen-presenting cells (APCs). These macrophage subtypes show a negative correlation within tumors, particularly during fecal microbiota transplantation. Depleting Spp1[+] TAMs in Spp1 conditional knockout mice boosts ICI efficacy and T cell infiltration, regardless of gut microbiota status, suggesting a potential upstream role of the gut microbiota and highlighting the crucial negative impact of Spp1[+] TAMs during macrophage reprogramming on immunotherapy outcomes. Mechanistically, we propose a γδ T cell-APC-CD8[+] T cell axis, where gut microbiota and ICIs enhance Cd40lg expression on γδ T cells, activating Cd40 overexpressing APCs (e.g., Cd74[+] TAMs) through CD40-CD40L-related NF-κB signaling and boosting CD8[+] T cell responses via CD86-CD28 interactions. These findings highlight the potential importance of γδ T cells and SPP1-related macrophage reprogramming in activating CD8[+] T cells, as well as the synergistic effect of gut microbiota and ICIs in immunotherapy through modulating the TME.},
}

Animals
*Gastrointestinal Microbiome/immunology/genetics/drug effects
*Tumor Microenvironment/immunology/genetics/drug effects
Mice
*Single-Cell Analysis
*Immunotherapy
CD8-Positive T-Lymphocytes/immunology
Humans
Gene Expression Profiling
Transcriptome
*Neoplasms/immunology/genetics/therapy/microbiology
*Immune Checkpoint Inhibitors/pharmacology
Mice, Knockout
Macrophages/immunology

@article {pmid40311999,
year = {2025},
author = {Liu, A and Wang, B and Wang, M and Tang, R and Xu, W and Xiao, W},
title = {L-theanine alleviates ulcerative colitis by repairing the intestinal barrier through regulating the gut microbiota and associated short-chain fatty acids.},
journal = {Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association},
volume = {},
number = {},
pages = {115497},
doi = {10.1016/j.fct.2025.115497},
pmid = {40311999},
issn = {1873-6351},
abstract = {Ulcerative colitis (UC) is closely related to impaired intestinal barrier function and imbalanced gut microbial communities. L-theanine shows great potential in maintaining intestinal integrity and regulating the gut microbiota and associated short-chain fatty acids (SCFAs). However, whether L-theanine can alleviate UC by repairing the intestinal barrier through these regulatory processes remains unclear. In this study, L-theanine was used to optimize the gut microbiota, and the restorative effect and mechanism of L-theanine in UC by repairing the gut barrier through the gut microbiota and SCFAs were investigated via fecal microbiota transplantation. The findings revealed that L-theanine regulated the gut microbiota structure, increased SCFA contents, and promoted gut barrier repair in UC mice. Moreover, L-theanine upregulated the protein and mRNA expression of G-protein-coupled receptor 43 (GPR43), AKT, and phosphatidylinositide 3-kinase (PI3K). These results indicated that L-theanine alleviates UC by repairing the gut barrier via regulating the gut microbiota and SCFAs through the GPR43/PI3K/AKT signaling pathway activation. This study provides a method of preventing and treating UC via L-theanine as a safe food dietary supplement.},
}

@article {pmid40309228,
year = {2025},
author = {Li, Y and Wu, YT and Wu, H},
title = {Management of hepatic encephalopathy following transjugular intrahepatic portosystemic shunts: Current strategies and future directions.},
journal = {World journal of gastroenterology},
volume = {31},
number = {15},
pages = {103512},
pmid = {40309228},
issn = {2219-2840},
mesh = {Humans ; *Portasystemic Shunt, Transjugular Intrahepatic/adverse effects ; *Hepatic Encephalopathy/etiology/therapy/prevention & control/diagnosis ; *Hypertension, Portal/surgery/etiology ; *Liver Cirrhosis/complications/surgery ; *Postoperative Complications/therapy/etiology/prevention & control ; Quality of Life ; Stents ; Treatment Outcome ; Biomarkers/blood ; Fecal Microbiota Transplantation ; },
abstract = {Transjugular intrahepatic portosystemic shunts (TIPSs) are generally used for the management of complications of portal hypertension in patients with decompensated cirrhosis. However, hepatic encephalopathy (HE), which impairs neuropsychiatric function and motor control, remains the primary adverse effect of TIPS, limiting its utility. Prompt prevention and treatment of post-TIPS HE are critical, as they are strongly associated with readmission rates and poor quality of life. This review focuses on the main pathophysiological mechanisms underlying post-TIPS HE, explores advanced biomarkers and predictive tools, and discusses current management strategies and future directions to prevent or reverse HE following TIPS. These strategies include preoperative patient assessment, individualized shunt diameter optimization, spontaneous portosystemic shunt embolization during the TIPS procedure, postoperative preventive and therapeutic measures such as nutrition management, medical therapy, fecal microbiota transplantation, and stent reduction.},
}

Humans
*Portasystemic Shunt, Transjugular Intrahepatic/adverse effects
*Hepatic Encephalopathy/etiology/therapy/prevention & control/diagnosis
*Hypertension, Portal/surgery/etiology
*Liver Cirrhosis/complications/surgery
*Postoperative Complications/therapy/etiology/prevention & control
Quality of Life
Stents
Treatment Outcome
Biomarkers/blood
Fecal Microbiota Transplantation

@article {pmid40309194,
year = {2025},
author = {Tang, CT and Wu, Y and Tao, Q and Zeng, CY and Chen, YX},
title = {Thalidomide mitigates Crohn's disease colitis by modulating gut microbiota, metabolites, and regulatory T cell immunity.},
journal = {Journal of pharmaceutical analysis},
volume = {15},
number = {4},
pages = {101121},
pmid = {40309194},
issn = {2214-0883},
abstract = {Thalidomide (THA) is renowned for its potent anti-inflammatory properties. This study aimed to elucidate its underlying mechanisms in the context of Crohn's disease (CD) development. Mouse colitis models were established by dextran sulfate sodium (DSS) treatment. Fecal microbiota and metabolites were analyzed by metagenomic sequencing and mass spectrometry, respectively. Antibiotic-treated mice served as models for microbiota depletion and transplantation. The expression of forkhead box P3[+] (FOXP3[+]) regulatory T cells (Tregs) was measured by flow cytometry and immunohistochemical assay in colitis model and patient cohort. THA inhibited colitis in DSS-treated mice by altering the gut microbiota profile, with an increased abundance of probiotics Bacteroides fragilis, while pathogenic bacteria were depleted. In addition, THA increased beneficial metabolites bile acids and significantly restored gut barrier function. Transcriptomic profiling revealed that THA inhibited interleukin-17 (IL-17), IL-1β and cell cycle signaling. Fecal microbiota transplantation from THA-treated mice to microbiota-depleted mice partly recapitulated the effects of THA. Specifically, increased level of gut commensal B. fragilis was observed, correlated with elevated levels of the microbial metabolite 3alpha-hydroxy-7-oxo-5beta-cholanic acid (7-ketolithocholic acid, 7-KA) following THA treatment. This microbial metabolite may stable FOXP3 expression by targeting the receptor FMR1 autosomal homolog 1 (FXR1) to inhibit autophagy. An interaction between FOXP3 and FXR1 was identified, with binding regions localized to the FOXP3 domain (aa238-335) and the FXR1 domain (aa82-222), respectively. Conclusively, THA modulates the gut microbiota and metabolite profiles towards a more beneficial composition, enhances gut barrier function, promotes the differentiation of FOXP3[+] Tregs and curbs pro-inflammatory pathways.},
}

@article {pmid40309103,
year = {2025},
author = {Cong, X and Liu, X and Zhou, D and Xu, Y and Liu, J and Tong, F},
title = {Characterization and comparison of the fecal bacterial microbiota in Red Back Pine Root Snake (Oligodon formosanus) and Chinese Slug-Eating Snake (Pareas chinensis).},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1575405},
pmid = {40309103},
issn = {1664-302X},
abstract = {INTRODUCTION: The gastrointestinal tracts and oral cavities of animals harbor complex microbial communities that assist hosts in nutrient absorption and immune responses, thereby influencing behavior, development, reproduction, and overall health.

METHODS: We utilized metagenomic sequencing technology to conduct a detailed analysis of the fecal bacterial communities of six Red Back Pine Root Snakes (Oligodon formosanus, XT) and three Chinese Slug-Eating Snakes (Pareas chinensis, Z) individuals. The microbial composition was assessed through taxonomic profiling, alpha diversity analysis, and functional annotation using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database.

RESULTS: The results indicated that Proteobacteria, Bacteroidetes, Firmicutes, Verrucomicrobia, Actinobacteria, and Fusobacteria were the dominant phyla in XT samples, while Z samples additionally contained Patescibacteria. Alpha diversity analysis revealed significant differences in species abundance at the family level, with Z samples exhibiting higher microbial richness than XT. Furthermore, KEGG analysis showed that XT had higher functional gene abundance in pathways related to transcription, translation, environmental adaptation, membrane transport, cellular communities (prokaryotes), motility, and replication/repair compared to Z.

