@article {pmid40255763,
year = {2025},
author = {Rathore, K and Shukla, N and Naik, S and Sambhav, K and Dange, K and Bhuyan, D and Imranul Haq, QM},
title = {The Bidirectional Relationship Between the Gut Microbiome and Mental Health: A Comprehensive Review.},
journal = {Cureus},
volume = {17},
number = {3},
pages = {e80810},
pmid = {40255763},
issn = {2168-8184},
abstract = {The gut microbiome plays a fundamental role in mental health, influencing mood, cognition, and emotional regulation through the gut-brain axis. This bidirectional communication system connects the gastrointestinal and CNS, facilitated by microbial metabolites, neurotransmitters, and immune interactions. Recent research highlights the association between gut dysbiosis and psychiatric disorders, including anxiety, depression, and stress-related conditions. Key findings indicate that altered microbial diversity, decreased short-chain fatty acid (SCFA) production, and increased neuroinflammation contribute to mental health disturbances. This paper explores the mechanism linking the gut microbiome to brain function, including microbial neurotransmitter synthesis, vagus nerve signaling, and hypothalamic-pituitary-adrenal (HPA) axis modulation. Additionally, it evaluates the potential of microbiome-targeted interventions, such as probiotics, prebiotics, dietary modifications, and fecal microbiota transplantation (FMT), in alleviating psychiatric symptoms. Microbiome sequencing and bioinformatics advances further support the development of personalized microbiome-based mental health interventions. Despite promising evidence, challenges such as inter-individual variability, methodological inconsistencies, and the need for longitudinal studies remain. Future research should focus on standardizing microbiome assessment techniques and optimizing therapeutic applications. Integrating precision psychiatry with microbiome-based diagnostics holds immense potential in transforming mental health treatment.},
}

@article {pmid40254304,
year = {2025},
author = {Fehily, SR and Wright, EK and Basnayake, C and Wilson-O'Brien, AL and Stanley, A and Marks, EP and Russell, EE and Hamilton, AL and Bryant, RV and Costello, SP and Kamm, MA},
title = {Faecal microbiota transplantation in Crohn's disease: an Australian randomised placebo-controlled trial protocol.},
journal = {BMJ open},
volume = {15},
number = {4},
pages = {e094714},
pmid = {40254304},
issn = {2044-6055},
mesh = {Humans ; *Crohn Disease/therapy ; *Fecal Microbiota Transplantation/methods ; Australia ; Randomized Controlled Trials as Topic ; Treatment Outcome ; Remission Induction ; Adult ; Male ; Gastrointestinal Microbiome ; Female ; Multicenter Studies as Topic ; },
abstract = {INTRODUCTION: The enteric microbiota drives inflammation in Crohn's disease. Yet, there are no placebo controlled trials evaluating the efficacy and safety of faecal microbiota transplantation (FMT) in inducing and maintaining remission in patients with active Crohn's disease. The Microbial Restoration (MIRO) study aims to establish this evidence.

METHODS AND ANALYSIS: At two specialist inflammatory bowel disease centres, 120 enrolled patients will have a 3-week period of diet optimisation (removal of ultra-processed foods) together with a 7-day course of antibiotics (to facilitate subsequent FMT engraftment). Patients will then be stratified to upper gut (for disease proximal to the splenic flexure) or lower gut (distal to the splenic flexure) disease. Patients will then be randomised in a 2:1 ratio to receive anaerobically prepared stool or placebo for 8 weeks either by gastroscopy, or colonoscopy and enemas. Clinical response at 8 weeks (Crohn's Disease Activity Index (CDAI) reduction ≥100 points or to <150 points) is the primary outcome measure. Non-responders to placebo and partial responders to FMT (CDAI decrease <100 but >70) receive FMT for weeks 8-16.Patients achieving clinical response from FMT after 8 or 16 weeks will be randomised in a 1:1 ratio to either a 44-week maintenance phase of FMT or placebo. Patients will receive FMT from one donor throughout the study.The MIRO study will establish whether FMT is an effective and safe therapy to induce and maintain remission in patients with active Crohn's disease.

ETHICS AND DISSEMINATION: Ethical approval has been received by the St Vincent's Hospital Melbourne Human Research Ethics Committee (HREC-A 084/21). The results will be disseminated in peer-reviewed journals and presented at international conferences.

TRIAL REGISTRATION NUMBER: ClinicalTrials.gov: NCT04970446; Registered on 20 July 2021.},
}

Humans
*Crohn Disease/therapy
*Fecal Microbiota Transplantation/methods
Australia
Randomized Controlled Trials as Topic
Treatment Outcome
Remission Induction
Adult
Male
Gastrointestinal Microbiome
Female
Multicenter Studies as Topic

@article {pmid40253186,
year = {2025},
author = {Hao, Y and Wang, C and Wang, L and Hu, L and Duan, T and Zhang, R and Yang, X and Li, T},
title = {Nondigestible stachyose alleviates cyclophosphamide-induced small intestinal mucosal injury in mice by regulating intestinal exosomal miRNAs, independently of the gut microbiota.},
journal = {Food research international (Ottawa, Ont.)},
volume = {209},
number = {},
pages = {116258},
doi = {10.1016/j.foodres.2025.116258},
pmid = {40253186},
issn = {1873-7145},
mesh = {Animals ; *Cyclophosphamide/adverse effects/toxicity ; *Gastrointestinal Microbiome/drug effects ; *MicroRNAs/metabolism/genetics ; *Intestinal Mucosa/drug effects/pathology/metabolism ; *Oligosaccharides/pharmacology ; Mice ; *Intestine, Small/drug effects/pathology/metabolism ; *Exosomes/metabolism/drug effects/genetics ; Male ; Oxidative Stress/drug effects ; Mice, Inbred C57BL ; Cytokines/metabolism ; Prebiotics ; Permeability ; Germ-Free Life ; Tight Junction Proteins/metabolism ; },
abstract = {Stachyose has traditionally been considered to exert prebiotic effects primarily through its interaction with gut microbiota. However, this study reveals a novel mechanism by which stachyose alleviates cyclophosphamide (CY)-induced small intestinal mucosa disruption by regulating the intestinal exosomal miRNAs, without relying on the gut microbiota. Specifically, stachyose significantly mitigates CY-caused damage to the intestinal permeability, oxidative stress, and the structure of intestinal villi and crypts in pseudo-germ-free (PGF) mice. The immunofluorescence staining and qPCR analyses show that stachyose treatment restores CY-caused abnormal changes on the levels of tight junction proteins including MUC2, Occludin, Claudin-1, and ZO-1, and pro-inflammatory cytokines including TNF-α, IL-1β, and IL-2. Furthermore, by conducting fecal miRNA transplantation experiment, we further demonstrated that, similar to stachyose, stachyose-shaped intestinal miRNAs protect against CY-induced intestinal mucosal damage in PGF mice. In summary, this study provides new scientific evidence for the direct interaction between nondigestible stachyose and the proximal small intestine. It also opens new avenues for further investigation into the systemic nutritional functions of stachyose, particularly the health benefits of stachyose in the upper gastrointestinal tract.},
}

Animals
*Cyclophosphamide/adverse effects/toxicity
*Gastrointestinal Microbiome/drug effects
*MicroRNAs/metabolism/genetics
*Intestinal Mucosa/drug effects/pathology/metabolism
*Oligosaccharides/pharmacology
Mice
*Intestine, Small/drug effects/pathology/metabolism
*Exosomes/metabolism/drug effects/genetics
Male
Oxidative Stress/drug effects
Mice, Inbred C57BL
Cytokines/metabolism
Prebiotics
Permeability
Germ-Free Life
Tight Junction Proteins/metabolism

@article {pmid40253185,
year = {2025},
author = {Yang, H and Zhao, Y and Zhang, R and Zhao, L and Yang, H and Liao, X},
title = {CiLi (Rosa roxburghii Tratt.) polyphenols improve colitis via gut microbiota-lipid mediator-immunity axis.},
journal = {Food research international (Ottawa, Ont.)},
volume = {209},
number = {},
pages = {116257},
doi = {10.1016/j.foodres.2025.116257},
pmid = {40253185},
issn = {1873-7145},
mesh = {*Gastrointestinal Microbiome/drug effects ; Animals ; *Polyphenols/pharmacology ; *Colitis/drug therapy/chemically induced/microbiology/immunology ; Mice ; Mice, Inbred C57BL ; Oxidative Stress/drug effects ; Dextran Sulfate ; Dysbiosis ; Male ; Lipid Metabolism/drug effects ; Disease Models, Animal ; Colon/drug effects ; Fatty Acids, Volatile ; },
abstract = {Dysbiosis of gut microbiome is one of the most important factors leading to inflammatory bowel disease (IBD). Intake of phytochemicals from fruits and vegetables is an effective way to improve IBD, but how these bioactivators regulate gut microbiota to exert healthy effects remains unclear. Here, we found that pretreatment with CiLi juice, particularly its polyphenol component, alleviated dextran sulfate sodium (DSS)-induced colitis while preserving intestinal barrier integrity. CiLi polyphenols (CL_PP) reduced inflammation and oxidative stress in colon tissue and enriched fecal short-chain fatty acids. Importantly, CL_PP significantly regulated the gut microbiome diversity, increasing beneficial bacteria (e.g., Clostridia_UCG-014, f_Muribaculaceae and Ileibacterium_valens) while decreasing harmful bacteria (Escherichia-Shigella and Romboutsia). Multiomics analysis revealed that CL_PP upregulated bioactive lipid metabolites, particularly those derived from polyunsaturated fatty acids (e.g., resolvin D2, prostaglandin A1, and glycerophosphocholine) related gene expressions (Pltp, Alox15 and Pld4). Additionally, CL-PP downregulated the oxidative stress markers (oxidized glutathione and glutathione peroxidase 3), and immune cell markers (CD8 and CD68). Fecal microbiota transplantation confirmed that the fecal microbiota from CL_PP-treated mice exhibited anti-colitis effects. These effects were diminished in antibiotic-treated mice, underscoring the importance of the gut microbiota in mediating the CL_PP's anti-inflammatory benefits. This study suggests that CL_PP is a potential modulator of gut microbiome dysbiosis for the prevention and treatment of colitis.},
}

*Gastrointestinal Microbiome/drug effects
Animals
*Polyphenols/pharmacology
*Colitis/drug therapy/chemically induced/microbiology/immunology
Mice
Mice, Inbred C57BL
Oxidative Stress/drug effects
Dextran Sulfate
Dysbiosis
Male
Lipid Metabolism/drug effects
Disease Models, Animal
Colon/drug effects
Fatty Acids, Volatile

@article {pmid40253128,
year = {2025},
author = {Zuo, G and Li, M and Guo, X and Wang, L and Yao, Y and Huang, JA and Liu, Z and Lin, Y},
title = {Fu brick tea supplementation ameliorates non-alcoholic fatty liver disease and associated endotoxemia via maintaining intestinal homeostasis and remodeling hepatic immune microenvironment.},
journal = {Food research international (Ottawa, Ont.)},
volume = {209},
number = {},
pages = {116207},
doi = {10.1016/j.foodres.2025.116207},
pmid = {40253128},
issn = {1873-7145},
mesh = {*Non-alcoholic Fatty Liver Disease/immunology ; Animals ; *Endotoxemia ; Gastrointestinal Microbiome/drug effects ; Male ; Humans ; Homeostasis/drug effects ; *Tea/chemistry ; *Liver/immunology/drug effects/metabolism ; Rats ; Diet, High-Fat/adverse effects ; Caco-2 Cells ; Dysbiosis ; Rats, Sprague-Dawley ; *Dietary Supplements ; Intestines ; },
abstract = {Non-alcoholic fatty liver disease (NAFLD) is a prevalent disorder of excessive fat accumulation and inflammation in the liver that currently lacks effective therapeutic interventions. Fu brick tea (FBT) has been shown to ameliorate liver damage and modulate gut microbiota dysbiosis in NAFLD, but the potential mechanisms have not been comprehensively elucidated, especailly whether its hepatoprotective effects are determined to depend on the homeostasis of gut microbiota, intestinal barrier function and hepatic immune microenvironment. In this study, our results further demonstrated that FBT not only alleviated NAFLD symptoms and related endotoxemia in high-fat diet (HFD)-fed rats, but also attenuated intestinal barrier dysfunction and associated inflammation, also confirmed in Caco-2 cell experiment. Meanwhile, FBT intervention significantly relieved HFD-induced gut microbiota dysbiosis, characterized by increased diversity and composition, particularly facilitating beneficial microbes, including short chain fatty acids (SCFAs) and bile acids producers, such as Blautia and Fusicatenibacter, and inhibiting Gram-negative bacteria, such as Prevotella_9 and Phascolarctobacterium. Also, the gut microbiota-dependent hepatoprotective effects of FBT were verified by fecal microbiota transplantation (FMT) experiment. Thus, the beneficial moulation of gut microbiota altered by FBT in levels of SCFAs, bile acids and lipopolysaccharides, intestinal barrier function and TLR4/NF-κB pathway contributed to alleviate liver steatosis and inflammation. Additionally, the hepatoprotective effects of FBT was further demonstrated by suppressing Kupffer cell activation and regulating lipid metabolism using an ex vivo model of liver organoid. Therefore, FBT supplementation can maintain intenstinal homeostasis and remodel hepatic immune microenvironment to prevent NAFLD and associated endotoxemia.},
}

*Non-alcoholic Fatty Liver Disease/immunology
Animals
*Endotoxemia
Gastrointestinal Microbiome/drug effects
Male
Humans
Homeostasis/drug effects
*Tea/chemistry
*Liver/immunology/drug effects/metabolism
Rats
Diet, High-Fat/adverse effects
Caco-2 Cells
Dysbiosis
Rats, Sprague-Dawley
*Dietary Supplements
Intestines

@article {pmid40252900,
year = {2025},
author = {Sahebi, K and Arianejad, M and Azadi, S and Hosseinpour-Soleimani, F and Kazemi, R and Tajbakhsh, A and Negahdaripour, M},
title = {The Interplay between Gut Microbiome, Epigenetics, and Substance Use Disorders: from Molecular to Clinical Perspectives.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {177630},
doi = {10.1016/j.ejphar.2025.177630},
pmid = {40252900},
issn = {1879-0712},
abstract = {Substance use disorders (SUDs) involve a complex series of central and peripheral pathologies, leading to impairments in cognitive, behavioral, and physiological processes. Emerging evidence indicates a more significant role for the microbiome-gut-brain axis (MGBA) in SUDs than previously recognized. The MGBA is interconnected with various body systems by producing numerous metabolites, most importantly short-chain fatty acids (SCFAs), cytokines, and neurotransmitters. These mediators influence the human body's epigenome and transcriptome. While numerous epigenetic alterations in different brain regions have been reported in SUD models, the intricate relationship between SUDs and the MGBA suggests that the gut microbiome may partially contribute to the underlying mechanisms of SUDs. Promising results have been observed with gut microbiome-directed interventions in patients with SUDs, including prebiotics, probiotics, antibiotics, and fecal transplantation. Nonetheless, the long-term epigenetic effects of these interventions remain unexplored. Moreover, various confounding factors and study limitations have hindered the identification of molecular mechanisms and clinical applications of gut microbiome interventions in SUDs. In the present review, we will (i) provide a comprehensive discussion on how the gut microbiome influences SUDs, with an emphasis on epigenetic alterations; (ii) discuss the current evidence on the bidirectional relationship of gut microbiome and SUDs, highlighting potential targets for intervention; and (iii) review recent advances in gut microbiome-directed therapies, along with their limitations and future directions.},
}

@article {pmid40252828,
year = {2025},
author = {Zhao, Y and Zhao, W and Chai, X and Sun, P and Huang, J and Guo, X and Zhang, L and Ren, D and Yi, C and Zhu, X and Zhao, S},
title = {Reshaping the gut microbiota: A novel oppinion of Eucommiae cortex polysaccharide alleviate learning and memory impairments in Alzheimer's disease.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2025.04.025},
pmid = {40252828},
issn = {2090-1224},
abstract = {BACKGROUND: Alzheimer's disease (AD), which is a chronic neurodegenerative disorder, is marked by the progressive deteriorations in learning and memory capabilities. The microbiota-gut-brain axis has come to be regarded as a crucial element in relation to the pathogenesis as well as the treatment of AD. Eucommiae cortex polysaccharides (EPs), being among the most plentiful substances present in the Eucommiae cortex, show the potential to exert immunomodulatory and neuroprotective function. However, whether EPs are protective against AD and their mechanism of action remain to be investigated OBJECTIVES: We hypothesize that EPs can regulate brain glutamine metabolism through gut microbiota and the butyric acid metabolized by them, improve oxidative stress and autophagy in the brain, and thus alleviate AD.