DISCUSSION: This study provides a comparative analysis of their gut microbiomes, offering valuable insights for future research on zoonotic diseases, host-microbe interactions, and ecological, evolutionary, behavioral, and seasonal influences on snake microbiota. These findings contribute to a broader understanding of microbial ecology in reptiles and its implications for conservation and disease dynamics.},
}

@article {pmid40308808,
year = {2025},
author = {Wei, H and Mai, ZL and Ma, BT and Chang, B},
title = {Creeping fat: A promising radiological predictor in small bowel Crohn's disease.},
journal = {World journal of gastroenterology},
volume = {31},
number = {16},
pages = {105186},
pmid = {40308808},
issn = {2219-2840},
mesh = {Humans ; *Crohn Disease/diagnostic imaging/therapy/pathology ; *Intestine, Small/diagnostic imaging/pathology ; Treatment Outcome ; Fecal Microbiota Transplantation ; Predictive Value of Tests ; Tomography, X-Ray Computed ; Magnetic Resonance Imaging ; *Adipose Tissue/diagnostic imaging/pathology ; Biological Products/therapeutic use ; },
abstract = {In this manuscript, we comment on the article by Hasnaoui et al. Specifically, we delve into the characteristic manifestation of Crohn's disease (CD) known as creeping fat (CF). Our primary focus is to investigate the potential of imaging features of CF in predicting the response of small bowel CD to biologic therapies and fecal microbiota transplantation. We believe that further research should be dedicated to developing methods for quantifying CF in order to provide more accurate predictive tools for the treatment of small bowel CD.},
}

Humans
*Crohn Disease/diagnostic imaging/therapy/pathology
*Intestine, Small/diagnostic imaging/pathology
Treatment Outcome
Fecal Microbiota Transplantation
Predictive Value of Tests
Tomography, X-Ray Computed
Magnetic Resonance Imaging
*Adipose Tissue/diagnostic imaging/pathology
Biological Products/therapeutic use

@article {pmid40307551,
year = {2025},
author = {Kennedy, MS and Freiburger, A and Cooper, M and Beilsmith, K and St George, ML and Kalski, M and Cham, C and Guzzetta, A and Ng, SC and Chan, FK and DeLeon, O and Rubin, D and Henry, CS and Bergelson, J and Chang, EB},
title = {Diet outperforms microbial transplant to drive microbiome recovery in mice.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {40307551},
issn = {1476-4687},
abstract = {A high-fat, low-fibre Western-style diet (WD) induces microbiome dysbiosis characterized by reduced taxonomic diversity and metabolic breadth[1,2], which in turn increases risk for a wide array of metabolic[3-5], immune[6] and systemic pathologies. Recent work has established that WD can impair microbiome resilience to acute perturbations such as antibiotic treatment[7,8], although little is known about the mechanism of impairment and the specific consequences for the host of prolonged post-antibiotic dysbiosis. Here we characterize the trajectory by which the gut microbiome recovers its taxonomic and functional profile after antibiotic treatment in mice on regular chow (RC) or WD, and find that only mice on RC undergo a rapid successional process of recovery. Metabolic modelling indicates that a RC diet promotes the development of syntrophic cross-feeding interactions, whereas in mice on WD, a dominant taxon monopolizes readily available resources without releasing syntrophic byproducts. Intervention experiments reveal that an appropriate dietary resource environment is both necessary and sufficient for rapid and robust microbiome recovery, whereas microbial transplant is neither. Furthermore, prolonged post-antibiotic dysbiosis in mice on WD renders them susceptible to infection by the intestinal pathogen Salmonella enterica serovar Typhimurium. Our data challenge widespread enthusiasm for faecal microbiota transplant (FMT) as a strategy to address dysbiosis, and demonstrate that specific dietary interventions are, at a minimum, an essential prerequisite for effective FMT, and may afford a safer, more natural and less invasive alternative.},
}

@article {pmid40307477,
year = {2025},
author = {Iyengar, A and Ramadass, B and Venkatesh, S and Mak, RH},
title = {Gut microbiota-targeted therapies in pediatric chronic kidney disease: gaps and opportunities.},
journal = {Pediatric nephrology (Berlin, Germany)},
volume = {},
number = {},
pages = {},
pmid = {40307477},
issn = {1432-198X},
abstract = {Given the complex relationship between the gut microbiome and chronic kidney disease (CKD), exploring the potential role and scope of microbiota-targeted therapies in pediatric CKD is highly relevant. We aim to provide an overview of gut-targeted therapeutic strategies, including nutritional interventions (fiber, phytochemicals, fermented foods, and traditional Chinese medicines), probiotics, synbiotics, oral absorbents, and fecal microbial transplantation. Enhancing physical activity and preventing constipation are additional strategies that may promote gut microbiome health. In a uremic environment, gut microbiota-targeted therapies could potentially rebalance the gut microbiota, improve gut barrier function, decrease uremic toxin concentrations, enhance the production of short-chain fatty acids (SCFA), and reduce inflammation. While research in adult CKD patients has provided insights into these approaches, there are limited data in children with CKD. This review aims to summarize potential targeted therapies for restoring a balanced gut microbiota, emphasizing the need for studies that evaluate their effects on clinical outcomes in pediatric CKD.},
}

@article {pmid40306604,
year = {2025},
author = {Lee, SH and Han, C and Shin, C},
title = {IUPHAR Review: Microbiota-Gut-Brain Axis and its role in Neuropsychiatric Disorders.},
journal = {Pharmacological research},
volume = {},
number = {},
pages = {107749},
doi = {10.1016/j.phrs.2025.107749},
pmid = {40306604},
issn = {1096-1186},
abstract = {The human gut microbiome, composed of a vast array of microorganisms that have co-evolved with humans, is crucial for the development and function of brain systems. Research has consistently shown bidirectional communication between the gut and the brain through neuronal, endocrine, and immunological, and chemical pathways. Recent neuroscience studies have linked changes in the microbiome and microbial metabolites to various neuropsychiatric disorders such as autism, depression, anxiety, schizophrenia, eating disorders, and neurocognitive disorders. Novel metagenome-wide association studies have confirmed these microbiome variations in large samples and expanded our understanding of the interactions between human genes and the gut microbiome. The causal relationship between gut microbiota and neuropsychiatric disorders is being elucidated through the establishment of large cohort studies incorporating microbiome data and advanced statistical techniques. Ongoing animal and human studies focused on the microbiota-gut-brain axis are promising for developing new prevention and treatment strategies for neuropsychiatric conditions. The scope of these studies has broadened from microbiome-modulating therapies including prebiotics, probiotics, synbiotics and postbiotics to more extensive approaches such as fecal microbiota transplantation. Recent systematic reviews and meta-analyses have strengthened the evidence base for these innovative treatments. Despite extensive research over the past decade, many intriguing aspects still need to be elucidated regarding the role and therapeutic interventions of the microbiota-gut-brain axis in neuropsychiatric disorders.},
}

@article {pmid40306274,
year = {2025},
author = {Kim, SH and White, Z and Gainullina, A and Kang, S and Kim, J and Dominguez, JR and Choi, Y and Cabrera, I and Plaster, M and Takahama, M and Czepielewski, RS and Yeom, J and Gunzer, M and Hay, N and David, O and Chevrier, N and Sano, T and Kim, KW},
title = {IL-10 sensing by lung interstitial macrophages prevents bacterial dysbiosis-driven pulmonary inflammation and maintains immune homeostasis.},
journal = {Immunity},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.immuni.2025.04.004},
pmid = {40306274},
issn = {1097-4180},
abstract = {Crosstalk between the immune system and the microbiome is critical for maintaining immune homeostasis. Here, we examined this communication and the impact of immune-suppressive IL-10 signaling on pulmonary homeostasis. We found that IL-10 sensing by interstitial macrophages (IMs) is required to prevent spontaneous lung inflammation. Loss of IL-10 signaling in IMs initiated an inflammatory cascade through the activation of classical monocytes and CD4[+] T cell subsets, leading to chronic lung inflammation with age. Analyses of antibiotic-treated and germ-free mice established that lung inflammation in the animals lacking IL-10 signaling was triggered by commensal bacteria. 16S rRNA sequencing revealed Delftia acidovorans and Rhodococcus erythropolis as potential drivers of lung inflammation. Intranasal administration of these bacteria or transplantation of human fecal microbiota elicited lung inflammation in gnotobiotic Il10-deficient mice. These findings highlight that IL-10 sensing by IMs contributes to pulmonary homeostasis by preventing lung inflammation caused by commensal dysbiosis.},
}

@article {pmid40305972,
year = {2025},
author = {Jiang, ZM and Fang, ZY and Yang, X and Ji, XX and Zhao, YY and Lin, BY and Weng, ZB and Liu, EH},
title = {Glycyrrhetinic acid ameliorates gastric mucosal injury by modulating gut microbiota and its metabolites via Thbs1/PI3K-Akt/p53 pathway.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {142},
number = {},
pages = {156745},
doi = {10.1016/j.phymed.2025.156745},
pmid = {40305972},
issn = {1618-095X},
abstract = {BACKGROUND: Dysbiosis of the gut microbiota is pivotal in the development of gastric mucosa injury (GMI). Glycyrrhetinic acid (GA) is a bioactive triterpenoid compound abundantly present in licorice roots. Although GA's potential in mitigating GMI is recognized, its precise mechanism remains elusive, particularly concerning the role of gut microbiota.

PURPOSE: This study aimed to explore the protective effects and mechanisms of GA in preventing HCl/ethanol-induced GMI in rats.

RESULTS: This study demonstrated the protective effects of GA on gastric mucosa, evidenced by enhanced morphology and structure as revealed through H&E staining. Utilizing fecal microbiota transplantation, GA was found to significantly mitigate oxidative damage, inflammation, and expression of apoptosis-related genes in GMI rats by a gut microbiota-dependent mechanism. 16S rRNA sequencing and metabolomics profiling revealed that GA ameliorated HCl/ethanol-triggered intestinal dysbiosis and imbalances in sphingolipid, arginine, and tryptophan metabolism. By promoting the prevalence of Bifidobacterium longum subsp. infantis (B. infantis) in the gut microbiota, GA improved metabolic disturbances linked to injury. Furthermore, its action mechanism was related to the inhibition of the Thbs1/PI3K-Akt/p53 signaling pathway.

CONCLUSION: The administration of GA improves GMI by mitigating intestinal dysbiosis and fostering colonization of B. infantis. GA offers therapeutic potential for GMI by modulating the Thbs1/PI3K-Akt/p53 pathway, thus alleviating inflammatory responses associated with gut microbiota imbalance.},
}

@article {pmid40305678,
year = {2025},
author = {Wang, Y and Wang, X and Chen, Z and Zheng, J and Liu, X and Zheng, Y and Zheng, Z and Xu, Z and Zhang, Y and Chen, K and Zhang, Y and Yu, L and Ding, Y},
title = {Akkermansia muciniphila exacerbates acute radiation-induced intestinal injury by depleting mucin and enhancing inflammation.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wraf084},
pmid = {40305678},
issn = {1751-7370},
abstract = {Dysbiosis of gut microbiota plays a crucial role in acute radiation-induced intestinal injury. However, studies on the influence of gut microbiota on acute radiation-induced intestinal injury are inconsistent. In this study, we established an acute radiation-induced intestinal injury mouse model and performed fecal microbiota transplantation to explore the role of the gut microbiota in acute radiation-induced intestinal injury. We observed a significant increase in Akkermansia muciniphila following irradiation, whereas fecal microbiota transplantation effectively reduced Akkermansia muciniphila levels. Contrary to expectations, Akkermansia muciniphila supplementation increased acute radiation-induced intestinal injury and mortality. Mechanistically, post-radiation Akkermansia muciniphila upregulates mucin metabolism genes and consumes mucin, thinning the mucosal barrier and promoting the adhesion and translocation of potential pathogens to epithelial cells, thus exacerbating acute radiation-induced intestinal injury. This enables Akkermansia muciniphila to use mucin as an energy source. Additionally, Akkermansia muciniphila increases the inflammatory macrophage changes and secretion of inflammatory cytokines, leading to a decrease in epithelial stem cell density and inhibition of goblet cell differentiation, further exacerbating acute radiation-induced intestinal injury. Our findings suggest that in certain intestinal environments, the addition of Akkermansia muciniphila may worsen radiation-induced intestinal damage; thus, alternative approaches to reverse the dysbiosis associated with radiotherapy should be explored.},
}

@article {pmid40305219,
year = {2025},
author = {Alves Costa Silva, C and Almonte, AA and Zitvogel, L},
title = {Oncobiomics: Leveraging Microbiome Translational Research in Immuno-Oncology for Clinical-Practice Changes.},
journal = {Biomolecules},
volume = {15},
number = {4},
pages = {},
pmid = {40305219},
issn = {2218-273X},
mesh = {Humans ; *Neoplasms/immunology/microbiology/therapy/metabolism ; *Translational Research, Biomedical ; *Microbiota ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/microbiology/immunology ; },
abstract = {Growing evidence suggests that cancer should not be viewed solely as a genetic disease but also as the result of functional defects in the metaorganism, including disturbances in the gut microbiota (i.e., gut dysbiosis). The human microbiota plays a critical role in regulating epithelial barrier function in the gut, airways, and skin, along with host metabolism and systemic immune responses against microbes and cancer. Collaborative international networks, such as ONCOBIOME, are essential in advancing research equity and building microbiome resources to identify and validate microbiota-related biomarkers and therapies. In this review, we explore the intricate relationship between the microbiome, metabolism, and cancer immunity, and we propose microbiota-based strategies to improve outcomes for individuals at risk of developing cancer or living with the disease.},
}

Humans
*Neoplasms/immunology/microbiology/therapy/metabolism
*Translational Research, Biomedical
*Microbiota
*Gastrointestinal Microbiome/immunology
Dysbiosis/microbiology/immunology

@article {pmid40304829,
year = {2025},
author = {Alum, EU and Uti, DE and Ugwu, OP and Alum, BN and Edeh, FO and Ainebyoona, C},
title = {Unveiling the microbial orchestra: exploring the role of microbiota in cancer development and treatment.},
journal = {Discover oncology},
volume = {16},
number = {1},
pages = {646},
pmid = {40304829},
issn = {2730-6011},
abstract = {The human microbiota comprises a diverse microbial ecosystem that significantly impacts health and disease. Among its components, the gut microbiota plays a crucial role in regulating metabolic, immunologic, and inflammatory responses. Dysbiosis, an imbalance in microbial composition, has been linked to carcinogenesis through mechanisms such as chronic inflammation, metabolic disturbances, epigenetic modifications, and immune system dysregulation. Additionally, dysbiosis influences the efficacy and toxicity of cancer therapies. Given these associations, there is growing interest in leveraging the microbiota as a biomarker for cancer detection and outcome prediction. Notably, distinct microbial signatures have been identified across various cancer types, suggesting their potential as diagnostic markers. Furthermore, modulation of the microbiota presents a promising avenue for improving cancer treatment outcomes through strategies such as antibiotics, prebiotics, probiotics, fecal microbiota transplantation, dietary interventions, small-molecule inhibitors, and phage therapy. To explore these relationships, we conducted a comprehensive literature review using Web of Science, Scopus, PubMed, MEDLINE, Embase, and Google Scholar as our primary online databases, focusing on indexed peer-reviewed articles up to the present year. This review aims to elucidate the role of dysbiosis in cancer development, examine the molecular mechanisms involved, and assess the impact of microbiota on cancer therapies. Additionally, we highlight microbiota-based therapeutic strategies and discuss their potential applications in cancer management. A deeper understanding of the intricate interplay between the microbiota and cancer may pave the way for novel approaches to cancer prevention, early detection, and treatment optimization.},
}

@article {pmid40302307,
year = {2025},
author = {Hoffmann, DE and Javitt, GH and Kelly, CR and Keller, JJ and Baunwall, SMD and Hvas, CL},
title = {Fecal microbiota transplantation: a tale of two regulatory pathways.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2493901},
pmid = {40302307},
issn = {1949-0984},
mesh = {*Fecal Microbiota Transplantation/history/methods/standards/adverse effects ; Humans ; *Gastrointestinal Microbiome ; United States ; Europe ; },
abstract = {Fecal microbiota transplantation (FMT) is a procedure involving the transfer of intestinal microbiota from a healthy donor to a patient to restore a functional intestinal microbiome. First described in modern science in 1958, the use of FMT has been practiced for decades, but only during the past dozen years have clinical frameworks and legal regulations from competent authorities been developed. Future development of microbiota-derived medical therapies will be shaped by the regulatory frameworks of various jurisdictions. This review examines the historical development and status of FMT regulations in the United States and Europe, with particular attention to their respective approaches to ensuring the safety and quality of the therapeutic product and patient access.},
}

*Fecal Microbiota Transplantation/history/methods/standards/adverse effects
Humans
*Gastrointestinal Microbiome
United States
Europe

@article {pmid40301246,
year = {2025},
author = {Liu, X and Cui, J and Tan, X and Yu, Y and Niu, J and Wang, Q},
title = {Short-Chain Fatty Acids Alleviate Perioperative Neurocognitive Disorders Through BDNF/PI3K/Akt Pathway in Middle-Aged Rats.},
journal = {Molecular neurobiology},
volume = {},
number = {},
pages = {},
pmid = {40301246},
issn = {1559-1182},
support = {246Z7702G//Central Government - Guided Local Science and Technology Development Fund/ ; },
abstract = {Perioperative neurocognitive disorders (PND), characterized by persistent cognitive impairment lasting from days to years, present substantial clinical challenges in elderly surgical populations, profoundly compromising functional independence, quality of life, and long-term prognosis. We aimed to investigate the effects of short-chain fatty acids (SCFAs) treatment on PND via mediating Brain-derived neurotrophic factor (BDNF)/Phosphatidylinositol3-kinase (PI3K)/Protein kinase B (Akt) pathway. Using 16S rDNA sequencing targeting the V3-V4 hypervariable regions, we first demonstrated significant gut microbiota dysbiosis in PND model rats, accompanied by altered SCFAs profiles. Subsequent fecal microbiota transplantation (FMT) experiments established causal relationships between PND-associated microbial alterations and spatial cognitive deficits. Mechanistically, SCFAs supplementation attenuated neuronal damage and restored synaptic plasticity, as evidenced by Nissl staining quantification (reduced chromatolysis), TUNEL assay (decreased apoptosis rate), and immunohistochemical analysis (upregulated NeuN expression). Molecular investigations revealed that SCFAs-mediated cognitive improvement involved BDNF upregulation and subsequent PI3K/Akt pathway activation, ultimately enhancing neuronal survival and synaptic integrity. Notably, PND animals exhibited characteristic neuropathological features including synaptic density reduction (PSD-95 downregulation), neuroinflammation amplification (IL-6 elevation), and apoptosis activation-all significantly reversed by SCFA intervention. Our findings establish a novel gut-brain axis mechanism wherein microbiota-derived SCFAs may exert neuroprotection through BDNF-dependent PI3K/Akt signaling, and offer potential therapeutic strategies for PND management.},
}

@article {pmid40301116,
year = {2025},
author = {Kamath, S and Bryant, RV and Costello, SP and Day, AS and Forbes, B and Haifer, C and Hold, G and Kelly, CR and Li, A and Pakuwal, E and Stringer, A and Tucker, EC and Wardill, HR and Joyce, P},
title = {Translational strategies for oral delivery of faecal microbiota transplantation.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2025-335077},
pmid = {40301116},
issn = {1468-3288},
abstract = {Faecal microbiota transplantation (FMT) has emerged as a transformative therapy for Clostridioides difficile infections and shows promise for various GI and systemic diseases. However, the poor patient acceptability and accessibility of 'conventional' FMT, typically administered via colonoscopies or enemas, hinders its widespread clinical adoption, particularly for chronic conditions. Oral administration of FMT (OralFMT) overcomes these limitations, yet faces distinct challenges, including a significant capsule burden, palatability concerns and poor microbial viability during gastric transit. This review provides a comprehensive analysis of emerging strategies that aim to advance OralFMT by: (1) refining processing technologies (eg, lyophilisation) that enable manufacturing of low-volume FMT formulations for reducing capsule burden and (2) developing delivery technologies that improve organoleptic acceptability and safeguard the microbiota for targeted colonic release. These advancements present opportunities for OralFMT to expand its therapeutic scope, beyond C. difficile infections, towards chronic GI conditions requiring frequent dosing regimens. While this review primarily focuses on optimising OralFMT delivery, it is important to contextualise these advancements within the broader shift towards defined microbial consortia. Live biotherapeutic products (LBPs) offer an alternative approach, yet the interplay between OralFMT and LBPs in clinical practice remains unresolved. We postulate that continued innovation in OralFMT and LBPs via a multidisciplinary approach can further increase therapeutic efficacy and scalability by enabling disease site targeting, co-delivery of therapeutic compounds and overcoming colonisation resistance. Realising these goals positions OralFMT as a cornerstone of personalised care across a range of diseases rooted in microbiome health.},
}

@article {pmid40300858,
year = {2025},
author = {Almonte, AA and Zitvogel, L},
title = {Gut reactions: harnessing microbial metabolism to fuel next-generation cancer immunotherapy.},
journal = {Journal for immunotherapy of cancer},
volume = {13},
number = {4},
pages = {},
pmid = {40300858},
issn = {2051-1426},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Immunotherapy/methods ; *Neoplasms/therapy/immunology ; },
abstract = {Immunotherapies, including immune checkpoint inhibitors and chimeric antigen receptor-T cell therapies, depend heavily on a healthy and diverse gut microbiome for optimal efficacy. Dysbiosis, or an imbalance in gut microbial composition and function, can diminish immunotherapy responses by altering immune cell trafficking and metabolic output. Key microbial metabolites such as short-chain fatty acids and modified bile acids shape host immunity and influence T-cell function, while their disruption can foster an immunosuppressive microenvironment. Emerging strategies to restore a balanced microbiome and boost treatment outcomes include dietary interventions, supplementation with beneficial microbes, and fecal microbiota transplantation. Despite these advances, challenges remain in defining dysbiosis, identifying reliable biomarkers, and tailoring microbiota-centered interventions. Nevertheless, as our understanding evolves, the gut microbiome holds promise as an integral component of personalized cancer immunotherapy.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Immunotherapy/methods
*Neoplasms/therapy/immunology