METHODS: In the present study, we used EPs (0.25 % w/w in food) and fecal microbiota transplantation, as well as butyrate supplementation (0.1 M in water), to intervene in AD mice. Multi-omics were used to determine the mechanism by which EPs improve AD-related learning and memory impairments.

RESULTS: Our results suggest that EPs, functioning as a prebiotic, alleviated learning and memory impairments in AD mice. Mechanistically, EPs are able to reshape the gut microbiota, promote the growth of gut microbiota involved in short-chain fatty acid metabolism, particularly butyrate-producing microbes. The butyrate produced by these microbes improves the brain microenvironment by modulating oxidative stress and autophagy mediated by brain glutamate metabolism, improving learning and memory impairments in AD mice, and inhibiting the formation and deposition of beta-amyloid proteins. Fecal microbiota transplantation (FMT) and butyrate supplementation further confirm this conclusion.

CONCLUSIONS: Our results highlighted that EPs can alleviate learning and memory impairments in AD with a gut microbiota-dependent manner and that butyric acid metabolized by butyric acid-metabolizing bacteria in the gut plays a central role in regulating brain glutamine metabolism to improve brain microenvironmental homeostasis. Meanwhile, the present study provides new insights into the treatment of AD with natural products.},
}

@article {pmid40252432,
year = {2025},
author = {Wang, R and Gan, C and Gong, B and Huang, J and Lou, Z and Wang, D and Yan, R and Li, G and Xiong, T and Guo, J},
title = {Tongfu Xingshen capsule alleviates stroke-associated pneumonia-induced multiple organ injuries by modulating the gut microbiota and sphingolipid metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {142},
number = {},
pages = {156756},
doi = {10.1016/j.phymed.2025.156756},
pmid = {40252432},
issn = {1618-095X},
abstract = {BACKGROUND: Stroke-associated pneumonia (SAP) represents a major complication and cause of death in patients suffering from intracerebral haemorrhage (ICH). It's urgent to develop more effective therapeutic strategies. Tongfu Xingshen capsule (TFXS) is a traditional Chinese medicine that has been utilised in clinical studies for the treatment of ICH and SAP, but the underlying mechanisms remain to be fully elucidated.

PURPOSE: This study aims to explore the therapeutic effects and mechanisms of TFXS on SAP using an aspiration-induced Klebsiella pneumoniae infection-complicating ICH rat model and an intratracheal injection of lipopolysaccharide (LPS)-induced acute lung injury-complicating ICH rat model.

METHODS: The chemical components of TFXS are characterised using ULPLC-Q Exactive-Orbitrap-MS. The therapeutic effects of TFXS are evaluated through neurological scoring, histopathology analysis, magnetic resonance imaging, immunofluorescence, Alcian blue-nuclear fast red staining, myeloperoxidase activity assessment, leukocyte counting, and ELISA. To investigate the underlying mechanisms, faecal microbiota transplantation, 16S rRNA sequencing, untargeted metabolomics, and Spearman correlation analyses are performed.

RESULTS: A total of 60 compounds are identified in TFXS. Pharmacological analysis reveals that TFXS significantly mitigates neurological deficits, enhances haematoma absorption, attenuates brain damage and neuroinflammation, and improves pneumonia and pulmonary injury by reducing the infiltration of leukocytes and lymphocytes, as well as suppressing the infiltration and overactivation of neutrophils. TFXS also alleviates intestinal lesions and barrier damage by increasing acidic mucins and the expression of the tight junction protein zonula occludens-1 (ZO-1). Mechanistically, TFXS ameliorates pneumonia and pulmonary injury in a gut microbiota-dependent manner. It reverses sphingolipid metabolism disorders and ceramide accumulation by modulating SAP-induced gut microbiota dysbiosis and enhancing the abundance of probiotics, including Lactobacillus, Allobaculum and Enterococcus.

CONCLUSION: TFXS exerts anti-inflammatory and protective effects on the brain, lung, and gut by alleviating gut microbiota dysbiosis and sphingolipid metabolism disorders. These findings highlight TFXS as a promising therapeutic candidate for the treatment of SAP.},
}

@article {pmid40252102,
year = {2025},
author = {Vassallo, GA and Dionisi, T and De Vita, V and Augello, G and Gasbarrini, A and Pitocco, D and Addolorato, G},
title = {The role of fecal microbiota transplantation in diabetes.},
journal = {Acta diabetologica},
volume = {},
number = {},
pages = {},
pmid = {40252102},
issn = {1432-5233},
abstract = {Fecal microbiota transplantation (FMT) has emerged as a potential therapeutic strategy for modulating gut dysbiosis in diabetes mellitus. This review critically evaluates preclinical and clinical evidence on FMT in type 1 (T1D) and type 2 diabetes (T2D). Studies suggest that FMT can restore microbial diversity, improve glycemic control, and modulate immune responses, with varying effects across diabetes subtypes. In T1D, preclinical models demonstrate that FMT influences regulatory T-cell expansion and β-cell preservation, though clinical translation remains limited. In T2D, FMT has shown transient improvements in insulin sensitivity, with sustained effects observed only in patients with specific microbiome signatures. However, heterogeneity in patient responses, donor variability, and methodological limitations complicate its clinical application. This review highlights the interplay between FMT, immune modulation, and microbial metabolism, advocating for phenotype-stratified trials and multi-omics integration to enhance therapeutic precision.},
}

@article {pmid40251524,
year = {2025},
author = {Pan, Q and Guo, F and Chen, J and Huang, H and Huang, Y and Liao, S and Xiao, Z and Wang, X and You, L and Yang, L and Huang, X and Xiao, H and Liu, HF and Pan, Q},
title = {Exploring the role of gut microbiota modulation in the long-term therapeutic benefits of early MSC transplantation in MRL/lpr mice.},
journal = {Cellular & molecular biology letters},
volume = {30},
number = {1},
pages = {49},
pmid = {40251524},
issn = {1689-1392},
support = {82070757//National Natural Science Foundation of China/ ; 82270770//National Natural Science Foundation of China/ ; 82400841//National Natural Science Foundation of China/ ; 2022B1212030003//Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Noncommunicable Diseases/ ; 2022A1515220028//Guangdong Basic and Applied Basic Research Foundation Enterprise Joint Fund/ ; 2021A05060//Zhanjiang Science and Technology Project (Competitive)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; Mice, Inbred MRL lpr ; *Mesenchymal Stem Cell Transplantation/methods ; *Lupus Erythematosus, Systemic/therapy/microbiology ; Mice ; Fecal Microbiota Transplantation ; Humans ; Mesenchymal Stem Cells/cytology/metabolism ; Female ; Disease Models, Animal ; Receptors, Aryl Hydrocarbon/metabolism ; Cytokines/metabolism ; },
abstract = {BACKGROUND: Systemic lupus erythematosus (SLE), influenced by gut microbiota dysbiosis, is characterized by autoimmune and inflammatory responses. Human umbilical cord-derived mesenchymal stem cell (hUC-MSC) transplantation is an effective and safe treatment for refractory or severe SLE; however, the long-term efficacy and mechanisms of early hUC-MSC therapeutic benefits in SLE need further investigation.

METHODS: Here, lupus-prone MRL/MpJ-Fas[lpr] (MRL/lpr) mice were divided into three groups: the control (Ctrl) group received saline injections, while the MSC and MSC-fecal microbiota transplantation (FMT) groups received early hUC-MSC transplants at weeks 6, 8, and 10. The MSC-FMT group also underwent FMT from the Ctrl group between weeks 9 and 13.

RESULTS: Our results showed that early MSC treatment extended therapeutic effects up to 12 weeks, reducing autoantibodies, proinflammatory cytokines, B cells, and improving lupus nephritis. It also modulated the gut microbiota, increasing the abundance of beneficial bacteria, such as Lactobacillus johnsonii and Romboutsia ilealis, which led to higher levels of plasma tryptophan and butyrate metabolites. These metabolites activate the aryl hydrocarbon receptor (AHR), upregulate the Cyp1a1 and Cyp1b1 gene, enhance the zonula occludens 1 (ZO-1) protein, promote intestinal repair, and mitigate SLE progression. Notably, FMT from lupus mice significantly reversed hUC-MSC benefits, suggesting that the modulation of the gut microbiota plays a crucial role in the therapeutic response observed in MRL/lpr mice.

CONCLUSIONS: This research innovatively explores the early therapeutic window for MSCs in SLE, highlighting the partial mechanisms through which hUC-MSCs modulate the gut microbiota-tryptophan-AHR axis, thereby ameliorating SLE symptoms.},
}

Animals
*Gastrointestinal Microbiome
Mice, Inbred MRL lpr
*Mesenchymal Stem Cell Transplantation/methods
*Lupus Erythematosus, Systemic/therapy/microbiology
Mice
Fecal Microbiota Transplantation
Humans
Mesenchymal Stem Cells/cytology/metabolism
Female
Disease Models, Animal
Receptors, Aryl Hydrocarbon/metabolism
Cytokines/metabolism

@article {pmid40250802,
year = {2025},
author = {Hirai, J},
title = {Extended-pulsed Fidaxomicin Therapy for Recurrent Clostridioides difficile Infection After Standard Vancomycin and Fidaxomicin Failure: A Case Report.},
journal = {Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy},
volume = {},
number = {},
pages = {102709},
doi = {10.1016/j.jiac.2025.102709},
pmid = {40250802},
issn = {1437-7780},
abstract = {Clostridioides difficile infection (CDI) is a leading cause of healthcare-associated diarrhea. Recurrence occurs in up to 60% of patients following multiple episodes, posing a major clinical challenge. While vancomycin (VCM) and fidaxomicin (FDX) are recommended first-line therapies, treatment failures and recurrences are not uncommon. Extended-pulsed fidaxomicin (EPFX) has been proposed to reduce recurrence, especially in high-risk patients, though the evidence remains limited for those with multiple prior relapses. We report the case of a 66-year-old man with advanced esophageal and gastric cancer who experienced four episodes of recurrent CDI despite standard treatment with VCM and FDX. Given the unavailability of bezlotoxumab (BEZ) in Japan and the limited accessibility of fecal microbiota transplantation (FMT), EPFX was selected as a salvage regimen. After both EPFX and pulse-tapered oral VCM were explained, the patient and physician elected to initiate EPFX, consisting of 200 mg twice daily for five days followed by 200 mg every other day for 20 days. No further recurrences were observed for over four months, and no adverse effects were noted. This case supports the use of EPFX in patients with multiple high-risk features-including advanced age, active malignancy, and prior treatment failures-despite the EXTEND trial's exclusion of patients with ≥3 recurrences. The favorable pharmacokinetic properties of FDX may have contributed to its efficacy. Importantly, the patient's medication, nutritional, and oncologic status remained stable throughout treatment, suggesting that EPFX played a pivotal role in achieving remission. EPFX may offer a viable option for patients with recurrent CDI refractory to standard therapies.},
}

@article {pmid40248060,
year = {2025},
author = {Liu, HJ and Wu, MC and Gau, SY},
title = {Role of gut microbiota and mesenteric adipose tissue in the pathology of Crohn's disease: Potential therapeutic targets.},
journal = {World journal of gastroenterology},
volume = {31},
number = {13},
pages = {102291},
pmid = {40248060},
issn = {2219-2840},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology/physiology ; *Crohn Disease/microbiology/therapy/pathology/immunology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; *Adipose Tissue/pathology ; Treatment Outcome ; Mesentery/pathology ; Colitis, Ulcerative/microbiology/therapy/immunology/pathology ; Remission Induction ; Animals ; Intestinal Mucosa/microbiology/pathology/immunology ; Dysbiosis/therapy/immunology/microbiology ; },
abstract = {This editorial comments on the article by Wu et al in the World Journal of Gastroenterology. The article explored the relationship between mesenteric adipose tissue, creeping fat, inflammation, and gut microbiota in Crohn's disease (CD). We discussed three key aspects of the interaction between gut microbiota and inflammatory bowel disease (IBD): The physiological functions of the gut microbiota, the potential role of probiotics in IBD treatment; and the effect of fecal microbiota transplantation (FMT) in combating IBD. IBD, comprising CD and ulcerative colitis (UC), is influenced by the gut microbiota. Changes in gut microbiota composition disrupt intestinal function and promote chronic inflammation, but the exact mechanisms remain unclear. Probiotics have demonstrated some efficacy in inducing remission in UC, though their effectiveness in CD is still debated. FMT shows promise in treating IBD, especially UC, by restoring gut microbiota diversity and inducing clinical remission. As for CD, FMT has potential, but more studies are needed to confirm its long-term effectiveness and safety. Dietary approaches may help manage IBD symptoms or disease activity, but patient adherence is crucial. Clinicians and researchers must recognize the importance of the gut microbiota and the need for personalized therapies targeting microbial imbalances.},
}

Humans
*Gastrointestinal Microbiome/immunology/physiology
*Crohn Disease/microbiology/therapy/pathology/immunology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
*Adipose Tissue/pathology
Treatment Outcome
Mesentery/pathology
Colitis, Ulcerative/microbiology/therapy/immunology/pathology
Remission Induction
Animals
Intestinal Mucosa/microbiology/pathology/immunology
Dysbiosis/therapy/immunology/microbiology

@article {pmid40247656,
year = {2025},
author = {Bonazzi, E and De Barba, C and Lorenzon, G and Maniero, D and Bertin, L and Barberio, B and Facciotti, F and Caprioli, F and Scaldaferri, F and Zingone, F and Savarino, EV},
title = {Recent developments in managing luminal microbial ecology in patients with inflammatory bowel disease: from evidence to microbiome-based diagnostic and personalized therapy.},
journal = {Expert review of gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1080/17474124.2025.2495087},
pmid = {40247656},
issn = {1747-4132},
abstract = {INTRODUCTION: Inflammatory bowel disease (IBD), including Crohn's disease and ulcerative colitis, is a chronic condition characterized by abnormal immune responses and intestinal inflammation. Emerging evidence highlights the vital role of gut microbiota in IBD's onset and progression. Recent advances have shaped diagnostic and therapeutic strategies, increasingly focusing on microbiome-based personalized care. Methodology: this review covers studies from 2004 to 2024, reflecting the surge in research on luminal microbial ecology in IBD. Human studies were prioritized, with select animal studies included for mechanistic insights. Only English-language, peer-reviewed articles - clinical trials, systematic reviews, and meta-analyses - were considered. Studies without clinical validation were excluded unless offering essential insights. Searches were conducted using PubMed, Scopus, and Web of Science.