@article {pmid40300731,
year = {2025},
author = {Mahmoud, AA and Wang, X and Liao, X and Zhang, S and Ding, T and Ahn, J},
title = {Impact of prophages on gut microbiota and disease associations.},
journal = {Microbial pathogenesis},
volume = {204},
number = {},
pages = {107642},
doi = {10.1016/j.micpath.2025.107642},
pmid = {40300731},
issn = {1096-1208},
abstract = {The gut microbiota plays an important role in maintaining host health by affecting various physiological functions. Among the diverse microbial communities in the gut, prophages are integral components of bacterial genomes, contributing significantly to bacterial evolution, ecology and pathogenicity. Prophages are capable of switching to lytic cycles in response to various internal and external factors. Factors that induce prophage induction include DNA damage, oxidative stress, nutrient availability, host immune response, quorum sensing, diet, secondary metabolites, antibiotics, and lifestyle changes. Prophage induction could contribute to both gut homeostasis and dysbiosis. Importantly, the connections between prophage induction and disorders such as inflammatory bowel disease, ulcerative colitis, and bacterial vaginosis highlight the dual roles of prophages in both health and disease. Although therapeutic approaches such as phage therapy (PT), fecal microbiota transplants (FMT), and fecal virome transplants (FVT) have gained attention, the concept of dietary prophage induction therapy offers a novel, targeted method to modulate gut microbiota. In spite of recent advances in understanding the role of prophages in gut health, the exact mechanisms by which they influence gut health remain only partially understood. Therefore, further research is needed to elucidate additional molecular mechanisms of prophage induction pathways and to explore their implications for gut microbiota dynamics and disease associations. This review discusses the molecular mechanisms and key factors that trigger prophage induction in the gut. Insights into these processes could lead to innovative therapeutic strategies that utilize prophages to support gut health.},
}

@article {pmid40300372,
year = {2025},
author = {Liu, Z and Zhang, H and Wang, J and Yao, Y and Wang, X and Liu, Y and Fang, W and Liu, X and Zheng, Y},
title = {Clca1 deficiency exacerbates colitis susceptibility via impairment of mucus barrier integrity and gut microbiota homeostasis.},
journal = {Microbiological research},
volume = {297},
number = {},
pages = {128191},
doi = {10.1016/j.micres.2025.128191},
pmid = {40300372},
issn = {1618-0623},
abstract = {The intestinal mucus barrier has emerged as a promising therapeutic target for inflammatory bowel disease. Understanding its regulatory mechanisms is critical for elucidating ulcerative colitis (UC) pathogenesis, improving diagnostics, guiding treatments, and preventing relapse. Chloride Channel Accessory 1 (Clca1), a constituent of the mucus layer, remains understudied in colitis. Here, we investigated Clca1's role in mucosal immunity and intestinal homeostasis using experimental colitis models. Clca1-deficient (Clca1[-/-]) mice displayed compromised mucus layer integrity, reduced neutrophil infiltration, and gut microbiota dysbiosis. Notably, Clca1[-/-] mice exhibited exacerbated colitis severity following dextran sulfate sodium (DSS) challenge, accompanied by a diminished goblet cell populations. Fecal microbiota transplantation (FMT) studies revealed that gut microbiota critically modulates divergent phenotypic outcomes between genotypes. Our findings establish Clca1 as a multifunctional regulator of mucus barrier integrity through mechanisms involving goblet cell maintenance, neutrophil-mediated immunity, and host-microbiota crosstalk. These results advance the understanding of UC pathogenesis and identify Clca1-associated pathways as potential targets for barrier restoration therapies.},
}

@article {pmid40299998,
year = {2025},
author = {Cao, J and Wang, X and Lei, Y and Jiang, X and Kannan, K and Li, M},
title = {Health Risks of Low-Dose Dietary Exposure to Triphenyl Phosphate and Diphenyl Phosphate in Mice: Insights from the Gut-Liver Axis.},
journal = {Environmental science & technology},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.est.4c08270},
pmid = {40299998},
issn = {1520-5851},
abstract = {Aryl phosphate esters have been detected throughout the natural environment and in human blood samples, making it important to determine the health risks associated with exposure to triphenyl phosphate (TPHP) and its metabolite diphenyl phosphate (DPHP). Here, C57BL/6J male mice were exposed to TPHP or DPHP for 12 weeks at estimated daily intake doses of 0.1 and 7 μg/kg bw/day. TPHP intake affected the levels of short-chain fatty acids and bile acids in the gut, enhancing the production of 29 medium- and long-chain fatty acids in the liver by 3.72-fold and significantly increasing hepatic lipid and cholesterol levels. Metabolomic and molecular analysis confirmed that elevated liver cholesterol levels persisted after an 8 week recovery period. Gut microbiota-dependent cholesterol alterations were the toxic end points observed in TPHP-fed mice, as supported by the results of fecal microbiota transplantation. In DPHP-fed mice, serotonergic and glutamatergic synapses were simultaneously altered in the liver and intestine, corresponding to the reduction of five brain neurotransmitters (15.4-60.8%). Decreased liver carbohydrate levels and insulin resistance were observed in the DPHP-fed mice. These results suggest that TPHP and DPHP affect metabolism via different toxic modes, mediated through the gut-liver axis, providing novel insights into the mechanisms of organophosphate-ester-mediated metabolic disruption.},
}

@article {pmid40299512,
year = {2025},
author = {Eslami, M and Adampour, Z and Fadaee Dowlat, B and Yaghmayee, S and Motallebi Tabaei, F and Oksenych, V and Naderian, R},
title = {A Novel Frontier in Gut-Brain Axis Research: The Transplantation of Fecal Microbiota in Neurodegenerative Disorders.},
journal = {Biomedicines},
volume = {13},
number = {4},
pages = {},
pmid = {40299512},
issn = {2227-9059},
abstract = {The gut-brain axis (GBA) represents a sophisticated bidirectional communication system connecting the central nervous system (CNS) and the gastrointestinal (GI) tract. This interplay occurs primarily through neuronal, immune, and metabolic pathways. Dysbiosis in gut microbiota has been associated with multiple neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), multiple sclerosis (MS), and amyotrophic lateral sclerosis (ALS). In recent years, fecal microbiota transplantation (FMT) has gained attention as an innovative therapeutic approach, aiming to restore microbial balance in the gut while influencing neuroinflammatory and neurodegenerative pathways. This review explores the mechanisms by which FMT impacts the gut-brain axis. Key areas of focus include its ability to reduce neuroinflammation, strengthen gut barrier integrity, regulate neurotransmitter production, and reinstate microbial diversity. Both preclinical and clinical studies indicate that FMT can alleviate motor and cognitive deficits in PD and AD, lower neuroinflammatory markers in MS, and enhance respiratory and neuromuscular functions in ALS. Despite these findings, several challenges remain, including donor selection complexities, uncertainties about long-term safety, and inconsistencies in clinical outcomes. Innovations such as synthetic microbial communities, engineered probiotics, and AI-driven analysis of the microbiome hold the potential to improve the precision and effectiveness of FMT in managing neurodegenerative conditions. Although FMT presents considerable promise as a therapeutic development, its widespread application for neurodegenerative diseases requires thorough validation through well-designed, large-scale clinical trials. It is essential to establish standardized protocols, refine donor selection processes, and deepen our understanding of the molecular mechanisms behind its efficacy.},
}

@article {pmid40299326,
year = {2025},
author = {Hauser, G and Benjak Horvat, I and Rajilić-Stojanović, M and Krznarić-Zrnić, I and Kukla, M and Aljinović-Vučić, V and Mikolašević, I},
title = {Intestinal Microbiota Modulation by Fecal Microbiota Transplantation in Nonalcoholic Fatty Liver Disease.},
journal = {Biomedicines},
volume = {13},
number = {4},
pages = {},
pmid = {40299326},
issn = {2227-9059},
abstract = {Numerous factors are involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD), which are responsible for its development and progression as an independent entity, but also thanks to their simultaneous action. This is explained by the hypothesis of multiple parallel hits. These factors are insulin resistance, lipid metabolism alteration, oxidative stress, endoplasmic reticulum stress, inflammatory cytokine liberation, gut microbiota dysbiosis or gut-liver axis activation. This is a systematic review which has an aim to show the connection between intestinal microbiota and the role of its disbalance in the development of NAFLD. The gut microbiota is made from a wide spectrum of microorganisms that has a systemic impact on human health, with a well-documented role in digestion, energy metabolism, the stimulation of the immune system, synthesis of essential nutrients, etc. It has been shown that dysbiosis is associated with all three stages of chronic liver disease. Thus, the modulation of the gut microbiota has attracted research interest as a novel therapeutic approach for the management of NAFLD patients. The modification of microbiota can be achieved by substantial diet modification and the application of probiotics or prebiotics, while the most radical effects are observed by fecal microbiota transplantation (FMT). Given the results of FMT in the context of metabolic syndrome (MetS) and NAFLD in animal models and scarce pilot studies on humans, FMT seems to be a promising treatment option that could reverse intestinal dysbiosis and thereby influence the course of NAFLD.},
}

@article {pmid40298931,
year = {2025},
author = {Gao, X and Fu, N and Ben, Q and Bu, X},
title = {A Meta-Analysis of the Effects of Gut Microbiota-Based Interventions on Gastrointestinal and Behavioral Symptoms in Children With Autism Spectrum Disorder.},
journal = {Nutrition reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/nutrit/nuaf050},
pmid = {40298931},
issn = {1753-4887},
abstract = {CONTEXT: Despite an increasing body of research showing gut microbiota-based interventions can improve gastrointestinal (GI) symptoms and behavioral symptoms in both humans and animals, there are still disagreements about its impact on autism spectrum disorder (ASD) in children.

OBJECTIVE: The goal of this systematic review and meta-analysis was to fully investigate the effects of gut microbiota-based interventions (eg, fecal microbiota transplantation, probiotics, prebiotics) on GI and behavioral symptoms in children with ASD.

DATA SOURCES: The PubMed, Web of Science, the Cochrane Library, China National Knowledge Infrastructure, and Scopus databases were searched from inception to August 25, 2024.

DATA EXTRACTION: Data were extracted by 2 reviewers independently, and discrepancies in authors' judgments were resolved by discussion or consulting a third author.

DATA ANALYSIS: The scale score of GI and behavioral symptoms before and after the intervention was extracted from included trials to evaluate the therapeutic effects of gut microbiota-based therapy in children with autism.