AREAS COVERED: we explore mechanisms for managing IBD-related microbiota, including microbial markers for diagnosis and novel therapies such as fecal microbiota transplantation, metabolite-based treatments, and precision microbiome modulation. Additionally, we review technologies and diagnostic tools used to analyze gut microbiota composition and function in clinical settings. Emerging data supporting personalized therapeutic strategies based on individual microbial profiles are discussed.

EXPERT OPINION: Standardized microbiome research integration into clinical practice will enhance precision in IBD care, signaling a shift toward microbiota-based personalized medicine.},
}

@article {pmid40246750,
year = {2025},
author = {Gefen, R and Dourado, J and Emile, SH and Wignakumar, A and Rogers, P and Aeschbacher, P and Garoufalia, Z and Horesh, N and Wexner, SD},
title = {Fecal microbiota transplantation for patients with ulcerative colitis: a systematic review and meta-analysis of randomized control trials.},
journal = {Techniques in coloproctology},
volume = {29},
number = {1},
pages = {103},
pmid = {40246750},
issn = {1128-045X},
mesh = {Humans ; *Colitis, Ulcerative/therapy ; *Fecal Microbiota Transplantation/methods/adverse effects ; Randomized Controlled Trials as Topic ; Remission Induction/methods ; Treatment Outcome ; Male ; Female ; Adult ; Middle Aged ; Gastrointestinal Microbiome ; },
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) has been shown to restore gut microbiome composition with an acceptable safety profile. FMT in inflammatory bowel disease, specifically ulcerative colitis (UC), has been investigated. We aimed to assess the efficacy of FMT in inducing UC remission.

METHODS: PubMed, Scopus, Google Scholar, and clinicaltrials.gov were searched for randomized control trials that assessed FMT in inducing UC remission. The primary outcome was combined clinical and endoscopic remission. Secondary outcomes were clinical remission, endoscopic remission, post-treatment overall adverse events, and colitis. Sensitivity analyses, meta-regression, bias assessment, and grading of certainty of evidence were performed.

RESULTS: A total of 14 studies including 600 patients (55.8% male; median age 40.7 years) were assessed. FMT was used in 299 patients and associated with significantly higher odds of combined clinical and endoscopic remission (OR 2.25, 95% CI 1.54, 3.3; p < 0.0001), clinical remission (OR 2.02, 95% CI 1.4, 2.93; p = 0.0002), and endoscopic remission (OR 1.95, 95% CI 1.17, 3.28; p = 0.011). The odds of post-treatment overall adverse events (OR 1.24, 95% CI 0.79, 1.95; p = 0.34) and colitis (OR 0.85, 95% CI 0.52, 1.93; p = 0.512) were similar between groups. Compared with baseline, FMT was more effective when biologics (OR 2.71), steroids (OR 2.27), or methotrexate (OR 3.07) were used as pre-FMT treatment. Oral delivery of FMT (OR 3.15) and pooled donors (OR 3.32) led to higher odds of remission. On meta-regression, pooled donors and methotrexate pre-treatment were associated with an increased likelihood of remission.

CONCLUSIONS: FMT is promising in inducing UC remission. Administration of medical treatments before FMT may help achieve higher remission rates. Current evidence shows that oral delivery of FMT and multidonor FMT may confer better results.},
}

Humans
*Colitis, Ulcerative/therapy
*Fecal Microbiota Transplantation/methods/adverse effects
Randomized Controlled Trials as Topic
Remission Induction/methods
Treatment Outcome
Male
Female
Adult
Middle Aged
Gastrointestinal Microbiome

@article {pmid40246463,
year = {2025},
author = {Xia, S and Yan, C and Cai, G and Xu, Q and Zou, H and Gu, J and Yuan, Y and Liu, Z and Bian, J},
title = {Gut dysbiosis exacerbates inflammatory liver injury induced by environmentally relevant concentrations of nanoplastics via the gut-liver axis.},
journal = {Journal of environmental sciences (China)},
volume = {155},
number = {},
pages = {250-266},
doi = {10.1016/j.jes.2024.11.022},
pmid = {40246463},
issn = {1001-0742},
mesh = {Animals ; *Dysbiosis/chemically induced ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Microplastics/toxicity ; Liver/drug effects ; *Environmental Pollutants/toxicity ; *Chemical and Drug Induced Liver Injury ; Inflammation/chemically induced ; Male ; *Nanoparticles/toxicity ; },
abstract = {As an emerging and potentially threatening pollutant, nanoplastics (NPs) have received considerable global attention. Due to their physical properties and diminutive size, NPs ingestion can more easily cross biological barriers and enter the human and animal body. Despite reports of hepatotoxicity associated with NPs, their impact and potential underlying mechanisms remain elusive. In this study, we investigated the impact of NPs at concentrations found in the environment on the gut flora, intestinal barrier function, liver pyroptosis, and inflammation in mice following 12 weeks of exposure. To further validate the involvement of gut flora in inflammatory liver damage caused by NPs, we utilized antibiotics to remove the intestinal flora and performed fecal microbiota transplantation. We confirmed that NPs exposure altered the gut microbiota composition, with a notable rise in the proportions of Alloprevotella and Ileibacterium while causing a decrease in the relative proportions of Dubosiella. This disruption also affected the gut barrier, increasing lipopolysaccharides in circulation and promoting liver pyroptosis. Importantly, mice receiving fecal transplants from NPs-treated mice showed intestinal barrier damage, liver pyroptosis, and inflammation. However, NPs effects on the intestinal barrier and liver pyroptosis were attenuated by antibiotics depletion of the commensal microbiota. In summary, our current research revealed that extended exposure to environmentally relevant concentrations of NPs resulted in inflammatory damage to the liver. Additionally, we have identified for the first time that imbalances in intestinal flora are crucial in liver pyroptosis induced by NPs.},
}

Animals
*Dysbiosis/chemically induced
*Gastrointestinal Microbiome/drug effects
Mice
*Microplastics/toxicity
Liver/drug effects
*Environmental Pollutants/toxicity
*Chemical and Drug Induced Liver Injury
Inflammation/chemically induced
Male
*Nanoparticles/toxicity

@article {pmid40246176,
year = {2025},
author = {Adıgüzel, E and Yılmaz, ŞG and Atabilen, B and Şeref, B},
title = {Microbiome modulation as a novel therapeutic modality for anxiety disorders: A review of clinical trials.},
journal = {Behavioural brain research},
volume = {487},
number = {},
pages = {115595},
doi = {10.1016/j.bbr.2025.115595},
pmid = {40246176},
issn = {1872-7549},
abstract = {Anxiety disorders are one of the major conditions in psychiatry characterized by symptoms such as worry, social and performance fears, unexpected and/or triggered panic attacks, anticipatory anxiety, and avoidance behaviors. Recent developments have drawn attention to the putative involvement of peripheral systems in the control of anxiety, and the gut microbiota has come to light as an emerging peripheral target for anxiety. The relationship between the gut-brain axis, a bidirectional communication network between the central nervous system (CNS) and enteric nervous system (ENS), and anxiety has been the subject of some recent studies. Therefore, this systematic review analyzed clinical trials evaluating the potential of microbiome modulation methods in mitigating and ameliorating anxiety disorders. Clinical studies on probiotic, prebiotic, synbiotic supplements, dietary interventions, and fecal microbiota transplantation in anxiety disorders were screened. All of the studies examined the effects of probiotic intervention. One of these studies compared a prebiotic-rich diet with probiotic supplementation. Longitudinal analyses showed that the probiotic intervention alleviated anxiety. However, most of the controlled studies reported that the probiotic intervention did not make a difference compared to placebo. Thus, the current findings suggest that it is too early to consider the promising role of microbiome modulation in the treatment of anxiety disorders. However, it is obvious that more clinical research is needed to clarify issues such as probiotic strains, prebiotic types, and their doses that may be effective on anxiety disorders.},
}

@article {pmid40245946,
year = {2025},
author = {Vinit, N and Glenisson, M and Leroy, J and Sarnacki, S and Crétolle, C and Beaudoin, S},
title = {Anatomical correction and early outcomes of one-step ventral and dorsal proctoplasty in girls with low anorectal malformations.},
journal = {European journal of pediatric surgery : official journal of Austrian Association of Pediatric Surgery ... [et al] = Zeitschrift fur Kinderchirurgie},
volume = {},
number = {},
pages = {},
doi = {10.1055/a-2590-5697},
pmid = {40245946},
issn = {1439-359X},
abstract = {INTRODUCTION: Rectoperineal (RPF) and rectovestibular fistula (RVF) are the most common forms of low anorectal malformations (ARM) in girls, and lead to difficult stooling, thus demanding early surgical correction. This study's aim was to assess early outcomes associated with one-step ventral and dorsal proctoplasty in RPF/RVF.

MATERIALS AND METHODS: All female infants who consecutively underwent one-step proctoplasty for RPF/RVF at our institution (2012-2022) were retrospectively included. Reviewed data included: age at procedure, congenital anomalies, fistula location, preoperative symptoms, intraoperative findings, operative time, postoperative complications, and bowel functional outcome. Success of the technique, defined as spontaneous bowel movement at last follow-up without anal dilation, was assessed. Secondary outcomes included resolution of preoperative symptoms, and Krickenbeck score and fecal continence in girls older than three at last follow-up. No preoperative bowel preparation was necessary.

RESULTS: None of the 77 included girls (median age at surgery: 3.2 months [2.3-7.3]) had prior colostomy. In every case, intraoperative findings included: ventral defect of the external anal sphincter, abnormal attachment of the bulbospongiosus muscles to the fistula and posterior ledge, thus justifying both ventral and dorsal reconstructions. The median operative time was 34 min [27-38], and the median hospital stay was 2 days [2-3]. Limited ventral skin dehiscence was the most common postoperative complication (31%), with limited effect on clinical outcome (one secondary anal stricture). No child required secondary colostomy or revision anoplasty. One child underwent secondary pull-through due to persistent megarectum. Preoperative symptoms resolved in 98% of cases. After a median follow-up of 27.6 months [9.8-48.3], all girls had spontaneous bowel movement and 21% had grade-2 constipation. The technique was successful in 97% of cases (two anal strictures treated with dilations).

CONCLUSIONS: RPF/RVF in female share abnormal anatomical characteristics. One-step ventral and dorsal proctoplasty allows precise anatomical correction of low ARM in girls.},
}

@article {pmid40245774,
year = {2025},
author = {Zhang, X and Yin, Y and Chen, Y and Lin, L and Shen, S and Fang, F and Wang, Q},
title = {Gut microbiota contributes to obstructive sleep apnea-induced hypertension by gut-heart axis in mice.},
journal = {International immunopharmacology},
volume = {155},
number = {},
pages = {114667},
doi = {10.1016/j.intimp.2025.114667},
pmid = {40245774},
issn = {1878-1705},
abstract = {BACKGROUND: The gut microbiome has been closely linked to obstructive sleep apnea (OSA)-associated hypertension (HTN). However, its precise role in the pathogenesis of OSA-induced HTN remains unclear.

METHODS: To clarify the causal relationship between gut dysbiosis and OSA-related HTN, C57BL6J mice were randomly assigned to four groups. Each group underwent fecal microbiota transplantation from healthy individuals (control), OSA patients (OSA group), OSA patients with pre-hypertension (OSA-pHTN group), or OSA patients with HTN (OSA-HTN group). The pro-hypertensive effects of the OSA gut microbiota were verified, and the composition and function of the gut microbiota were compared using 16S rDNA gene sequencing. Additionally, the gut microbiota-related lipopolysaccharide (LPS)/ Toll-like receptor 4 (TLR4)/nuclear factor-kappaB (NF-κB) pathway in aortic tissues was investigated.

RESULTS: Fecal microbiota transplantation induced increased systolic blood pressure and aortic injury in mice from the OSA, OSA-pHTN and OSA-HTN groups, whereas no significant injury was observed in the control group. These three groups exhibited dysbiosis and impaired intestinal barrier function as evidenced by a reduction in Akkermansia and decreased expression of zonula occludens-1 and Occludin proteins. In addition, LPS, TLR4 and phosphorylated NF-κB expression were increased in aortic tissue from the three groups, and immunofluorescence showed a significant upregulation of TLR4 expression in aortic endothelial cells compared to controls.