RESULTS: A total of 5722 records were identified, of which 13 included in narrative synthesis and 8 studies included a meta-analysis. The nonsignificant overall effect size of gut microbiota-based intervention on GI symptoms (standardized mean difference [SMD] = -0.34 [95% CI, -0.76 to 0.07]; P = .11) and behavioral symptoms (SMD = -0.18 [95% CI, -0.37 to 0.02]; P = .08) was observed. Nevertheless, we observed a significant effect size on behavioral symptoms in the subgroup of the intervention duration (SMD = -0.26 [95% CI, -0.49 to -0.03]; P = .02).

CONCLUSIONS: In children with autism, the proof supporting the validity of gut microbiota-based intervention on GI and behavioral symptoms should be interpreted cautiously. More randomized controlled trials with rigorous methodological quality are required to precisely confirm the curative benefits of gut microbiota-based interventions on GI and behavioral symptoms in children with autism.

PROSPERO registration no. CRD42024583213.},
}

@article {pmid40298495,
year = {2025},
author = {Cusumano, G and Flores, GA and Venanzoni, R and Angelini, P},
title = {The Impact of Antibiotic Therapy on Intestinal Microbiota: Dysbiosis, Antibiotic Resistance, and Restoration Strategies.},
journal = {Antibiotics (Basel, Switzerland)},
volume = {14},
number = {4},
pages = {},
pmid = {40298495},
issn = {2079-6382},
abstract = {The human gut microbiota-an intricate and dynamic ecosystem-plays a pivotal role in metabolic regulation, immune modulation, and the maintenance of intestinal barrier integrity. Although antibiotic therapy is indispensable for managing bacterial infections, it profoundly disrupts gut microbial communities. Such dysbiosis is typified by diminished diversity and shifts in community structure, especially among beneficial bacterial genera (e.g., Bifidobacterium and Eubacterium), and fosters antibiotic-resistant strains and the horizontal transfer of resistance genes. These alterations compromise colonization resistance, increase intestinal permeability, and amplify susceptibility to opportunistic pathogens like Clostridioides difficile. Beyond gastrointestinal disorders, emerging evidence associates dysbiosis with systemic conditions, including chronic inflammation, metabolic syndrome, and neurodegenerative diseases, underscoring the relevance of the microbiota-gut-brain axis. The recovery of pre-existing gut communities post-antibiotic therapy is highly variable, influenced by drug spectrum, dosage, and treatment duration. Innovative interventions-such as fecal microbiota transplantation (FMT), probiotics, synbiotics, and precision microbiome therapeutics-have shown promise in counteracting dysbiosis and mitigating its adverse effects. These therapies align closely with antibiotic stewardship programs aimed at minimizing unnecessary antibiotic use to preserve microbial diversity and curtail the spread of multidrug-resistant organisms. This review emphasizes the pressing need for microbiota-centered strategies to optimize antibiotic administration, promote long-term health resilience, and alleviate the disease burden associated with antibiotic-induced dysbiosis.},
}

@article {pmid40297591,
year = {2025},
author = {Pei, X and Liu, L and Han, Y},
title = {Advances in human microbiome and prostate cancer research.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1576679},
pmid = {40297591},
issn = {1664-3224},
mesh = {Humans ; *Prostatic Neoplasms/microbiology/therapy/immunology/metabolism/etiology ; Male ; *Microbiota ; *Gastrointestinal Microbiome ; Tumor Microenvironment/immunology ; Animals ; },
abstract = {Prostate cancer (PCa) is the second most common malignant tumor in men worldwide, and its metastatic and heterogeneous nature makes it significantly more difficult to treat. Recent studies have revealed the critical role of microbiota in PCa occurrence, progression, and treatment. Accumulating evidence from 16S rRNA and metagenomic sequencing suggests the presence of specific microbiota in prostate tissues and macrogenomics techniques: cancerous tissues are enriched with pro-inflammatory genera (e.g., Fusobacterium, Propionibacterium acnes), whereas commensal bacteria (e.g., Pseudomonas) are more common in paracancerous tissues. The microbiota drive tumor progression through activation of the NF-κB/STAT3 pathway to induce chronic inflammation, modulation of the immune microenvironment (e.g., Treg/Th17 imbalance and M2-type macrophage polarization), and metabolite (e.g., LPS, short-chain fatty acids)-mediated hormonal and epigenetic regulation. In terms of clinical translation, urinary microbiota characterization combined with metabolomics analysis may enhance diagnostic specificity, while gut flora modulation (e.g., probiotic interventions or fecal transplants) may improve resistance to androgen deprivation therapy. Current challenges include sequencing accuracy of low-biomass samples, limitations of causal mechanism validation models, and large cohort heterogeneity. In the future, it will be necessary to integrate multi-omics technologies to explore the bidirectional regulation of the "gut-prostate axis" and develop personalized therapeutic strategies targeting microorganisms. In this paper, we systematically review the interactions between microbiota and PCa and their clinical potentials to provide a theoretical basis for precision diagnosis and treatment.},
}

Humans
*Prostatic Neoplasms/microbiology/therapy/immunology/metabolism/etiology
Male
*Microbiota
*Gastrointestinal Microbiome
Tumor Microenvironment/immunology
Animals

@article {pmid40297203,
year = {2025},
author = {Nguyen, JDK and Yohannes, KG and Setiady, I and Phillips, EC and Hays, RA and Behm, BW and Warren, CA and Shin, JH},
title = {Factors associated with failure of fecal microbiota transplant for recurrent Clostridioides difficile infection.},
journal = {Therapeutic advances in gastroenterology},
volume = {18},
number = {},
pages = {17562848251334517},
pmid = {40297203},
issn = {1756-283X},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) has emerged as a prevalent and recurrent antibiotic-associated infection. Fecal microbiota transplantation (FMT) is the most effective treatment for recurrent CDI (rCDI). Despite high success rates, FMT is ineffective in 5%-20% of cases. Factors associated with failure have not been clearly defined.

OBJECTIVES: In this study, we seek to identify factors predictive of FMT failure.

DESIGN: Retrospective cohort study.

METHODS: A retrospective chart review was conducted on adult patients who were screened at the Complicated C. difficile Clinic at the University of Virginia Health System and received FMT for rCDI between 2013 and 2022. The primary outcome was failure of FMT, defined as either rCDI or all-cause death within 1 year.

RESULTS: In total, 240 patients underwent FMT: 70.4% were female, the median age was 68, and the median episode of CDI was 4. A total of 24.6% experienced failure within 1 year (18.3% had rCDI and 7.1% died). Age 70 or older (odds ratio (OR) = 2.66 (1.29-5.67)), ⩾4 episodes of CDI (OR = 3.13 (1.47-7.09)), and diabetes mellitus (OR = 2.82 (1.25-6.50)) were associated with failure on multivariate analysis.

CONCLUSION: Our study shows that FMT remains an effective treatment for rCDI. We highlight several factors associated with FMT failure, such as older age, ⩾4 episodes of CDI, and diabetes mellitus, and the need for additional research to clearly define causality.},
}

@article {pmid40296251,
year = {2025},
author = {Zheng, H and Chen, Y and Lu, S and Liu, Z and Ma, Y and Zhang, C and Zhang, Y and Zhang, J and Liu, C and Chu, M and Pei, F and Liu, S and Duan, L},
title = {Mechanosensory Piezo2 regulated by gut microbiota participates in the development of visceral hypersensitivity and intestinal dysmotility.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2497399},
pmid = {40296251},
issn = {1949-0984},
mesh = {*Gastrointestinal Microbiome/physiology ; Animals ; Humans ; Mice ; *Irritable Bowel Syndrome/microbiology/physiopathology/metabolism/therapy ; *Ion Channels/metabolism/genetics ; Male ; Female ; Fecal Microbiota Transplantation ; *Gastrointestinal Motility ; Adult ; Middle Aged ; Colon/metabolism ; Mice, Inbred C57BL ; Feces/microbiology ; Fusobacterium/physiology ; Dysbiosis/microbiology ; Disease Models, Animal ; Ganglia, Spinal/metabolism ; Akkermansia ; },
abstract = {The gut microbiota plays a crucial role in the manifestation of intestinal dysfunction associated with irritable bowel syndrome (IBS). The mechanosensory Piezo2 has been implicated in the regulation of intestinal function. However, it remains unclear whether Piezo2 is modulated by the gut microbiota, thus contributing to the development of visceral hypersensitivity and gut dysmotility. The study enrolled patients with diarrhea-predominant IBS (IBS-D) alongside healthy controls (HC). Questionnaires, rectal barostat test, and colonoscopy with mucosal biopsy were conducted. Fecal microbiota transplantation (FMT) was performed using samples from HC or IBS-D patients, and interventions with Akkermansia muciniphila or Fusobacterium varium were carried out on colon- or dorsal root ganglion (DRG)- Piezo2 knockdown pseudo-germ-free mice. Visceral sensitivity and intestinal motility were assessed. Piezo2 levels were detected using western blot and immunofluorescence. Fecal 16S rRNA sequencing and cecum untargeted metabolomics analysis, followed by molecular docking predictions of Piezo2, were also performed. The ratio of Piezo2[+]/5-HT[+] cells was lower in IBS-D patients, positively correlated with visceral sensation and intestinal dysbiosis. The mice that received FMT from IBS-D patients exhibited colonic dysmotility and visceral hypersensitivity, along with elevated Piezo2 protein levels in the colon and DRG. Knockdown of Piezo2 in the colon or DRG ameliorated the FMT-induced colonic dysmotility and visceral hypersensitivity. Fecal 16S rRNA sequencing revealed distinct microbiota composition. Notably, Fusobacterium varium, but not Akkermansia muciniphila, induced gut dysmotility and visceral hypersensitivity, effects that could be alleviated by colon or DRG Piezo2 knockdown. Additionally, Fusobacterium varium lead to increased Piezo2 protein levels, as well as elevated levels of indole-3-acetic acid and indole-3-acrylic acid, which were predicted to bind to Piezo2, causing disturbances. Piezo2 can be regulated by gut microbiota and involved in visceral hypersensitivity and colonic dysmotility, with Fusobacterium varium playing a crucial role.},
}

*Gastrointestinal Microbiome/physiology
Animals
Humans
Mice
*Irritable Bowel Syndrome/microbiology/physiopathology/metabolism/therapy
*Ion Channels/metabolism/genetics
Male
Female
Fecal Microbiota Transplantation
*Gastrointestinal Motility
Adult
Middle Aged
Colon/metabolism
Mice, Inbred C57BL
Feces/microbiology
Fusobacterium/physiology
Dysbiosis/microbiology
Disease Models, Animal
Ganglia, Spinal/metabolism
Akkermansia

@article {pmid40295906,
year = {2025},
author = {Ahmadi, A and Shokoohizadeh, L and Sheikhesmaili, F and Mirzaei, MK and Mohammadi, A and Nikkhoo, B and Khodaei, H and Alikhani, MY and Yousefimashouf, R},
title = {Gut microbiomes and treatment-resistant ulcerative colitis: a case-control study using qPCR.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {254},
pmid = {40295906},
issn = {1471-2180},
mesh = {Humans ; *Colitis, Ulcerative/microbiology/drug therapy ; Case-Control Studies ; *Gastrointestinal Microbiome/genetics ; Male ; Adult ; Female ; Feces/microbiology ; Middle Aged ; Real-Time Polymerase Chain Reaction ; *Bacteria/genetics/classification/isolation & purification ; Young Adult ; },
abstract = {BACKGROUND: The gut microbiome has been identified as a pivotal factor in ulcerative colitis (UC), given its role as the main reservoir of microbes in the body. This community of microorganisms, present in variable concentrations in the digestive tract, makes a wide range of beneficial roles for the host. However, the role of the gut microbiome in patients with refractory UC is still significant, so this study aimed to further investigate the role of these bacteria in patients with refractory UC.

METHODS: This case-control study was conducted on stool samples from four distinct groups: the first group comprised new patients diagnosed with ulcerative colitis (all of them had responded to treatment after follow-up) (N = 24); the second group consisted of patients with treatment-resistant ulcerative colitis (N = 23); the third group included first-degree relatives of group 1 patients (N = 24); and the fourth group consisted of first-degree relatives of group 2 patients (N = 23). The research tools employed in this study included a questionnaire, quantitative real-time PCR (qPCR) test, and culture on stool samples.

RESULT: The mean age of patients in groups 1 and 2 was 45.88 ± 18.51 and 41.30 ± 13.01 years, while the mean age of controls in groups 3 and 4 was 37.29 ± 9.62 and 40.96 ± 13.01 years, respectively. Stool culture results for pathogenic bacteria were negative in all four groups. The of history of consuming dairy products containing probiotics was highest in Group 1, with 22 (91.67%) subjects, while the lowest was observed in Group 3, with 16 (66.67%). The highest history of self-administered antibiotic use was observed in Group 2, with 13 cases (56.52%), while the lowest was noted in Group 3, with 4 cases (16.67%). The findings indicated a statistically significant relationship (P < 0.05) between Groups 2 and 4 with respect to the E. coli and Bifidobacterium ssp. microbial population. Additionally, a significant relationship was identified between the Lactobacillus ssp., Bifidobacterium ssp., and Bacteroides ssp. microbial community between groups 1 and 2 (P < 0.05).

CONCLUSION: The findings of this study demonstrated that several intestinal microbiomes have a substantial impact on the management of ulcerative colitis. The results of this study suggest that by comparing the gut microbiome of treatment-resistant and individuals newly diagnosed with ulcerative colitis, we can gain a better understanding of microbiome differences that may influence treatment outcomes. The results of this study may also lead to the identification of new therapeutic strategies that are based on regulating the gut microbiome. These strategies could include the use of fecal microbiome transplantation (FMT), probiotics, prebiotics, or specific bacteria-based therapies.},
}

Humans
*Colitis, Ulcerative/microbiology/drug therapy
Case-Control Studies
*Gastrointestinal Microbiome/genetics
Male
Adult
Female
Feces/microbiology
Middle Aged
Real-Time Polymerase Chain Reaction
*Bacteria/genetics/classification/isolation & purification
Young Adult

@article {pmid40295607,
year = {2025},
author = {Mohammadi, M and Rahimi, K and Rezaie, A and Tabandeh, MR},
title = {The role of fecal microbiota transplantation on the NLRP3-Caspase 1 pathway and anxiety like behavioral in the ulcerative colitis model in rats.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {14831},
pmid = {40295607},
issn = {2045-2322},
mesh = {Animals ; *Caspase 1/metabolism/genetics ; *Fecal Microbiota Transplantation/methods ; *NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/genetics ; *Anxiety/therapy/metabolism/etiology ; Rats ; Signal Transduction ; Male ; *Colitis, Ulcerative/therapy/chemically induced/metabolism ; Disease Models, Animal ; Hippocampus/metabolism ; Behavior, Animal ; Colon/metabolism/pathology ; Acetic Acid ; Interleukin-18/metabolism ; },
abstract = {The purpose of this study was to investigate the function of the NLRP3-Caspase 1 signaling pathway in the colon during fecal microbiota transplantation (FMT) in colitis induced by acetic acid. Additionally, the study aimed to determine the impact of FMT on anxiety behaviors by analyzing the function of the NLRP3-Caspase 1 signaling pathway in the hippocampus. A total of twenty-four rats were selected randomly for the study and divided into two groups, a control group, and an acid acetic-induced colitis group. The acid acetic-induced colitis group further consisted of three subgroups: untreated acid acetic-induced colitis group, mesalazine 0.3 gr/kg group, and FMT group. After 6 days, the colon was evaluated for macroscopic and microscopic damage, and the signaling pathway NLRP3-Caspase1-related genes in the colon and hippocampus were analyzed. Additionally, anxiety-related behaviors of the rats were observed. FMT decreased colonic mRNA expression levels of NLRP3, NF-кB, and Caspase1 and pro-inflammatory cytokines (IL-1β and IL-18). Also, FMT reduced the expression of NLRP3, NF-κB, and Caspase1 protein levels as well as pro-inflammatory cytokines IL-1β and IL-18 in the hippocampus, resulting in a reduction of anxiety behaviors in the open field and elevated plus maze tests in the colitis model. FMT may improve acetic acid-induced colitis by regulating the NLRP3-Caspase1 signaling pathway in the colon. It also reduced colitis-induced anxiety behavior by regulating the expression of proteins related to the NLRP3-Caspase 1 pathway in the hippocampus.},
}

Animals
*Caspase 1/metabolism/genetics
*Fecal Microbiota Transplantation/methods
*NLR Family, Pyrin Domain-Containing 3 Protein/metabolism/genetics
*Anxiety/therapy/metabolism/etiology
Rats
Signal Transduction
Male
*Colitis, Ulcerative/therapy/chemically induced/metabolism
Disease Models, Animal
Hippocampus/metabolism
Behavior, Animal
Colon/metabolism/pathology
Acetic Acid
Interleukin-18/metabolism

@article {pmid40295196,
year = {2025},
author = {Sun, J and Shi, L and Xu, F and Sun, H and Liu, Y and Sun, J and Zhou, Q},
title = {Naringenin Inhibits Colorectal Cancer associated with a High-Fat Diet through Modulation of Gut Microbiota and IL-6/STAT3 Pathway.},
journal = {Journal of microbiology and biotechnology},
volume = {35},
number = {},
pages = {e2412029},
doi = {10.4014/jmb.2412.12029},
pmid = {40295196},
issn = {1738-8872},
mesh = {*Flavanones/pharmacology ; *Gastrointestinal Microbiome/drug effects ; *Colorectal Neoplasms/drug therapy/microbiology/prevention & control/etiology/metabolism ; *STAT3 Transcription Factor/metabolism ; *Diet, High-Fat/adverse effects ; Animals ; *Interleukin-6/metabolism ; Mice ; Male ; Signal Transduction/drug effects ; Fecal Microbiota Transplantation ; Humans ; Mice, Inbred C57BL ; Bacteria/drug effects/classification/genetics ; },
abstract = {Colorectal cancer (CRC) is a worldwide health issue. It causes illness and death in millions of people each year. A positive correlation has been observed between the intake of dietary fat and the development of CRC. The composition of gut microbiota exhibits a significant correlation with pathophysiologic processes in intestine. Clinical treatment remains inadequate due to the complex pathogenic mechanisms of CRC triggered by a high-fat diet (HFD). Naringenin, a flavonoid from grapefruit, has anti-cancer activity. Our findings suggest that naringenin enhances gut microbiota diversity by increasing the abundance of beneficial bacterial species while reducing opportunistic pathogenic bacteria. The fecal microbiota transplantation assay (FMT) demonstrated that the anti-HFD-CRC activity of naringenin depended on the gut microbiota. Furthermore, naringenin antagonized the IL-6/STAT3 pathway. These results suggest that naringenin may be a potential treatment for HFD-CRC.},
}

*Flavanones/pharmacology
*Gastrointestinal Microbiome/drug effects
*Colorectal Neoplasms/drug therapy/microbiology/prevention & control/etiology/metabolism
*STAT3 Transcription Factor/metabolism
*Diet, High-Fat/adverse effects
Animals
*Interleukin-6/metabolism
Mice
Male
Signal Transduction/drug effects
Fecal Microbiota Transplantation
Humans
Mice, Inbred C57BL
Bacteria/drug effects/classification/genetics

@article {pmid40294087,
year = {2025},
author = {Duarte, L and Magne, F and Gotteland, M},
title = {Gut microbiota in patients with metabolic, dysfunction-associated steatotic liver disease.},
journal = {Current opinion in clinical nutrition and metabolic care},
volume = {},
number = {},
pages = {},
pmid = {40294087},
issn = {1473-6519},
abstract = {PURPOSE OF REVIEW: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a highly prevalent condition that can progress to fibrosis, steatohepatitis, and hepatocellular carcinoma. This review examines recent advances concerning the role of gut microbiota in MASLD and microbiota-focused interventions to positively impact disease outcome.

RECENT FINDINGS: Dysbiotic microbiota and a compromised gut barrier facilitate the translocation of microbial-associated molecular patterns and harmful metabolites into the portal circulation and liver, where they exacerbate inflammatory and fibrogenic processes. Conversely, other bacterial metabolites have protective effects in the liver. Therefore, microbiota homeostasis is essential for maintaining liver health.