CONCLUSION: This study demonstrates the pro-hypertensive effects of gut microbiota in OSA, mediated through the gut-derived LPS/TLR4/NF-κB pathway. These findings may guide the development of therapeutic strategies focused on restoring gut microbiome homeostasis.},
}

@article {pmid40244948,
year = {2025},
author = {Zhou, H and Zhuang, Y and Liang, Y and Chen, H and Qiu, W and Xu, H and Zhou, H},
title = {Curcumin exerts anti-tumor activity in colorectal cancer via gut microbiota-mediated CD8[+] T Cell tumor infiltration and ferroptosis.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d4fo04045g},
pmid = {40244948},
issn = {2042-650X},
abstract = {Colorectal cancer (CRC), as a high-incidence malignancy, continues to present significant challenges in prevention, screening, and treatment. Curcumin (Cur) exhibits notable anti-inflammatory and anticancer properties. Despite its poor solubility in water and low bioavailability, high concentrations of Cur are detected in the gastrointestinal tract after oral administration, suggesting that it may directly interact with the gut microbiota and exert regulatory effects. This study aims to explore the mechanisms by which Cur improves CRC by modulating gut microbiota. Firstly, we evaluated the effect of Cur on CRC cell viability in vitro using the MTT assay, and the results showed a significant inhibitory effect on CRC cell growth. The IC50 values for Cur in CT26 and RKO cells were 23.52 μM, 16.11 μM, and 13.62 μM at 24, 48, and 72 hours, respectively, and 26.3 μM, 16.52 μM, and 14.22 μM at 24, 48, and 72 hours, respectively. Cur induced apoptosis and caused G2 phase cell cycle arrest in tumor cells. Subsequently, we established a CRC mouse model. Oral administration of Cur at 15 mg kg[-1] and 30 mg kg[-1] inhibited CRC progression, as evidenced by reduced tumor volume, histological analysis, immunohistochemistry, and an increased number of CD8[+] T cells infiltrating the tumors. Ferroptosis in tumor cells was also observed. Cur partially restored the gut microbiota of CRC mice, altering the abundance and diversity of the gut microbiota and affecting serum metabolite distribution, with significant increases in the abundance of SCFA-producing microbes such as Lactobacillus and Kineothrix. To verify causality, we designed a fecal microbiota transplantation (FMT) experiment. Compared with CRC mice, the fecal microbiota from Cur-treated mice significantly alleviated CRC symptoms, including slowed tumor growth, enhanced CD8[+] T cell tumor infiltration, and induced ferroptosis in tumor cells. Additionally, when gut microbiota was depleted with antibiotics, Cur's antitumor effects disappeared, suggesting that Cur mitigates CRC in a gut microbiota-dependent manner. These findings provide new insights into the mechanisms underlying CRC and propose novel therapeutic interventions, emphasizing the interaction between gut microbiota and immune responses within the tumor immune microenvironment (TIME).},
}

@article {pmid40244415,
year = {2025},
author = {Nista, EC and Parello, S and Brigida, M and Amadei, G and Saviano, A and De Lucia, SS and Petruzziello, C and Migneco, A and Ojetti, V},
title = {Exploring the Role of Gut Microbiota and Probiotics in Acute Pancreatitis: A Comprehensive Review.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40244415},
issn = {1422-0067},
mesh = {*Probiotics/therapeutic use ; *Gastrointestinal Microbiome ; Humans ; *Pancreatitis/microbiology/therapy ; Fecal Microbiota Transplantation ; Animals ; Acute Disease ; },
abstract = {Acute pancreatitis (AP) is a common and potentially severe gastrointestinal condition characterized by acute inflammation of the pancreas. The pathophysiology of AP is multifactorial and intricate, involving a cascade of events that lead to pancreatic injury and systemic inflammation. The progression of AP is influenced by many factors, including genetic predispositions, environmental triggers, and immune dysregulation. Recent studies showed a critical involvement of the gut microbiota in shaping the immune response and modulating inflammatory processes during AP. This review aims to provide a comprehensive overview of the emerging role of gut microbiota and probiotics in AP. We analyzed the implication of gut microbiota in pathogenesis of AP and the modification during an acute attack. The primary goals of microbiome-based therapies, which include probiotics, prebiotics, antibiotics, fecal microbiota transplantation, and enteral nutrition, are to alter the composition of the gut microbial community and the amount of metabolites derived from the microbiota. By resetting the entire flora or supplementing it with certain beneficial organisms and their byproducts, these therapeutic approaches aim to eradicate harmful microorganisms, reducing inflammation and avoiding bacterial translocation and the potential microbiota-based therapeutic target for AP from nutrition to pre- and probiotic supplementation to fecal transplantation.},
}

*Probiotics/therapeutic use
*Gastrointestinal Microbiome
Humans
*Pancreatitis/microbiology/therapy
Fecal Microbiota Transplantation
Animals
Acute Disease

@article {pmid40244136,
year = {2025},
author = {Wu, Z and Yan, S and Zhang, H and Ma, Z and Du, R and Liu, Z and Li, X and Cao, G and Song, Y},
title = {Oral Sheep Milk-Derived Exosome Therapeutics for Cadmium-Induced Inflammatory Bowel Disease.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40244136},
issn = {1422-0067},
support = {No. 2022JBGS0021//Inner Mongolia Autonomous Region "Jiebangguashuai" project of China/ ; No. 2022ZD0401403//The Scientific and Technological Innovation 2030 - major project funding/ ; 10000-23122101/021//2024 Inner Mongolia University "Steed Plan" high-level talent funding/ ; },
mesh = {Animals ; Mice ; *Exosomes/metabolism ; *Cadmium/toxicity ; Gastrointestinal Microbiome ; *Milk/chemistry ; Sheep ; *Inflammatory Bowel Diseases/therapy/chemically induced/etiology/microbiology ; Disease Models, Animal ; Fecal Microbiota Transplantation ; Administration, Oral ; },
abstract = {Cadmium (Cd) contamination in plants and soil poses significant risks to livestock, particularly sheep. Cd exposure often leads to severe gastrointestinal diseases in sheep that are difficult to treat. Milk-derived exosomes, particularly those from sheep milk (SM-Exo), have shown potential in treating gastrointestinal disorders, though their efficacy in Cd-induced colitis remains unclear. In this study, we investigated the therapeutic potential of SM-Exo in a Cd-induced colitis model. Hu sheep were exposed to Cd, and their fecal microbiota were collected to prepare bacterial solutions for fecal microbiota transplantation (FMT) in mice. The changes in gut microbiota and gene expression were analyzed through microbiome and transcriptomics. Our results showed that prior to treatment, harmful bacteria (e.g., Bacteroides and Parabacteroides) were increased in FMT mice. SM-Exo treatment increased beneficial bacteria, particularly Lachnoclostridium, and activated the Cyclic Adenosine Monophosphate (cAMP) pathway, upregulating genes like Adcy1, Adcy3, CREB, and Sst. These changes were linked to reduced Cd-induced cell death and alleviation of colonic inflammation. In conclusion, SM-Exo appears to be a promising treatment for Cd-induced colitis, likely through modulation of the gut microbiota and activation of the cAMP pathway.},
}

Animals
Mice
*Exosomes/metabolism
*Cadmium/toxicity
Gastrointestinal Microbiome
*Milk/chemistry
Sheep
*Inflammatory Bowel Diseases/therapy/chemically induced/etiology/microbiology
Disease Models, Animal
Fecal Microbiota Transplantation
Administration, Oral

@article {pmid40243936,
year = {2025},
author = {Ma, B and Barathan, M and Ng, MH and Law, JX},
title = {Oxidative Stress, Gut Microbiota, and Extracellular Vesicles: Interconnected Pathways and Therapeutic Potentials.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40243936},
issn = {1422-0067},
support = {FF-2024-115/1//National University of Malaysia/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Oxidative Stress ; *Extracellular Vesicles/metabolism ; Animals ; Dysbiosis/metabolism ; Signal Transduction ; Reactive Oxygen Species/metabolism ; Antioxidants ; Probiotics/therapeutic use ; Inflammation ; },
abstract = {Oxidative stress (OS) and gut microbiota are crucial factors influencing human health, each playing a significant role in the development and progression of chronic diseases. This review provides a comprehensive analysis of the complex interplay between these two factors, focusing on how an imbalance between reactive oxygen species (ROS) and antioxidants leads to OS, disrupting cellular homeostasis and contributing to a range of conditions, including metabolic disorders, cardiovascular diseases, neurological diseases, and cancer. The gut microbiota, a diverse community of microorganisms residing in the gastrointestinal tract, is essential for regulating immune responses, metabolic pathways, and overall health. Dysbiosis, an imbalance in the gut microbiota composition, is closely associated with chronic inflammation, metabolic dysfunction, and various diseases. This review highlights how the gut microbiota influences and is influenced by OS, complicating the pathophysiology of many conditions. Furthermore, emerging evidence has identified extracellular vesicles (EVs) as critical facilitators of cellular crosstalk between the OS and gut microbiota. EVs also play a crucial role in signaling between the gut microbiota and host tissues, modulating immune responses, inflammation, and metabolic processes. The signaling function of EVs holds promise for the development of targeted therapies aimed at restoring microbial balance and mitigating OS. Personalized therapeutic approaches, including probiotics, antioxidants, and fecal microbiota transplantation-based strategies, can be used to address OS-related diseases and improve health outcomes. Nonetheless, further research is needed to study the molecular mechanisms underlying these interactions and the potential of innovative interventions to offer novel strategies for managing OS-related diseases and enhancing overall human health.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Oxidative Stress
*Extracellular Vesicles/metabolism
Animals
Dysbiosis/metabolism
Signal Transduction
Reactive Oxygen Species/metabolism
Antioxidants
Probiotics/therapeutic use
Inflammation

@article {pmid40243802,
year = {2025},
author = {Xiong, Y and Guo, J and Yu, W and Zeng, D and Song, C and Zhou, L and Anatolyevna, NL and Baranenko, D and Xiao, D and Zhou, Y and Lu, W},
title = {Molecular Mechanism of Microgravity-Induced Intestinal Flora Dysbiosis on the Abnormalities of Liver and Brain Metabolism.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40243802},
issn = {1422-0067},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Liver/metabolism/pathology ; *Brain/metabolism ; *Dysbiosis/metabolism/microbiology/etiology ; Mice ; *Weightlessness/adverse effects ; Male ; Space Flight ; Weightlessness Simulation/adverse effects ; Mice, Inbred C57BL ; Metabolomics/methods ; },
abstract = {Space flight has many adverse effects on the physiological functions of astronauts. Certain similarities have been observed in some physiological processes of rodents and astronauts in space, although there are also differences. These similarities make rodents helpful models for initial investigations into space-induced physiological changes. This study uses a 3D-Clinostat to simulate microgravity and explores the role of microgravity in space flight-induced liver and brain abnormalities by comparing changes in the gut microbiota, serum metabolites, and the function and physiological biochemistry of liver and brain tissues between the simulated microgravity (SMG) group mice and the wild type (WT) group mice. The study, based on hematoxylin-eosin (HE) staining, 16S sequencing technology, and non-targeted metabolomics analysis, shows that the gut tissue morphology of the SMG group mice is abnormal, and the structure of the gut microbiota and the serum metabolite profile are imbalanced. Furthermore, using PICRUST 2 technology, we have predicted the functions of the gut microbiota and serum metabolites, and the results indicate that the liver metabolism and functions (including lipid metabolism, amino acid metabolism, and sugar metabolism, etc.) of the SMG group mice are disrupted, and the brain tissue metabolism and functions (including neurotransmitters and hormone secretion, etc.) are abnormal, suggesting a close relationship between microgravity and liver metabolic dysfunction and brain dysfunction. Additionally, the high similarity in the structure of the gut microbiota and serum metabolite profile between the fecal microbiota transplant (FMT) group mice and the SMG group mice, and the physiological and biochemical differences in liver and brain tissues compared to the WT group mice, suggest that microgravity induces imbalances in the gut microbiota, which in turn triggers abnormalities in liver and brain metabolism and function. Finally, through MetaMapp analysis and Pearson correlation analysis, we found that valeric acid, a metabolite of gut microbiota, is more likely to be the key metabolite that relates to microgravity-induced gut microbiota abnormalities, disorders of amino acid and lipid metabolism, and further induced metabolic or functional disorders in the liver and brain. This study has significant practical application value for deepening the understanding of the adaptability of living organisms in the space environment.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Liver/metabolism/pathology
*Brain/metabolism
*Dysbiosis/metabolism/microbiology/etiology
Mice
*Weightlessness/adverse effects
Male
Space Flight
Weightlessness Simulation/adverse effects
Mice, Inbred C57BL
Metabolomics/methods

@article {pmid40243712,
year = {2025},
author = {Murgiano, M and Bartocci, B and Puca, P and di Vincenzo, F and Del Gaudio, A and Papa, A and Cammarota, G and Gasbarrini, A and Scaldaferri, F and Lopetuso, LR},
title = {Gut Microbiota Modulation in IBD: From the Old Paradigm to Revolutionary Tools.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40243712},
issn = {1422-0067},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Inflammatory Bowel Diseases/therapy/microbiology ; Fecal Microbiota Transplantation/methods ; Probiotics/therapeutic use ; Animals ; Prebiotics ; },
abstract = {Inflammatory bowel diseases (IBDs) are chronic inflammatory disorders primarily comprising two main conditions: ulcerative colitis and Crohn's disease. The gut microbiota's role in driving inflammation in IBD has garnered significant attention, yet the precise mechanisms through which the microbiota influences IBD pathogenesis remain largely unclear. Given the limited therapeutic options for IBD, alternative microbiota-targeted therapies-including prebiotics, probiotics, postbiotics, and symbiotics-have been proposed. While these approaches have shown promising results, microbiota modulation is still mainly considered an adjunct therapy to conventional treatments, with a demonstrated impact on patients' quality of life. Fecal microbiota transplantation (FMT), already approved for treating Clostridioides difficile infection, represents the first in a series of innovative microbiota-based therapies under investigation. Microbial biotherapeutics are emerging as personalized and cutting-edge tools for IBD management, encompassing next-generation probiotics, bacterial consortia, bacteriophages, engineered probiotics, direct metabolic pathway modulation, and nanotherapeutics. This review explores microbial modulation as a therapeutic strategy for IBDs, highlighting current approaches and examining promising tools under development to better understand their potential clinical applications in managing intestinal inflammatory disorders.},
}

Humans
*Gastrointestinal Microbiome
*Inflammatory Bowel Diseases/therapy/microbiology
Fecal Microbiota Transplantation/methods
Probiotics/therapeutic use
Animals
Prebiotics

@article {pmid40243656,
year = {2025},
author = {Li, X and Yang, W and Weng, Y and Zhao, Y and Chen, H and Chen, Y and Qiu, J and Jiang, B and Li, C and Lai, Y},
title = {Scutellarin Alleviates CCl4-Induced Liver Fibrosis by Regulating Intestinal Flora and PI3K/AKT Signaling Axis.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40243656},
issn = {1422-0067},
support = {No. 81360511//National Natural Science Foundation of China/ ; No.KY2319102140//Dali University Research and Development Fund/ ; },
mesh = {Animals ; *Apigenin/pharmacology/chemistry/therapeutic use ; *Gastrointestinal Microbiome/drug effects ; *Glucuronates/pharmacology/chemistry ; *Proto-Oncogene Proteins c-akt/metabolism ; Male ; Rats ; *Phosphatidylinositol 3-Kinases/metabolism ; *Signal Transduction/drug effects ; *Liver Cirrhosis/drug therapy/chemically induced/metabolism/pathology ; Carbon Tetrachloride/toxicity ; Rats, Sprague-Dawley ; Molecular Docking Simulation ; },
abstract = {Liver fibrosis is a pathological manifestation of chronic liver disease developing to the terminal stage, and there is a lack of effective therapeutic drugs in clinical practice. Scutellarin (SCU) is a flavonoid extracted from Erigeron breviscapus (Vaniot.) Hand.-Mazz., which has significant anti-liver-fibrosis efficacy, but its mode of action remains incompletely understood. A liver fibrosis model was built with male Sprague Dawley rats induced with the disease by CCl4 to evaluate the therapeutic effect of drugs. 16S rRNA sequencing and metabolomics were used to analyze the regulatory effects of SCU on intestinal flora and host metabolism; antibiotics were administered to eliminate gut microbiota and fecal microbiota transplantation (FMT) experiments were used to verify the mechanism. The mechanistic basis underlying SCU's hepatic anti-fibrotic effects was screened by network pharmacology combined with transcriptomics, combined with molecular docking, qPCR, and WB verification. The results showed that SCU may play an anti-liver-fibrosis role by correcting the imbalance of gut flora and regulating the linoleic acid and purine metabolic pathways. In addition, SCU can downregulate the levels of proteins and genes related to the PI3K/AKT axis. In summary, SCU alleviates liver fibrosis by reversing intestinal flora imbalance, regulating the metabolic profile, and inhibiting the PI3K/AKT axis.},
}