SUMMARY: Levels of harmful bacterial metabolites including ethanol, NH3, trimethylamine-L-oxide, 2-oleylglycerol, and litocholic acid are often increased in patients with MASLD. Conversely, short-chain fatty acids, indole derivatives, histidine, and the acids taurodeoxycholic, 3-succinylcholic, and hyodeoxycholic are decreased. The main aim of current interventions/treatments is to reduce harmful metabolites and increase beneficial ones. These interventions include drugs (pemafibrate, metformin, obeticholic acid), natural compounds (silymarin, lupeol, dietary fiber, peptides), exogenous bacteria (probiotics, gut symbionts), special diets (Mediterranean diet, time-restricted feeding), as well as microbiota transplantation, and phage therapy. Most improve gut permeability, liver inflammation, and fibrosis through microbiota regulation, and are promising alternatives for MASLFD management. However, most results come from animal studies, while clinical trials in MASLD patients are lacking. Further research is therefore needed in this area.},
}

@article {pmid40292220,
year = {2025},
author = {Ma, P and Wang, R and Chen, H and Zheng, J and Yang, W and Meng, B and Liu, Y and Lu, Y and Zhao, J and Gao, H},
title = {Fecal microbiota transplantation alleviates lipopolysaccharide-induced osteoporosis by modulating gut microbiota and long non-coding RNA TUG1 expression.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1535666},
pmid = {40292220},
issn = {2235-2988},
mesh = {Animals ; *RNA, Long Noncoding/genetics/metabolism ; *Gastrointestinal Microbiome/genetics ; *Osteoporosis/therapy/chemically induced/microbiology ; *Fecal Microbiota Transplantation/methods ; *Lipopolysaccharides/adverse effects ; Mice, Inbred C57BL ; Mice ; Disease Models, Animal ; RNA, Ribosomal, 16S/genetics ; Femur/pathology/diagnostic imaging ; Core Binding Factor Alpha 1 Subunit/metabolism ; X-Ray Microtomography ; Male ; },
abstract = {PURPOSE: To study whether fecal microbiota transplantation (FMT) can alleviate lipopolysaccharide (LPS)-induced osteoporosis (OP) by regulating the composition and abundance of gut microbiota and the expression level of long non-coding RNA (lncRNA) TUG1.

METHODS: Twenty C57BL/6 mice were selected. Two mice were randomly designated as fecal donors, while the remaining mice were randomly divided into control group, LPS group, and LPS + FMT group. Each group consisted of 6 mice. The mice in the LPS and LPS + FMT groups were intraperitoneally injected with LPS to establish the OP model, and the mice in the LPS + FMT group were treated with donor feces by gavage. Micro-CT was used to scan the femur specimens of mice, and the bone structural parameters of the control and LPS groups were compared to verify the effectiveness of the OP model. HE staining was used to compare the microstructure of femurs in the 3 groups. 16S rRNA gene sequencing was used to analyze the composition and abundance of gut microbiota in mice. Immunofluorescence staining was used to compare the expression levels of Runt-related transcription factor 2 (RUNX2) in the femur of the 3 groups. Real-time quantitative reverse transcription PCR (qRT-PCR) was used to compare the expression levels of lncRNA TUG1 in the intestines and serum of mice in the 3 groups.

RESULTS: Micro-CT showed that compared with the control group, the mice in the LPS group had more bone loss. The bone mineral density, trabecular number, and trabecular thickness of the control group was higher, and the trabecular separation was smaller. The models were validated effectively. HE staining showed that compared with the control group, the bone trabeculae in the LPS group were thinner and sparse, while that in the LPS + FMT group were dense and clear. The 16s rRNA sequencing showed that the abundance of Bacteroides and Lactobacillus in LPS+FMT group was significantly higher than that in LPS group. Immunofluorescence staining showed that the RUNX2 level in the control group and LPS + FMT group was similar, and both were higher than that in the LPS group. The qRT-PCR results showed that the TUG1 mRNA level in the control group and LPS + FMT group was similar and significantly higher than that in the LPS group.

CONCLUSION: FMT can enhance osteoblast levels and improve bone structure by modulating the abundance of gut microbiota in OP mice (such as increasing Bacteroides and Lactobacillus populations) and promoting the expression of lncRNA TUG1, thereby alleviating LPS-induced OP.},
}

Animals
*RNA, Long Noncoding/genetics/metabolism
*Gastrointestinal Microbiome/genetics
*Osteoporosis/therapy/chemically induced/microbiology
*Fecal Microbiota Transplantation/methods
*Lipopolysaccharides/adverse effects
Mice, Inbred C57BL
Mice
Disease Models, Animal
RNA, Ribosomal, 16S/genetics
Femur/pathology/diagnostic imaging
Core Binding Factor Alpha 1 Subunit/metabolism
X-Ray Microtomography
Male

@article {pmid40292216,
year = {2025},
author = {Bu, F and Chen, K and Chen, S and Jiang, Y},
title = {Gut microbiota and intestinal immunity interaction in ulcerative colitis and its application in treatment.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1565082},
pmid = {40292216},
issn = {2235-2988},
mesh = {Humans ; *Colitis, Ulcerative/immunology/therapy/microbiology ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; *Immunity, Mucosal ; Intestinal Mucosa/immunology/microbiology ; Animals ; },
abstract = {Ulcerative colitis (UC) is a chronic, non-specific inflammatory bowel disease characterized by inflammation and injury of the colonic mucosa, exhibiting an increasing global incidence. Although research into UC pathogenesis is ongoing, the precise mechanisms remain to be fully elucidated. Studies indicate that UC development results from a complex interplay of factors, including genetic predisposition, environmental exposures, gut microbial dysbiosis, and immune dysregulation. Specifically, UC pathogenesis involves aberrant immune responses triggered by interactions between the host and gut microbiota. A complex, dynamic relationship exists between the microbial community and the host immune system throughout UC pathogenesis. Accumulating evidence suggests that changes in microbiota composition significantly impact gut immunity. This review will examine the intricate balance between the gut microbiota and mucosal immunity in UC progression and discuss potential therapeutic applications, providing a reference for further clinical treatment of this patient population.},
}

Humans
*Colitis, Ulcerative/immunology/therapy/microbiology
*Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
*Immunity, Mucosal
Intestinal Mucosa/immunology/microbiology
Animals

@article {pmid40291934,
year = {2025},
author = {Mattar, L and Thalib, HI and Alnuwaimi, M and Alsaadi, H and Allouji, HA and Alyafei, J and Alshowiman, L and Alsobyani, N and Hassan, FES},
title = {Challenges of concurrent HIV infection in the course and management of Crohn's disease.},
journal = {Journal of medicine and life},
volume = {18},
number = {3},
pages = {171-178},
pmid = {40291934},
issn = {1844-3117},
mesh = {Humans ; *Crohn Disease/therapy/complications/immunology ; *HIV Infections/complications/immunology ; Disease Progression ; Probiotics/therapeutic use ; Gastrointestinal Microbiome ; },
abstract = {Crohn's disease (CD) is a chronic transmural bowel inflammation with a multifactorial etiology involving genetic predisposition and immune dysregulation in response to environmental triggers. In patients with human immunodeficiency virus (HIV), an already compromised immune system further complicates the progression and management of CD, creating unique therapeutic challenges. Probiotics have recently gained attention as a potential therapeutic option for CD, especially due to their role in modulating the gut microbiota. However, their effectiveness in patients with HIV, especially in enhancing and maintaining remissions, remains underexplored. This review aimed to examine how HIV infection influences the course of inflammatory bowel disease (IBD) and its impact on CD management strategies. A systematic literature search was conducted using Google Scholar, PubMed, Springer, and Web of Science to identify studies on patients with HIV and CD. HIV infection significantly alters the progression and management of CD due to its impact on the immune system. The immunosuppressed state of patients with HIV can complicate both the diagnosis and treatment of CD, often requiring adjustments in therapeutic approaches, necessitating a careful, tailored approach.},
}

Humans
*Crohn Disease/therapy/complications/immunology
*HIV Infections/complications/immunology
Disease Progression
Probiotics/therapeutic use
Gastrointestinal Microbiome

@article {pmid40289872,
year = {2025},
author = {Gao, L and Zhang, Y and Hu, Z and Chen, S and Wang, Q and Zeng, Y and Yin, H and Zhao, J and Zhan, Y and Gao, C and Xin, Y and Chen, B and van der Veen, S and Zhao, M and Fang, D and Lu, Q},
title = {Microbiota-Derived Inosine Suppresses Systemic Autoimmunity via Restriction of B Cell Differentiation and Migration.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2409837},
doi = {10.1002/advs.202409837},
pmid = {40289872},
issn = {2198-3844},
support = {2022YFC3601800//National Key R&D Program of China/ ; 32141004//Special Program of National Natural Science Foundation of China/ ; 2021-I2M-1-059//CAMS Innovation Fund for Medical Sciences (CIFMS) No/ ; 2024-I2M-ZH-020//CAMS Innovation Fund for Medical Sciences (CIFMS) No/ ; 2020-RC320-003//Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences/ ; NO.82430102//Key Program of the National Natural Science Foundation of China/ ; 82404154//National Natural Science Foundation of China/ ; },
abstract = {The role of gut microbiota dysbiosis in systemic lupus erythematosus (SLE) pathogenesis remains elusive. Here, it is shown that fecal microbiota transplantation (FMT) from healthy mice to lupus mice ameliorates lupus-like symptoms. Microbiota reconstitution effectively reduces systemic class switch recombination (CSR) and elevates immunoglobulin heavy chain (IGH) naïve isotype. Microbiota profiling reveals an enrichment of Lactobacillus johnsonii post-FMT, with a significant correlation to purine metabolites. Importantly, the L. johnsonii-derived inosine, an intermediate metabolite in purine metabolism, effectively alleviates lupus pathogenesis in mice. Inosine inhibits B cell differentiation and reduces renal B cell infiltration to protect mice from lupus. At the molecular level, inosine reprograms B cells through the eDDxtracellular signal-regulated kinase (ERK)-hypoxia-inducible factor-1alpha (HIF-1α) signaling pathway. Therefore, this study highlights the discovery of a novel microbial metabolite modulating autoimmunity and suggests its potential for innovative microbiome-based therapeutic approaches.},
}

@article {pmid40289678,
year = {2025},
author = {Xu, Z and Li, L and Cheng, L and Gu, Z and Hong, Y},
title = {Maternal obesity and offspring metabolism: revisiting dietary interventions.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d4fo06233g},
pmid = {40289678},
issn = {2042-650X},
abstract = {Maternal obesity increases the risk of metabolic disorders in offspring. Understanding the mechanisms underlying the transgenerational transmission of metabolic diseases is important for the metabolic health of future generations. More research is needed to elucidate the mechanisms underlying the associated risks and their clinical implications because of the inherently complex nature of transgenerational metabolic disease transmission. Diet is a well-recognized risk factor for the development of obesity and other metabolic diseases, and rational dietary interventions are potential therapeutic strategies for their prevention. Despite extensive research on the physiological effects of diet on health and its associated mechanisms, little work has been devoted to understanding the effects of early-life dietary interventions on the metabolic health of offspring. In addition, existing dietary interventions are insufficient to meet clinical needs. Here, we discuss the literature on the effects of maternal obesity on the metabolic health of offspring, focusing on the mechanisms underlying the transgenerational transmission of metabolic diseases. We revisit current dietary interventions and describe their strengths and weaknesses in ameliorating maternal obesity-induced metabolism-related disorders in offspring. We also propose innovative strategies, such as the use of precision nutrition and fecal microbiota transplantation, which may limit the vicious cycle of intergenerational metabolic disease transmission.},
}