Animals
*Apigenin/pharmacology/chemistry/therapeutic use
*Gastrointestinal Microbiome/drug effects
*Glucuronates/pharmacology/chemistry
*Proto-Oncogene Proteins c-akt/metabolism
Male
Rats
*Phosphatidylinositol 3-Kinases/metabolism
*Signal Transduction/drug effects
*Liver Cirrhosis/drug therapy/chemically induced/metabolism/pathology
Carbon Tetrachloride/toxicity
Rats, Sprague-Dawley
Molecular Docking Simulation

@article {pmid40243472,
year = {2025},
author = {Beyoğlu, D and Idle, JR},
title = {The Microbiome and Metabolic Dysfunction-Associated Steatotic Liver Disease.},
journal = {International journal of molecular sciences},
volume = {26},
number = {7},
pages = {},
pmid = {40243472},
issn = {1422-0067},
mesh = {Humans ; *Gastrointestinal Microbiome ; Animals ; Dysbiosis/microbiology ; *Fatty Liver/microbiology/metabolism/therapy ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Liver/microbiology/metabolism/pathology ; Bile Acids and Salts/metabolism ; },
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is a condition wherein excessive fat accumulates in the liver, leading to inflammation and potential liver damage. In this narrative review, we evaluate the tissue microbiota, how they arise and their constituent microbes, and the role of the intestinal and hepatic microbiota in MASLD. The history of bacteriophages (phages) and their occurrence in the microbiota, their part in the potential causation of MASLD, and conversely, "phage therapy" for antibiotic resistance, obesity, and MASLD, are all described. The microbiota metabolism of bile acids and dietary tryptophan and histidine is defined, together with the impacts of their individual metabolites on MASLD pathogenesis. Both periodontitis and intestinal microbiota dysbiosis may cause MASLD, and how individual microorganisms and their metabolites are involved in these processes is discussed. Novel treatment opportunities for MASLD involving the microbiota exist and include fecal microbiota transplantation, probiotics, prebiotics, synbiotics, tryptophan dietary supplements, intermittent fasting, and phages or their holins and endolysins. Although FDA is yet to approve phage therapy in clinical use, there are multiple FDA-approved clinical trials, and this may represent a new horizon for the future treatment of MASLD.},
}

Humans
*Gastrointestinal Microbiome
Animals
Dysbiosis/microbiology
*Fatty Liver/microbiology/metabolism/therapy
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Liver/microbiology/metabolism/pathology
Bile Acids and Salts/metabolism

@article {pmid40243365,
year = {2025},
author = {Ismeurt-Walmsley, C and Giannoni, P and Servant, F and Mekki, L-N and Baranger, K and Rivera, S and Marin, P and Lelouvier, B and Claeysen, S},
title = {The same but different: impact of animal facility sanitary status on a transgenic mouse model of Alzheimer's disease.},
journal = {mBio},
volume = {},
number = {},
pages = {e0400124},
doi = {10.1128/mbio.04001-24},
pmid = {40243365},
issn = {2150-7511},
abstract = {UNLABELLED: The gut-brain axis has emerged as a key player in the regulation of brain function and cognitive health. Gut microbiota dysbiosis has been observed in preclinical models of Alzheimer's disease and patients. Manipulating the composition of the gut microbiota enhances or delays neuropathology and cognitive deficits in mouse models. Accordingly, the health status of the animal facility may strongly influence these outcomes. In the present study, we longitudinally analyzed the fecal microbiota composition and amyloid pathology of 5XFAD mice housed in a specific opportunistic pathogen-free (SOPF) and a conventional facility. The composition of the microbiota of 5XFAD mice after aging in conventional facility showed marked differences compared to WT littermates that were not observed when the mice were bred in SOPF facility. The development of amyloid pathology was also enhanced by conventional housing. We then transplanted fecal microbiota (FMT) from both sources into wild-type (WT) mice and measured memory performance, assessed in the novel object recognition test, in transplanted animals. Mice transplanted with microbiota from conventionally bred 5XFAD mice showed impaired memory performance, whereas FMT from mice housed in SOPF facility did not induce memory deficits in transplanted mice. Finally, 18 weeks of housing SOPF-born animals in a conventional facility resulted in the reappearance of specific microbiota compositions in 5XFAD vs WT mice. In conclusion, these results show a strong impact of housing conditions on microbiota-associated phenotypes and question the relevance of breeding preclinical models in specific pathogen-free (SPF) facilities.

IMPORTANCE: Housing conditions affect the composition of the gut microbiota. Gut microbiota of 6-month-old conventionally bred Alzheimer's mice is dysbiotic. Gut dysbiosis is absent in Alzheimer's mice housed in highly sanitized facilities. Transfer of fecal microbiota from conventionally bred mice affects cognition. Microbiota of mice housed in highly sanitized facilities has no effect on cognition.},
}

@article {pmid40243343,
year = {2025},
author = {Olesen, RH and Larsen, EB and Rubak, T and Baunwall, SMD and Paaske, SE and Gregersen, M and Foss, CH and Erikstrup, C and Krogh, CB and Ehlers, LH and Hvas, CL},
title = {Cost-Effectiveness of Hospital-at-Home and Fecal Microbiota Transplantation in Treating Older Patients With Clostridioides difficile.},
journal = {Clinical infectious diseases : an official publication of the Infectious Diseases Society of America},
volume = {},
number = {},
pages = {},
doi = {10.1093/cid/ciaf104},
pmid = {40243343},
issn = {1537-6591},
support = {NNF22OC0074080//Novo Nordisk Foundation/ ; },
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) primarily affects older patients with comorbid conditions and has a high mortality rate. Fecal microbiota transplantation (FMT) is effective and cost-effective for CDI. In a recent study, we demonstrated the clinical benefits of combining hospital-at-home care with FMT for older patients with CDI, but its cost-effectiveness remains unknown. The current study aimed to evaluate the cost-effectiveness of the intervention in patients aged ≥70 years with CDI, compared with standard treatment.

METHODS: The cost-utility analysis was conducted using data from a randomized clinical trial enrolling 217 patients, assessing the cost-effectiveness of the intervention over 90 days. Resource use was assessed from a healthcare sector perspective. Missing data were handled with proxy replacement and multiple imputation. Sensitivity analyses included probabilistic analysis, complete case analysis, adjustment of key unit prices, and a hospital perspective. A willingness-to-pay threshold was set to €22 994 or $24 863 per quality-adjusted life year (QALY).

RESULTS: In the base case analysis, the intervention was dominant, with mean cost savings of €2556 ($2764) and a mean gain of 0.004 QALY. Although resource use was higher, the intervention resulted in an average reduction of 6 hospital admission days per patient and increased odds of clinical resolution. The results remained robust across different perspectives, the exclusion of patients with missing data, and variations in hospital admission costs.

CONCLUSIONS: In patients aged ≥70 years with CDI, an intervention combining hospital-at-home care and FMT is cost-effective compared with standard treatment. The cost-effectiveness is mainly driven by fewer hospital admission days.},
}

@article {pmid40237231,
year = {2025},
author = {Saeedi, N and Pourabdolhossein, F and Dadashi, M and Suha, AJ and Janahmadi, M and Behzadi, G and Hosseinmardi, N},
title = {Faecal Microbiota Transplantation Modulates Morphine Addictive-Like Behaviours Through Hippocampal Metaplasticity.},
journal = {Addiction biology},
volume = {30},
number = {4},
pages = {e70034},
pmid = {40237231},
issn = {1369-1600},
support = {//Vice President of Research and Technology of Shahid Beheshti University of Medical Sciences/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; Male ; Rats, Wistar ; Rats ; *Morphine/pharmacology ; *Morphine Dependence/therapy/physiopathology ; *Neuronal Plasticity/drug effects/physiology ; *Hippocampus/drug effects/physiopathology ; Substance Withdrawal Syndrome ; Naloxone/pharmacology ; Gastrointestinal Microbiome ; Narcotic Antagonists/pharmacology ; Analgesics, Opioid/pharmacology ; },
abstract = {The microbiota-gut-brain axis has been implicated in the pathology of substance use disorders (SUDs). In light of the brain's capability to reorganize itself in response to intrinsic and extrinsic stimuli, opioid-induced dysbiosis is likely to contribute to addictive behaviour through modulating neuroplasticity. In this study, a faecal microbiota transplantation (FMT) from a saline-donor was performed on morphine-treated rats to evaluate the effects of gut microbiota on morphine-induced metaplasticity and addictive behaviours. Male Wistar rats were treated with subcutaneous injections of 10 mg/kg morphine sulphate every 12 h for 9 days in an effort to induce dependence. The withdrawal syndrome was precipitated by injecting naloxone (1.5 mg/kg, ip) after the final dose of morphine. The tolerance was induced by repeated morphine injections over a period of 7 days (10 mg/kg, once a day, ip). FMT was applied daily through gavage of processed faeces 1 week before and during the morphine treatment. Field potential recordings (i.e., fEPSP) were carried out to assess short-term and long-term synaptic plasticity in the CA1 area of the hippocampus following Schaffer-collateral stimulation. Animals subjected to FMT exhibited significant reductions in naloxone-precipitated withdrawal syndrome (one-way ANOVA, p < 0.05). Tolerance to the analgesic effects of morphine was not affected by FMT (two-way ANOVA, p > 0.05). Following high-frequency stimulation (HFS) to induce long-term potentiation (LTP), a greater fEPSP slope was observed in morphine-treated animals (unpaired t test, p < 0.05). FMT from saline-donor rats diminished morphine-induced augmented LTP (unpaired t test, p < 0.05). These results highlighted the alleviating effects of FMT from saline-donors on morphine-induced metaplasticity and dependence potentially by modulating the dysbiosis of gut microbiota.},
}

Animals
*Fecal Microbiota Transplantation/methods
Male
Rats, Wistar
Rats
*Morphine/pharmacology
*Morphine Dependence/therapy/physiopathology
*Neuronal Plasticity/drug effects/physiology
*Hippocampus/drug effects/physiopathology
Substance Withdrawal Syndrome
Naloxone/pharmacology
Gastrointestinal Microbiome
Narcotic Antagonists/pharmacology
Analgesics, Opioid/pharmacology

@article {pmid40237060,
year = {2025},
author = {Li, H and Lai, H and Xing, Y and Zou, S and Yang, X},
title = {Microbiota-gut-brain axis: Novel Potential Pathways for Developing Antiepileptogenic Drugs.},
journal = {Current neuropharmacology},
volume = {},
number = {},
pages = {},
doi = {10.2174/1570159X23666250414094040},
pmid = {40237060},
issn = {1875-6190},
abstract = {The treatment of epilepsy remains imperfect due to a lack of understanding of its pathogenesis. Although antiseizure medications can control most seizures, up to 30% of patients experience uncontrolled seizures, leading to refractory epilepsy. Therefore, elucidating the pathogenesis of epilepsy and exploring new avenues to design antiepileptic drugs may improve epilepsy treatment. Recent studies have identified an imbalance of the gut microbiota (GM) in both patients with epilepsy and various animal models of epilepsy. In response to this phenomenon, an increasing number of studies have focused on controlling seizures by regulating GM homeostasis, utilizing methods such as dietary restrictions, fecal microbiota transplantation, and the use of prebiotics. Surprisingly, these interventions have shown promising antiepileptic effects, suggesting that GM, through the regulatory role of the microbiota-gut-brain axis (gut-brain axis), may emerge as a novel strategy for treating epilepsy. This review aims to discuss the research progress on the relationship between GM and epilepsy, incorporating the latest clinical studies and animal experiments. We will specifically concentrate on the potential key role of the gut-brain axis in epileptogenesis, epilepsy development, and outcomes of epilepsy. Through a detailed analysis of the underlying mechanisms of the gut-brain axis, we aim to provide a more comprehensive perspective on understanding the pathophysiology of epilepsy and lay the groundwork for the development of new antiepileptic drugs in the future.},
}

@article {pmid40235083,
year = {2025},
author = {Brown, R and Barko, P and Ruiz Romero, JDJ and Williams, DA and Gochenauer, A and Nguyen-Edquilang, J and Suchodolski, JS and Pilla, R and Ganz, H and Lopez-Villalobos, N and Gal, A},
title = {The effect of lyophilised oral faecal microbial transplantation on functional outcomes in dogs with diabetes mellitus.},
journal = {The Journal of small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1111/jsap.13865},
pmid = {40235083},
issn = {1748-5827},
support = {//University of Illinois at Urbana-Champaign Companion Animal Research Grant Program/ ; },
abstract = {OBJECTIVES: We aimed to determine if oral faecal microbiota transplantation improves indices of glycaemic control, changes the faecal dysbiosis indices, alters faecal short-chain fatty acid and bile acid profiles and increases serum glucagon-like-peptide 1 concentrations in diabetic dogs.

MATERIALS AND METHODS: In this prospective randomised, placebo-controlled, double-blinded pilot study, we recruited nine diabetic dogs (five faecal microbiota transplantation and four placebo) and nine healthy controls.

RESULTS: Compared to healthy dogs, diabetic dogs had altered faecal short-chain fatty acid and bile acid profiles. In the first 30 days, the faecal microbiota transplantation group had a more rapid decline in interstitial glucose; however, the mean interstitial glucose of the faecal microbiota transplantation recipients did not differ from the placebo recipients at the end of the study. Compared with placebo, faecal microbiota transplantation recipients had a decreased 24-hour water intake at day 60 and increased faecal abundance of Faecalibacterium.

CLINICAL SIGNIFICANCE: This study provides a proof of concept for faecal microbiota transplantation in canine diabetes, and its data could inform the design of future large-scale studies. Further investigation is required to determine whether faecal microbiota transplantation would have any role as an adjunctive therapy in canine diabetes and to elucidate the mechanisms by which faecal microbiota transplantation may provide a beneficial clinical effect in canine diabetes.},
}

@article {pmid40235010,
year = {2025},
author = {Chen, M and Pan, J and Song, Y and Liu, S and Sun, P and Zheng, X},
title = {Effect of inulin supplementation in maternal fecal microbiota transplantation on the early growth of chicks.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {98},
pmid = {40235010},
issn = {2049-2618},
support = {20170204043NY2//key technology research. project of Changchun Key R&D Program, and the Outstanding Talents in Science and Technology Innovation/ ; 32472995//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Inulin/administration & dosage/pharmacology ; *Chickens/growth & development/microbiology ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome/drug effects ; Female ; Dietary Supplements ; Feces/microbiology ; Prebiotics/administration & dosage ; },
abstract = {BACKGROUND: Fecal microbial transplantation (FMT) is an important technology for treating diarrhea and enteritis. Additionally, FMT has been applied to improve productivity, alter abnormal behavior, relieve stress, and reduce burdens. However, some previous studies have reported that FMT may cause stress in acceptor animals. Inulin, a prebiotic, can promote growth, enhance immunity, and balance the gut microbiota. Currently, there are limited reports on the effects of combining FMT with inulin on early growth performance in chicks.

RESULTS: In this study, a total of 90 1-day-old chicks were randomly divided into the control group (CON), FMT group, and inulin group (INU). The CON group was fed a basic diet, whereas the FMT and INU groups received fecal microbiota transplantation and FMT with inulin treatment, respectively. Compared with the FMT and CON groups, the INU group presented significantly greater average daily gain (ADG) and average daily feed intake (ADFI) values (P < 0.05). However, the organ indices did not significantly change (P > 0.05). The ratio of the villi to crypts in the ileum significantly differed at 21 and 35 days (P < 0.05). In addition, the cecum concentrations of acetic acid and butyric acid significantly increased in the INU group (P < 0.05). In addition, gut inflammation and serum inflammation decreased in the INU group, and immune factors increased after inulin supplementation. (P < 0.05). Firmicutes and Bacteroidetes were the dominant phyla, with more than 90% of all sequences being identified as originating from these two phyla. Inulin supplementation during mother-sourced microbial transplantation significantly increased the abundance of Rikenella, Butyricicoccus, and [Ruminococcus], which contributed positively to the promotion of early intestinal health and facilitated the early growth of chicks.

CONCLUSION: The results of this study suggest that inulin supplementation in maternal fecal microbiota transplantation can effectively promote early growth and probiotic colonization, which favors the health of chicks. Video Abstract.},
}

Animals
*Inulin/administration & dosage/pharmacology
*Chickens/growth & development/microbiology
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome/drug effects
Female
Dietary Supplements
Feces/microbiology
Prebiotics/administration & dosage

@article {pmid40234859,
year = {2025},
author = {Senthilkumar, H and Arumugam, M},
title = {Gut microbiota: a hidden player in polycystic ovary syndrome.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {443},
pmid = {40234859},
issn = {1479-5876},
mesh = {Humans ; *Polycystic Ovary Syndrome/microbiology/physiopathology/therapy ; *Gastrointestinal Microbiome ; Female ; Animals ; Dysbiosis ; },
abstract = {Polycystic ovary syndrome (PCOS) is an endocrine disorder that affects reproductive-aged women worldwide, causing hormonal imbalances and ovarian dysfunction. PCOS affects metabolic health and increases the risk of obesity, insulin resistance, and cardiovascular disease, in addition to infertility. This review delves deeper into the connections of gut microbiota with PCOS pathophysiology, particularly into its impact on hormone metabolism, obesity, inflammation, and insulin resistance by way of short-chain fatty acids, lipopolysaccharides, and gut-brain axis. Studies also show that changes in the metabolic processes and immune responses are seen in changes in the gut microbiota in PCOS subjects, such as changes in the Bacteroidetes and Firmicutes groups. Some bacteria, like Escherichia and Shigella, have been associated with dysbiosis in patients with PCOS, leading to systemic inflammation and changed hormone levels, which further worsen the clinical symptoms. Therapeutic interventions targeting the gut microbiota comprise probiotics, prebiotics, and fecal microbiota transplantation; these have potential to alleviate the symptoms of PCOS. Other precision microbiome-based therapies include postbiotics, and CRISPR-Cas9 genome editing, which are relatively new avenues toward precision treatment. This complex interlink of gut microbiota and PCOS pathophysiology will open the avenues for possible treatments for hormonal imbalances and metabolic problems that characterize these complex disorders. The review here focuses on the requirement of further studies to be able to elucidate the specific pathways relating gut microbiota dysregulation to PCOS and, thus, improve microbiome-based therapies for better clinical outcomes in affected individuals.},
}

Humans
*Polycystic Ovary Syndrome/microbiology/physiopathology/therapy
*Gastrointestinal Microbiome
Female
Animals
Dysbiosis

@article {pmid40234406,
year = {2025},
author = {Sui, Y and Zhang, T and Ou, S and Li, G and Liu, L and Lu, T and Zhang, C and Cao, Y and Bai, R and Zhou, H and Zhao, X and Yuan, Y and Wang, G and Chen, H and Kong, R and Sun, B and Li, L},
title = {Statin therapy associated Lactobacillus intestinalis attenuates pancreatic fibrosis through remodeling intestinal homeostasis.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {59},
pmid = {40234406},
issn = {2055-5008},
support = {82270665//National Natural Science Foundation of China/ ; 82270666//National Natural Science Foundation of China/ ; },
mesh = {Animals ; Mice ; *Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/drug effects ; Homeostasis/drug effects ; Fibrosis ; Fecal Microbiota Transplantation ; Male ; *Pancreas/pathology/drug effects ; Macrophages/immunology ; Mice, Inbred C57BL ; CD8-Positive T-Lymphocytes/immunology ; *Intestines/microbiology/drug effects ; *Lactobacillus ; Disease Models, Animal ; *Probiotics/administration & dosage ; },
abstract = {Chronic pancreatitis (CP) is characterized by irreversible fibrotic destruction and impaired pancreatic function. CP disrupts lipid metabolism and causes the imbalance of gut microbiota which in turn exacerbates pancreatic fibrosis. Statins alter gut microbiota and exert anti-inflammatory effects, but its role in CP has not been fully elucidated. Here, we found that statins-associated higher abundance of Lactobacillus intestinalis (L.intestinalis) maintained gut homeostasis that restrained bacteria translocation from gut to the pancreas, which eventually aggravated pancreatic fibrosis through inhibiting CD8[+]T cells-dependent immunity. Fecal microbiota transplantation (FMT) or L.intestinalis administration inhibited the infiltration of CD8[+]T cells and macrophages that delayed CP progression. L.intestinalis restrained the recruitment of M1 macrophages and limited the release of Ccl2/7 in the colon, which prevented epithelial damage and epithelial barrier dysfunction through blocking Ccl2/7-Ccr1 signaling. Our findings elucidate that the utilization of statin therapy or supplementation of L.intestinalis can be potential approach for the therapies of CP.},
}

Animals
Mice
*Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use/pharmacology
*Gastrointestinal Microbiome/drug effects
Homeostasis/drug effects
Fibrosis
Fecal Microbiota Transplantation
Male
*Pancreas/pathology/drug effects
Macrophages/immunology
Mice, Inbred C57BL
CD8-Positive T-Lymphocytes/immunology
*Intestines/microbiology/drug effects
*Lactobacillus
Disease Models, Animal
*Probiotics/administration & dosage

@article {pmid40233040,
year = {2025},
author = {Pomej, K and Frick, A and Scheiner, B and Balcar, L and Pajancic, L and Klotz, A and Kreuter, A and Lampichler, K and Regnat, K and Zinober, K and Trauner, M and Tamandl, D and Gasche, C and Pinter, M},
title = {Study protocol: Fecal Microbiota Transplant combined with Atezolizumab/Bevacizumab in Patients with Hepatocellular Carcinoma who failed to achieve or maintain objective response to Atezolizumab/Bevacizumab - the FAB-HCC pilot study.},
journal = {PloS one},
volume = {20},
number = {4},
pages = {e0321189},
pmid = {40233040},
issn = {1932-6203},
mesh = {Aged ; Female ; Humans ; Male ; Middle Aged ; *Antibodies, Monoclonal, Humanized/therapeutic use/administration & dosage ; *Antineoplastic Combined Chemotherapy Protocols/therapeutic use ; *Bevacizumab/therapeutic use/administration & dosage ; *Carcinoma, Hepatocellular/therapy/drug therapy ; *Fecal Microbiota Transplantation/methods ; Gastrointestinal Microbiome ; *Liver Neoplasms/therapy/drug therapy ; Pilot Projects ; Clinical Trials, Phase II as Topic ; },
abstract = {BACKGROUND: The gut microbiota is often altered in chronic liver diseases and hepatocellular carcinoma (HCC), and increasing evidence suggests that it may influence response to cancer immunotherapy. Strategies to modulate the gut microbiome (i.e., fecal microbiota transplant (FMT)) may help to improve efficacy of immune checkpoint inhibitors (ICIs) or even overcome resistance to ICIs. Here, we describe the design and rationale of FAB-HCC, a single-center, single-arm, phase II pilot study to assess safety, feasibility, and efficacy of FMT from patients with HCC who responded to PD-(L)1-based immunotherapy or from healthy donors to patients with HCC who failed to achieve or maintain a response to atezolizumab plus bevacizumab.

METHODS: In this single-center, single-arm, phase II pilot study (ClinicalTrials.gov identifier: NCT05750030), we plan to include 12 patients with advanced HCC who failed to achieve or maintain a response to atezolizumab/bevacizumab. Patients will receive a single FMT via colonoscopy from donors with HCC who responded to PD-(L)1-based immunotherapy or from healthy individuals, followed by atezolizumab/bevacizumab every 3 weeks. The primary endpoint is safety, measured by incidence and severity of treatment-related adverse events. The main secondary endpoint is efficacy, as assessed by best radiological response according to RECISTv1.1 and mRECIST. Additional exploratory endpoints include data on the effect of FMT on recipient gut microbiota, as well as metagenomic analysis of stool samples, analyses of circulating immune cells and serum and stool proteomic, metabolomic and lipidomic signatures.

DISCUSSION: The results of this study will help to define the potential of FMT as add-on intervention in the systemic treatment of advanced HCC, with the potential to improve efficacy of immunotherapy or even overcome resistance.

TRIAL REGISTRATION: EudraCT Number: 2022-000234-42 Clinical trial registry & ID: ClinicalTrials.gov identifier: NCT05750030 (Registration date: 16.01.2023).},
}

Aged
Female
Humans
Male
Middle Aged
*Antibodies, Monoclonal, Humanized/therapeutic use/administration & dosage
*Antineoplastic Combined Chemotherapy Protocols/therapeutic use
*Bevacizumab/therapeutic use/administration & dosage
*Carcinoma, Hepatocellular/therapy/drug therapy
*Fecal Microbiota Transplantation/methods
Gastrointestinal Microbiome
*Liver Neoplasms/therapy/drug therapy
Pilot Projects
Clinical Trials, Phase II as Topic

@article {pmid40232107,
year = {2025},
author = {Ravizza, T and Volpedo, G and Riva, A and Striano, P and Vezzani, A},
title = {Intestinal microbiome alterations in pediatric epilepsy: Implications for seizures and therapeutic approaches.},
journal = {Epilepsia open},
volume = {},
number = {},
pages = {},
doi = {10.1002/epi4.70037},
pmid = {40232107},
issn = {2470-9239},
support = {PE0000006/DN.1553//National Recovery and Resilience Plan (NRRP)/ ; //AICE-FIRE/ ; },
abstract = {The intestinal microbiome plays a pivotal role in maintaining host health through its involvement in gastrointestinal, immune, and central nervous system (CNS) functions. Recent evidence underscores the bidirectional communication between the microbiota, the gut, and the brain and the impact of this axis on neurological diseases, including epilepsy. In pediatric patients, alterations in gut microbiota composition-called intestinal dysbiosis-have been linked to seizure susceptibility. Preclinical models revealed that gut dysbiosis may exacerbate seizures, while microbiome-targeted therapies, including fecal microbiota transplantation, pre/pro-biotics, and ketogenic diets, show promise in reducing seizures. Focusing on clinical and preclinical studies, this review examines the role of the gut microbiota in pediatric epilepsy with the aim of exploring its implications for seizure control and management of epilepsy. We also discuss mechanisms that may underlie mutual gut-brain communication and emerging therapeutic strategies targeting the gut microbiome as a novel approach to improve outcomes in pediatric epilepsy. PLAIN LANGUAGE SUMMARY: Reciprocal communication between the brain and the gut appears to be dysfunctional in pediatric epilepsy. The composition of bacteria in the intestine -known as microbiota- and the gastrointestinal functions are altered in children with drug-resistant epilepsy and animal models of pediatric epilepsies. Microbiota-targeted interventions, such as ketogenic diets, pre-/post-biotics administration, and fecal microbiota transplantation, improve both gastrointestinal dysfunctions and seizures in pediatric epilepsy. These findings suggest that the gut and its microbiota represent potential therapeutic targets for reducing drug-resistant seizures in pediatric epilepsy.},
}

@article {pmid40231893,
year = {2025},
author = {Vargas-Castellanos, E and Rincón-Riveros, A},
title = {Microsatellite Instability in the Tumor Microenvironment: The Role of Inflammation and the Microbiome.},
journal = {Cancer medicine},
volume = {14},
number = {8},
pages = {e70603},
pmid = {40231893},
issn = {2045-7634},
support = {C-012-2023//Hospital Universitario Mayor Méderi/ ; },
mesh = {Humans ; *Tumor Microenvironment/immunology/genetics ; *Microsatellite Instability ; *Neoplasms/genetics/microbiology/immunology/pathology ; *Inflammation/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; Animals ; Dysbiosis ; Immune Checkpoint Inhibitors/therapeutic use ; },
abstract = {BACKGROUND: Microsatellite instability (MSI) is a hallmark of DNA mismatch repair (MMR) deficiency that leads to genomic instability and increased cancer risk. The tumor microenvironment (TME) significantly influences MSI-driven tumorigenesis, and emerging evidence points to a critical role of the microbiome in shaping this complex interplay.

METHODS: This review comprehensively examines the existing literature on the intricate relationship between MSI, microbiome, and cancer development, with a particular focus on the impact of microbial dysbiosis on the TME.

RESULTS: MSI-high tumors exhibited increased immune cell infiltration owing to the generation of neoantigens. However, immune evasion mechanisms such as PD-1/CTLA-4 upregulation limit the efficacy of immune checkpoint inhibitors (ICIs) in a subset of patients. Pathobionts, such as Fusobacterium nucleatum and Bacteroides fragilis, contribute to MSI through the production of genotoxins, further promoting inflammation and oxidative stress within the TME.