@article {pmid40289444,
year = {2025},
author = {Grimstad, T and Carlsen, A and Kvaløy, JT and Bolstad, N and Warren, DJ and Aabakken, L and Lundin, KEA and Karlsen, L and Steinsbø, Ø and Omdal, R},
title = {Fatigue in Inflammatory Bowel Disease: No Effect of Serum Concentrations of Infliximab, Adalimumab or Anti-Drug Antibodies During Maintenance Therapy.},
journal = {Scandinavian journal of immunology},
volume = {101},
number = {5},
pages = {e70029},
doi = {10.1111/sji.70029},
pmid = {40289444},
issn = {1365-3083},
mesh = {Adult ; Aged ; Female ; Humans ; Male ; Middle Aged ; *Adalimumab/therapeutic use/blood/immunology ; Antibodies/blood ; C-Reactive Protein/metabolism ; *Colitis, Ulcerative/drug therapy ; *Crohn Disease/drug therapy ; Cross-Sectional Studies ; *Fatigue/drug therapy/etiology/blood ; Feces/chemistry ; *Inflammatory Bowel Diseases/drug therapy/complications ; *Infliximab/blood/therapeutic use/immunology ; Leukocyte L1 Antigen Complex/metabolism ; Severity of Illness Index ; },
abstract = {Several studies have shown that infliximab and adalimumab ameliorate fatigue in inflammatory bowel disease. We investigated whether serum levels of these agents above or below a selected threshold influence fatigue severity. In this cross-sectional study, we measured serum concentrations (s-) of infliximab and adalimumab and corresponding anti-drug antibody levels. Therapeutic thresholds were defined as s-infliximab ≥ 5.0 mg/L and s-adalimumab ≥ 7.0 mg/L. Disease activity was assessed using the Harvey-Bradshaw Index for Crohn's disease, Partial Mayo Score for ulcerative colitis, and C-reactive protein (CRP) and faecal calprotectin levels for both conditions. Fatigue was assessed with the Fatigue Visual Analog Scale and Fatigue Severity Scale, and depression was evaluated with the Hospital Anxiety and Depression Scale, Depression subscale. Of 171 included patients (112 with Crohn's disease, 59 with ulcerative colitis), 66 (38.6%) were on infliximab and 105 (61.4%) were on adalimumab. Scores on the two fatigue scales were similar for serum values above versus below therapeutic thresholds for both drugs and did not differ with versus without anti-drug antibodies against either drug. CRP was numerically higher with infliximab levels below versus above the threshold (p = 0.06), whereas both CRP and faecal calprotectin were increased with adalimumab below versus above the threshold (p = 0.022, p = 0.0242). In patients with inflammatory bowel disease on maintenance therapy, s-infliximab and s-adalimumab levels below or above therapeutic thresholds or the presence of anti-drug antibodies did not affect fatigue severity. Trial Registration: ClinicalTrials.gov identifier: NCT02134054.},
}

Adult
Aged
Female
Humans
Male
Middle Aged
*Adalimumab/therapeutic use/blood/immunology
Antibodies/blood
C-Reactive Protein/metabolism
*Colitis, Ulcerative/drug therapy
*Crohn Disease/drug therapy
Cross-Sectional Studies
*Fatigue/drug therapy/etiology/blood
Feces/chemistry
*Inflammatory Bowel Diseases/drug therapy/complications
*Infliximab/blood/therapeutic use/immunology
Leukocyte L1 Antigen Complex/metabolism
Severity of Illness Index

@article {pmid40288637,
year = {2025},
author = {La Rosa, F and Guzzardi, MA and Pardo-Tendero, M and Barone, M and Ruocco, C and Conti, G and Panetta, D and Riabitch, D and Bernardi, S and Giorgetti, A and Campani, D and Monleon, D and Nisoli, E and Brigidi, P and Iozzo, P},
title = {Effects of Children's microbiota on adipose and intestinal development in sex-matched mice persist into adulthood following a single fecal microbiota transplantation.},
journal = {Molecular metabolism},
volume = {},
number = {},
pages = {102157},
doi = {10.1016/j.molmet.2025.102157},
pmid = {40288637},
issn = {2212-8778},
abstract = {BACKGROUND: The global prevalence of obesity and type 2 diabetes, particularly among children, is rising, yet the long-term impacts of early-life fecal microbiota transplantation (FMT) on metabolic health remain poorly understood.

OBJECTIVES: To investigate how early-life FMT from children to young, sex-matched mice influences metabolic outcomes and adipose tissue function in later, adult life.

METHODS: Germ-free mice were colonized with fecal microbiota from either lean children or children with obesity. The impacts on brown adipose tissue (BAT), white adipose tissue (WAT), glucose metabolism, and gut health were analyzed in male and female mice. Microbial communities and metabolite profiles were characterized using sequencing and metabolomics.

RESULTS: Male mice receiving FMT from obese donors exhibited marked BAT whitening and impaired amino acid and glucose metabolism. In contrast, female recipients developed hyperglycemia, accompanied by gut barrier dysfunction and WAT impairment. Distinct microbial and metabolite profiles were associated with these phenotypes: Collinsella and trimethylamine in females; and Paraprevotella, Collinsella, Lachnospiraceae NK4A136, Bacteroides, Coprobacillus, and multiple metabolites in males. These phenotypic effects persisted despite changes in host environment and diet.

CONCLUSIONS: Early-life FMT induced long-lasting effects on the metabolic landscape, profoundly affecting adipose tissue function and systemic glucose homeostasis in adulthood. Donor dietary habits correlated with the fecal microbial profiles observed in recipient mice. These findings highlight the critical need for identifying and leveraging beneficial exposures during early development to combat obesity and diabetes.},
}

@article {pmid40288317,
year = {2025},
author = {Banerjee, A and Mal, S and Roy, P and Chatterji, U},
title = {Regulating environmental arsenic-mediated gut-brain toxicity using chitosan-conjugated luteolin gold nanoparticles.},
journal = {Ecotoxicology and environmental safety},
volume = {297},
number = {},
pages = {118250},
doi = {10.1016/j.ecoenv.2025.118250},
pmid = {40288317},
issn = {1090-2414},
abstract = {Anxiety and depression are two major contributors to global disease burden. Amongst various causal factors, exposure to even low doses of environmental heavy metals, like arsenic, can induce anxiety and depression-like behaviour in mammals. Ingestion of arsenic, primarily through contaminated drinking water, severely disrupts the gut microbes, thereby inducing structural and functional abnormalities in the brain. Fecal microbiota transplantation (FMT) from arsenic-exposed mice to recipient healthy mice (As-FMT) enriched LPS-secreting Gram-negative bacteria and upregulated the expression of TLR4 in intestinal epithelial cells. Consequently, inflammation, oxidative stress and compromised barrier integrity in the gut facilitated LPS translocation into the bloodstream and promoted systemic inflammation. The secretomes eventually affected the brain by activating microglia, altering neurotransmitter levels and reducing the glucocorticoid receptor (GR) expression, contributing to appearance of pyknotic nuclei in dentate gyrus of hippocampus and emergence of anxiety- and depression-like behaviour. Luteolin, a flavonoid, devoid of any apparent side-effects, yet known for its anti-inflammatory and antioxidant properties, showed potential in alleviating the gut-brain toxic effects. However, its limited solubility and bioavailability pose challenges for its effectiveness, for which chitosan-conjugated luteolin gold nanoparticles (CH-LuAuNPs) were synthesized. Interestingly, where FMT from arsenic-treated mice to healthy mice showed deleterious effects in the transplanted mice, FMT from arsenic-treated mice co-administered with CH-LuAuNP attenuated As-FMT-mediated disruption of the gut-brain axis. This study highlighted the critical contribution of healthy gut microbiota in preserving neurobehavioural physiology, as well as underscored the potential therapeutic benefits of luteolin nanoparticles in ameliorating arsenic-induced gut dysbiosis and consequent mental disorders.},
}

@article {pmid40287572,
year = {2025},
author = {Zou, T and Tang, X and Wang, H and Shang, X and Liang, X and Ma, X},
title = {Nanocrystalline cellulose-geniposide complex enhances gut-brain axis modulation for depression treatment.},
journal = {Communications biology},
volume = {8},
number = {1},
pages = {667},
pmid = {40287572},
issn = {2399-3642},
mesh = {Animals ; *Cellulose/chemistry/pharmacology ; Mice ; *Depression/drug therapy ; *Iridoids/pharmacology/chemistry ; *Nanoparticles/chemistry ; Gastrointestinal Microbiome/drug effects ; *Antidepressive Agents/pharmacology ; Male ; Fecal Microbiota Transplantation ; *Brain/drug effects/metabolism ; Mice, Inbred C57BL ; *Brain-Gut Axis/drug effects ; Disease Models, Animal ; },
abstract = {Depression, a major global health issue, is closely associated with imbalances in gut microbiota and altered intestinal functions. This study investigates the antidepressant potential of a composite of Geniposide (GP) and Nanocrystalline Cellulose (NCC), focusing on its effects on the gut-brain axis. Utilizing network pharmacology, GP was identified as a key compound targeting the BCL2 gene in depression management. Experimental approaches, including a chronic unpredictable mild stress (CUMS) model in mice, cellular assays, and fecal microbiota transplantation (FMT), were used to evaluate the composite's effectiveness. Results indicate that GP activates the adenosine monophosphate-activated protein kinase (AMPK) pathway by upregulating BCL2, enhancing intestinal barrier integrity, and balancing gut flora. These mechanisms contribute to its positive effects on hippocampal function and depressive-like behaviors in mice, suggesting that the GP-NCC composite could be a promising avenue for developing depression therapies that target gut health.},
}

Animals
*Cellulose/chemistry/pharmacology
Mice
*Depression/drug therapy
*Iridoids/pharmacology/chemistry
*Nanoparticles/chemistry
Gastrointestinal Microbiome/drug effects
*Antidepressive Agents/pharmacology
Male
Fecal Microbiota Transplantation
*Brain/drug effects/metabolism
Mice, Inbred C57BL
*Brain-Gut Axis/drug effects
Disease Models, Animal