CONCLUSIONS: The microbiome profoundly affects MSI-driven tumorigenesis. Modulation of the gut microbiota through interventions such as fecal microbiota transplantation, probiotics, and dietary changes holds promise for improving ICI response rates. Further research into cancer pharmacomicrobiomics, investigating the interplay between microbial metabolites and anticancer therapies, is crucial for developing personalized treatment strategies.},
}

Humans
*Tumor Microenvironment/immunology/genetics
*Microsatellite Instability
*Neoplasms/genetics/microbiology/immunology/pathology
*Inflammation/immunology/microbiology
*Gastrointestinal Microbiome/immunology
Animals
Dysbiosis
Immune Checkpoint Inhibitors/therapeutic use

@article {pmid40230225,
year = {2025},
author = {Fang, X and Zhang, Y and Huang, X and Miao, R and Zhang, Y and Tian, J},
title = {Gut microbiome research: Revealing the pathological mechanisms and treatment strategies of type 2 diabetes.},
journal = {Diabetes, obesity & metabolism},
volume = {},
number = {},
pages = {},
doi = {10.1111/dom.16387},
pmid = {40230225},
issn = {1463-1326},
support = {CI2021A01601//Scientific and Technological Innovation Project of China Academy of Chinese Medical Sciences/ ; HLCMHPP20230CZ40907//High Level Chinese Medical Hospital Promotion Project/ ; ZZ13-YQ-026//CACMS Outstanding Young Scientific and Technological Talents Program/ ; CI2021B008//Innovation Team Project of Science and Technology Innovation Engineering of China Academy of Chinese Medical Sciences/ ; 82474323//National Natural Science Foundation of China/ ; },
abstract = {The high prevalence and disability rate of type 2 diabetes (T2D) caused a huge social burden to the world. Currently, new mechanisms and therapeutic approaches that may affect this disease are being sought. With in-depth research on the pathogenesis of T2D and growing advances in microbiome sequencing technology, the association between T2D and gut microbiota has been confirmed. The gut microbiota participates in the regulation of inflammation, intestinal permeability, short-chain fatty acid metabolism, branched-chain amino acid metabolism and bile acid metabolism, thereby affecting host glucose and lipid metabolism. Interventions focusing on the gut microbiota are gaining traction as a promising approach to T2D management. For example, dietary intervention, prebiotics and probiotics, faecal microbiota transplant and phage therapy. Meticulous experimental design and choice of analytical methods are crucial for obtaining accurate and meaningful results from microbiome studies. How to design gut microbiome research in T2D and choose different machine learning methods for data analysis are extremely critical to achieve personalized precision medicine.},
}

@article {pmid40229514,
year = {2025},
author = {Du, J and Guan, Y and Zhang, E},
title = {Regulatory role of gut microbiota in immunotherapy of hepatocellular carcinoma.},
journal = {Hepatology international},
volume = {},
number = {},
pages = {},
pmid = {40229514},
issn = {1936-0541},
abstract = {BACKGROUND: The gut microbiota plays a role in triggering innate immunity and regulating the immune microenvironment (IME) of hepatocellular carcinoma (HCC) by acting on various signaling receptors and transcription factors through its metabolites and related molecules. Furthermore, there is an increasing recognition of the gut microbiota as a potential therapeutic target for HCC, given its ability to modulate the efficacy of immune checkpoint inhibitors (ICIs).

OBJECTIVE: This review will discuss the mechanisms of gut microbiota in modulating immunotherapy of HCC, the predictive value of efficacy, and the therapeutic strategies for modulating the gut microbiota in detail.

METHODS: We conducted a systematic literature search in PubMed, Embase, Scopus, Cochrane Library, China National Knowledge Infrastructure, and Wanfang Chinese databases for articles involving the influence of gut microbiota on HCC immunotherapy.

RESULTS: The mechanisms underlying the effect of gut microbiota on HCC immunotherapy include gut-liver axis, tumor immune microenvironment (TIME), and antibodies. Patients who benefit from ICIs exhibit a higher abundance of gut microbiota. Antibiotics, fecal microbiota transplantation (FMT), probiotics, and prebiotics are effective methods to regulate gut microbiota.

CONCLUSION: The strong connection between the liver and gut will provide numerous opportunities for the development of microbiome-based diagnostics, treatments, or prevention strategies for HCC patients.},
}

@article {pmid40229213,
year = {2025},
author = {Hoops, SL and Moutsoglou, D and Vaughn, BP and Khoruts, A and Knights, D},
title = {Metagenomic source tracking after microbiota transplant therapy.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2487840},
doi = {10.1080/19490976.2025.2487840},
pmid = {40229213},
issn = {1949-0984},
mesh = {Humans ; *Metagenomics/methods ; *Fecal Microbiota Transplantation ; *Gastrointestinal Microbiome/genetics ; Colitis, Ulcerative/therapy/microbiology ; *Bacteria/genetics/classification/isolation & purification ; RNA, Ribosomal, 16S/genetics ; *Metagenome ; Bayes Theorem ; Feces/microbiology ; },
abstract = {Reliable engraftment assessment of donor microbial communities and individual strains is an essential component of characterizing the pharmacokinetics of microbiota transplant therapies (MTTs). Recent methods for measuring donor engraftment use whole-genome sequencing and reference databases or metagenome-assembled genomes (MAGs) to track individual bacterial strains but lack the ability to disambiguate DNA that matches both donor and patient microbiota. Here, we describe a new, cost-efficient analytic pipeline, MAGEnTa, which compares post-MTT samples to a database comprised MAGs derived directly from donor and pre-treatment metagenomic data, without relying on an external database. The pipeline uses Bayesian statistics to determine the likely sources of ambiguous reads that align with both the donor and pre-treatment samples. MAGEnTa recovers engrafted strains with minimal type II error in a simulated dataset and is robust to shallow sequencing depths in a downsampled dataset. Applying MAGEnTa to a dataset from a recent MTT clinical trial for ulcerative colitis, we found the results to be consistent with 16S rRNA gene SourceTracker analysis but with added MAG-level specificity. MAGEnTa is a powerful tool to study community and strain engraftment dynamics in the development of MTT-based treatments that can be integrated into frameworks for functional and taxonomic analysis.},
}

Humans
*Metagenomics/methods
*Fecal Microbiota Transplantation
*Gastrointestinal Microbiome/genetics
Colitis, Ulcerative/therapy/microbiology
*Bacteria/genetics/classification/isolation & purification
RNA, Ribosomal, 16S/genetics
*Metagenome
Bayes Theorem
Feces/microbiology

@article {pmid40227949,
year = {2025},
author = {He, Y and Cai, J and Xie, X and Zhang, X and Qu, L and Liu, J and Cao, Y},
title = {Dimethyl Itaconate Alleviates Escherichia coli-Induced Endometritis Through the Guanosine-CXCL14 Axis via Increasing the Abundance of norank_f_Muribaculaceae.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2414792},
doi = {10.1002/advs.202414792},
pmid = {40227949},
issn = {2198-3844},
support = {2023YFD1801100//Key Technologies Research and Development Program of Anhui Province/ ; },
abstract = {Endometritis, a prevalent reproductive system disease with high incidence, leads to reproductive dysfunction in humans and animals, causing huge economic losses. Dimethyl itaconate (DI) has been demonstrated to exert protective effects in multiple inflammatory diseases. Nevertheless, the efficacy of DI in preventing endometritis and the role played by the gut microbiota remain unknown. In this study, it is found that DI ameliorated Escherichia coli (E. coli) induced endometritis in mice. The protective effect is abolished by antibiotic-induced depletion of the gut microbiota, and fecal microbiota transplantation (FMT) from DI-treated mice to recipient mice ameliorated E. coli-induced endometritis. Integrative multiomics reveals that DI promotes the multiplication of norank_f_Muribaculaceae in vivo, and supplementation of Muribaculum intestinale (DSM 28989), which belongs to the norank_f_Muribaculaceae genus, upregulates the level of guanosine in the uterus. Mechanistically, the protective effect of guanosine in endometritis is mediated by activating the expression of CXCL14 in uterine epithelial cells. Moreover, the antibody-neutralizing experiment of CXCL14 eliminated this protective effect. In conclusion, this study elucidates the significant role of the gut microbiota and its metabolites in the protection of DI against endometritis, and provides new evidence for the regulation of distal organ by the gut microbiota.},
}

@article {pmid40223320,
year = {2025},
author = {Yaghmaei, H and Taromiha, A and Nojoumi, SA and Soltanipur, M and Shahshenas, S and Rezaei, M and Mirhosseini, SM and Hosseini, SM and Siadat, SD},
title = {Role of Gut-Liver Axis in Non-Alcoholic Fatty Liver Disease.},
journal = {Iranian biomedical journal},
volume = {29},
number = {1 & 2},
pages = {1-8},
doi = {10.61186/ibj.4212},
pmid = {40223320},
issn = {2008-823X},
mesh = {*Non-alcoholic Fatty Liver Disease/microbiology ; Humans ; *Gastrointestinal Microbiome ; Animals ; *Liver/pathology/microbiology/metabolism ; Dysbiosis ; },
abstract = {Non-alcoholic fatty liver disease has emerged as a significant global health problem, mainly due to the increasing prevalence of obesity and metabolic syndrome. The gut microbiota plays an essential role in the development of NAFLD through the gut-liver axis. Dysbiosis of the GM is associated with the pathogenesis of NAFLD. Dietary choices and other lifestyle factors influence the composition of the GM and contribute to the development of NAFLD. At the phylum level, individuals with NAFLD show an increased level in Actinobacteria and Firmicutes, while Verrucomicrobia, Thermus, Proteobacteria, Lentiphaerae, and Fusobacteria are found to be decreased. Several genera, including Faecalibacterium and Akkermansia, exhibit alterations in NAFLD and are linked to disease progression. Modulating the GM through prebiotics, probiotics, or fecal microbiota transplantation represents a promising therapeutic strategy for NAFLD. This review summarizes the current understanding of GM changes in NAFLD, focusing on findings from both human and animal studies.},
}

*Non-alcoholic Fatty Liver Disease/microbiology
Humans
*Gastrointestinal Microbiome
Animals
*Liver/pathology/microbiology/metabolism
Dysbiosis

@article {pmid40221450,
year = {2025},
author = {Kim, KS and Noh, J and Kim, BS and Koh, H and Lee, DW},
title = {Refining microbiome diversity analysis by concatenating and integrating dual 16S rRNA amplicon reads.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {57},
pmid = {40221450},
issn = {2055-5008},
support = {RS-2021-NR056579//National Research Foundation of Korea (NRF)/ ; RS-2023-KH141436//Ministry of Health and Welfare (Ministry of Health, Welfare and Family Affairs)/ ; 200118770//Ministry of Trade, Industry and Energy (Ministry of Trade, Industry and Energy, Korea)/ ; },
mesh = {*RNA, Ribosomal, 16S/genetics ; Humans ; *Gastrointestinal Microbiome/genetics ; *Bacteria/classification/genetics/isolation & purification ; *Metagenomics/methods ; Sequence Analysis, DNA/methods ; Metagenome ; Colitis, Ulcerative/microbiology ; DNA, Bacterial/genetics ; Republic of Korea ; Phylogeny ; Feces/microbiology ; Biodiversity ; High-Throughput Nucleotide Sequencing ; },
abstract = {Understanding the role of human gut microbiota in health and disease requires insights into its taxonomic composition and functional capabilities. This study evaluates whether concatenating paired-end reads enhances data output for gut microbiome analysis compared to the merging approach across various regions of the 16S rRNA gene. We assessed this approach in both mock communities and Korean cohorts with or without ulcerative colitis. Our results indicate that using the direct joining method for the V1-V3 or V6-V8 regions improves taxonomic resolution compared to merging paired-end reads (ME) in post-sequencing data. While predicting microbial function based on 16S rRNA sequencing has inherent limitations, integrating sequencing reads from both the V1-V3 and V6-V8 regions enhanced functional predictions. This was confirmed by whole metagenome sequencing (WMS) of Korean cohorts, where our approach improved taxa detection that was lost using the ME method. Thus, we propose that the integrated dual 16S rRNA sequencing technique serves as a valuable tool for microbiome research by bridging the gap between amplicon sequencing and WMS.},
}

*RNA, Ribosomal, 16S/genetics
Humans
*Gastrointestinal Microbiome/genetics
*Bacteria/classification/genetics/isolation & purification
*Metagenomics/methods
Sequence Analysis, DNA/methods
Metagenome
Colitis, Ulcerative/microbiology
DNA, Bacterial/genetics
Republic of Korea
Phylogeny
Feces/microbiology
Biodiversity
High-Throughput Nucleotide Sequencing

@article {pmid40220715,
year = {2025},
author = {Chen, Y and Chen, Z and Liang, L and Li, J and Meng, L and Yuan, W and Xie, B and Zhang, X and Feng, L and Jia, Y and Fu, Z and Su, P and Tong, Z and Zhong, J and Liu, X},
title = {Multi-kingdom gut microbiota dysbiosis is associated with the development of pulmonary arterial hypertension.},
journal = {EBioMedicine},
volume = {115},
number = {},
pages = {105686},
doi = {10.1016/j.ebiom.2025.105686},
pmid = {40220715},
issn = {2352-3964},
abstract = {BACKGROUND: Gut microbiota dysbiosis has been implicated in pulmonary arterial hypertension (PAH). However, the exact roles and underlying mechanisms of multi-kingdom gut microbiota, including bacteria, archaea, and fungi, in PAH remain largely unclear.

METHODS: The shotgun metagenomics was used to analyse multi-kingdom gut microbial communities in patients with idiopathic PAH (IPAH) and healthy controls. Furthermore, fecal microbiota transplantation (FMT) was performed to transfer gut microbiota from IPAH patients or monocrotaline (MCT)-PAH rats to normal rats and from normal rats to MCT-PAH rats.

FINDINGS: Gut microbiota analysis revealed substantial alterations in the bacterial, archaeal, and fungal communities in patients with IPAH compared with healthy controls. Notably, FMT from IPAH patients or MCT-PAH rats induced PAH phenotypes in recipient rats. More intriguingly, FMT from normal rats to MCT-PAH rats significantly ameliorated PAH symptoms; restored gut bacteria, archaea, and fungi composition; and shifted the plasma metabolite profiles of MCT-PAH rats toward those of normal rats. In parallel, RNA-sequencing analysis demonstrated the expression of genes involved in key signalling pathways related to PAH. A panel of multi-kingdom markers exhibited superior diagnostic accuracy compared with single-kingdom panels for IPAH.

INTERPRETATION: Our findings established an association between multi-kingdom gut microbiota dysbiosis and PAH, thereby indicating the therapeutic potential of FMT in PAH. More importantly, apart from gut bacteria, gut archaea and fungi were also significantly associated with PAH pathogenesis, highlighting their indispensable role in PAH.

FUNDING: This work was supported by Noncommunicable Chronic Diseases-National Science and Technology Major Projects No. 2024ZD0531200, No. 2024ZD0531201 (Research on Prevention and Treatment of Cancer, Cardiovascular and Cerebrovascular Diseases, Respiratory Diseases, and Metabolic Diseases), the National Natural Science Foundation of China of China (No. 82170302, 82370432), Financial Budgeting Project of Beijing Institute of Respiratory Medicine (Ysbz2025004, Ysbz2025007), National clinical key speciality construction project Cardiovascular Surgery, Reform and Development Program of Beijing Institute of Respiratory Medicine (Ggyfz202417, Ggyfz202501), Clinical Research Incubation Program of Beijing Chaoyang Hospital Affiliated to Capital Medical University (CYFH202209).},
}

@article {pmid40220396,
year = {2025},
author = {Kou, G and Yao, S and Ullah, A and Fang, S and Guo, E and Bo, Y},
title = {Polystyrene microplastics impair brown and beige adipocyte function via the gut microbiota-adipose tissue crosstalk in high-fat diet mice.},
journal = {Journal of hazardous materials},
volume = {492},
number = {},
pages = {138225},
doi = {10.1016/j.jhazmat.2025.138225},
pmid = {40220396},
issn = {1873-3336},
abstract = {BACKGROUND: Microplastics (MPs) are pervasive in the environment and food. The potential health hazards of this emerging pollutant have raised significant concerns in recent years. However, the underlying mechanism by which MPs have any impact on brown and beige adipocytes in the context of obesity is yet to be investigated.

METHODS: The C57BL/6 J mice were randomly assigned to the HFD and HFD+MPs group for 12 weeks of exposure to explore the differences in brown and beige adipocyte function. The gut microbiota analysis, fecal microbiota transplantation and metabolomic profiling were carried out to further determine its potential mechanism.

RESULTS: The present work demonstrated that high-fat diet mice accumulate lipids and have reduced energy expenditure after three months of oral administration of MPs. In addition to escalating intestinal dysbiosis, exposing HFD mice to MPs induces thermogenic dysfunction in inguinal white adipose tissue and brown adipose tissue. Following the fecal microbiota transplantation, the accumulation of lipids and dysfunction in energy expenditure within the microbiota of recipient mice further elucidated the inhibitory effect of MPs.

CONCLUSIONS: Our results suggest that MPs induced the thermogenic dysfunction of BAT and iWAT by affecting gut microbiota composition. The present study highlights the mechanisms by which MPs produce thermogenic dysfunction in BAT and iWAT and disruption in the gastrointestinal microbiota.},
}

@article {pmid40220293,
year = {2025},
author = {Damiani, F and Giuliano, MG and Cornuti, S and Putignano, E and Tognozzi, A and Suckow, V and Kalscheuer, VM and Pizzorusso, T and Tognini, P},
title = {Multi-site investigation of gut microbiota in CDKL5 deficiency disorder mouse models: Targeting dysbiosis to improve neurological outcomes.},
journal = {Cell reports},
volume = {44},
number = {4},
pages = {115546},
doi = {10.1016/j.celrep.2025.115546},
pmid = {40220293},
issn = {2211-1247},
abstract = {Cyclin-dependent kinase-like 5 (CDKL5) deficiency disorder (CDD) is a rare neurodevelopmental disorder often associated with gastrointestinal (GI) issues and subclinical immune dysregulation, suggesting a link to the gut microbiota. We analyze the fecal microbiota composition in two CDKL5 knockout (KO) mouse models at postnatal days (P) 25, 32 (youth), and 70 (adulthood), revealing significant microbial imbalances, particularly during juvenile stages. To investigate the role of the intestinal microbiota in CDD and assess causality, we administer antibiotics, which lead to improved visual cortical responses and reduce hyperactivity. Additionally, microglia morphology changes, indicative of altered surveillance and activation states, are reversed. Strikingly, fecal transplantation from CDKL5 KO to wild-type (WT) recipient mice successfully transfers both visual response deficits and hyperactive behavior. These findings show that gut microbiota alterations contribute to the severity of neurological symptoms in CDD, shedding light on the interplay between microbiota, microglia, and neurodevelopmental outcomes.},
}

@article {pmid40219707,
year = {2025},
author = {Li, M and Bao, Y and Ren, J and Wei, W and Yu, X and He, X and Gulisima, M and Sheng, L and Zheng, N and Wan, J and Zhou, H and Zhao, L and Li, H},
title = {Aged Gut Microbiota Contributes to Cognitive Impairment and Hippocampal Synapse Loss in Mice.},
journal = {Aging cell},
volume = {},
number = {},
pages = {e70064},
doi = {10.1111/acel.70064},
pmid = {40219707},
issn = {1474-9726},
support = {21XD1403500//Shanghai Excellent Academic Leaders Program/ ; //"Youth Qi Huang Scholar" by State Administration of TCM/ ; 2021YFE0111800//2021 UK-China Health and Ageing Flagship Challenge/ ; 81871098//National Natural Science Foundation of China/ ; },
abstract = {Gut microbiota alteration during the aging process serves as a causative factor for aging-related cognitive decline, which is characterized by the early hallmark, hippocampal synaptic loss. However, the impact and mechanistic role of gut microbiota in hippocampal synapse loss during aging remains unclear. Here, we observed that the fecal microbiota of naturally aged mice successfully transferred cognitive impairment and hippocampal synapse loss to young recipients. Multi-omics analysis revealed that aged gut microbiota was characterized with obvious change in Bifidobacterium pseudolongum (B.p) and metabolite of tryptophan, indoleacetic acid (IAA) in the periphery and brain. These features were also reproduced in young recipients that were transplanted with aged gut microbiota. Fecal B.p abundance was reduced in patients with cognitive impairment compared to healthy subjects and showed a positive correlation with cognitive scores. Microbiota transplantation from patients who had fewer B.p abundances yielded worse cognitive behavior in mice than those with higher B.p abundances. Meanwhile, supplementation of B.p was capable of producing IAA and enhancing peripheral and brain IAA bioavailability, as well as improving cognitive behaviors and microglia-mediated synapse loss in 5 × FAD transgenic mice. IAA produced from B.p was shown to prevent microglia engulfment of synapses in an aryl hydrocarbon receptor-dependent manner. This study reveals that aged gut microbiota -induced cognitive decline and microglia-mediated synapse loss that is, at least partially, due to the deficiency in B.p and its metabolite, IAA. It provides a proof-of-concept strategy for preventing neurodegenerative diseases by modulating gut probionts and their tryptophan metabolites.},
}

@article {pmid40219669,
year = {2025},
author = {Murray, J and Kefayat, A and Finlayson, M and Seenan, JP and Hsu, R and Din, S},
title = {RCPE in association with the American College of Gastroenterology and the Scottish Society of Gastroenterology - Gastroenterology: A global perspective.},
journal = {The journal of the Royal College of Physicians of Edinburgh},
volume = {},
number = {},
pages = {14782715251332318},
doi = {10.1177/14782715251332318},
pmid = {40219669},
issn = {2042-8189},
abstract = {On 6 November 2024, the Royal College of Physicians of Edinburgh (RCPE) hosted its annual gastroenterology symposium, marking the first collaboration with the American College of Gastroenterology (ACG) and the Scottish Society of Gastroenterology (SSG). The event addressed key global challenges in gastroenterology, including obesity, liver disease, inflammatory bowel disease (IBD), the gut microbiome, endoscopy quality and artificial intelligence (AI) applications. Discussions emphasised the growing burden of metabolic dysfunction-associated steatotic liver disease (MASLD), with promising pharmacologic and endoscopic interventions emerging. Advances in microbiome-targeted therapies, including faecal microbiota transplantation (FMT), were explored for recurrent Clostridium difficile infection and IBD. Professor David Rubin delivered the esteemed Sir Stanley Davidson lecture, highlighting the era of disease modification in IBD, emphasising early intervention and personalised treatment strategies. The symposium also addressed the role of AI in improving endoscopic detection rates and optimising resource allocation. This international collaboration underscored the importance of a multidisciplinary approach to tackling global digestive diseases, integrating clinical innovation, policy interventions and technological advancements. The event fostered knowledge exchange among global experts, aiming to advance patient care and improve long-term outcomes in gastroenterology.},
}

@article {pmid40218893,
year = {2025},
author = {Młynarska, E and Barszcz, E and Budny, E and Gajewska, A and Kopeć, K and Wasiak, J and Rysz, J and Franczyk, B},
title = {The Gut-Brain-Microbiota Connection and Its Role in Autism Spectrum Disorders.},
journal = {Nutrients},
volume = {17},
number = {7},
pages = {},
pmid = {40218893},
issn = {2072-6643},
mesh = {Humans ; *Autism Spectrum Disorder/microbiology/therapy ; *Gastrointestinal Microbiome/physiology ; Dysbiosis/complications/microbiology ; *Brain/microbiology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; *Brain-Gut Axis ; },
abstract = {Autism spectrum disorder (ASD) is a group of complex neurodevelopmental conditions with a heterogeneous and multifactorial etiology that is not yet fully understood. Among the various factors that may contribute to ASD development, alterations in the gut microbiota have been increasingly recognized. Microorganisms in the gastrointestinal tract play a crucial role in the gut-brain axis (GBA), affecting nervous system development and behavior. Dysbiosis, or an imbalance in the microbiota, has been linked to both behavioral and gastrointestinal (GI) symptoms in individuals with ASD. The microbiota interacts with the central nervous system through mechanisms such as the production of short-chain fatty acids (SCFAs), the regulation of neurotransmitters, and immune system modulation. Alterations in its composition, including reduced diversity or an overabundance of specific bacterial taxa, have been associated with the severity of ASD symptoms. Dietary modifications, such as gluten-free or antioxidant-rich diets, have shown potential for improving gut health and alleviating behavioral symptoms. Probiotics, with their anti-inflammatory properties, may support neural health and reduce neuroinflammation. Fecal microbiota transplantation (FMT) is being considered, particularly for individuals with persistent GI symptoms. It has shown promising outcomes in enhancing microbial diversity and mitigating GI and behavioral symptoms. However, its limitations should be considered, as discussed in this narrative review. Further research is essential to better understand the long-term effects and safety of these therapies. Emphasizing the importance of patient stratification and phenotype characterization is crucial for developing personalized treatment strategies that account for individual microbiota profiles, genetic predispositions, and coexisting conditions. This approach could lead to more effective interventions for individuals with ASD. Recent findings suggest that gut microbiota may play a key role in innovative therapeutic approaches to ASD management.},
}

Humans
*Autism Spectrum Disorder/microbiology/therapy
*Gastrointestinal Microbiome/physiology
Dysbiosis/complications/microbiology
*Brain/microbiology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
*Brain-Gut Axis

@article {pmid40216789,
year = {2025},
author = {Shekarriz, S and Szamosi, JC and Whelan, FJ and Lau, JT and Libertucci, J and Rossi, L and Fontes, ME and Wolfe, M and Lee, CH and Moayyedi, P and Surette, MG},
title = {Detecting microbial engraftment after FMT using placebo sequencing and culture enriched metagenomics to sort signals from noise.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {3469},
pmid = {40216789},
issn = {2041-1723},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Metagenomics/methods ; *Colitis, Ulcerative/therapy/microbiology ; *Gastrointestinal Microbiome/genetics ; Feces/microbiology ; Male ; Female ; Placebos ; Adult ; Middle Aged ; },
abstract = {Fecal microbiota transplantation (FMT) has shown efficacy for the treatment of ulcerative colitis but with variable response between patients and trials. The mechanisms underlying FMT's therapeutic effects remains poorly understood but is generally assumed to involve engraftment of donor microbiota into the recipient's microbiome. Reports of microbial engraftment following FMT have been inconsistent between studies. Here, we investigate microbial engraftment in a previous randomized controlled trial (NCT01545908), in which FMT was sourced from a single donor, using amplicon-based profiling, shotgun metagenomics, and culture-enriched metagenomics. Placebo samples were included to estimate engraftment noise, and a significant level of false-positive engraftment was observed which confounds the prediction of true engraftment. We show that analyzing engraftment across multiple patients from a single donor enhances the accuracy of detection. We identified a unique set of genes engrafted in responders to FMT which supports strain displacement as the primary mechanism of engraftment in our cohort.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Metagenomics/methods
*Colitis, Ulcerative/therapy/microbiology
*Gastrointestinal Microbiome/genetics
Feces/microbiology
Male
Female
Placebos
Adult
Middle Aged

@article {pmid40216297,
year = {2025},
author = {Tanabe, M and Kunisawa, K and Saito, I and Ojika, H and Saito, K and Nabeshima, T and Mouri, A},
title = {High-cellulose diet ameliorates cognitive impairment by modulating gut microbiota and metabolic pathways in mice.},
journal = {The Journal of nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tjnut.2025.04.004},
pmid = {40216297},
issn = {1541-6100},
abstract = {BACKGROUND: Nutrition is a key factor in cognitive function, and safe dietary interventions are promising to prevent cognitive impairment in pediatric psychiatric disorders. We previously demonstrated that childhood social isolation (SI) stress affects colonic function, leading to cognitive impairment. Cellulose, an insoluble dietary fiber, shows benefits to intestinal health, but its potential impact on cognitive impairment has not been explored.

OBJECTIVES: This study investigated whether a high-cellulose diet ameliorates cognitive impairment induced by SI through modulation of gut microbiota and metabolic pathways.

METHODS: C57BL/6J male mice (3 weeks old; n=10-15/group) were randomly divided into two groups: individually housed (SI) group and housed five mice per cage (GH) group. Each group received either a normal diet (5% cellulose) or a high-cellulose diet (30% cellulose) for 5 weeks daily until the end of the behavioral testing. We evaluated behavior abnormalities, gut microbiota composition, and metabolites, and performed two-way ANOVA.

RESULTS: Intake of a high-cellulose diet ameliorated cognitive impairment, including decreased time spent in a novel location of SI mice in novel object location test (NOLT; +30%; p < 0.01) with reduction of Iba-1 positive cells, microglia, in the hippocampus (-33%; p < 0.05). The high-cellulose diet indicated significant difference in gut microbiota clustering plots (p < 0.01) and enhanced the variation in malate-aspartate shuttle pathways in SI mice (p < 0.01). Notably, fecal microbiota transplantation (FMT) from SI mice fed a high-cellulose diet after antibiotic treatment, replicated amelioration of cognitive impairment in NOLT (+46%; p < 0.01). Additionally, the FMT replicated a decrease of Iba-1 positive cells indicating suppressed hippocampal microglial activation (-52%; p < 0.01), and enhanced the variation in malate-aspartate shuttle pathways (p < 0.01).

CONCLUSIONS: These findings suggest that a high-cellulose diet may ameliorate pediatric-specific cognitive impairment through modulation of the gut microbiota and metabolic pathways.},
}

@article {pmid40211390,
year = {2025},
author = {Wang, Z and Gao, X and Ji, H and Shao, M and Ni, B and Fei, S and Sun, L and Chen, H and Tan, R and Du, M and Gu, M},
title = {Characterization of gut microbiota and metabolites in renal transplant recipients during COVID-19 and prediction of one-year allograft function.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {420},
pmid = {40211390},
issn = {1479-5876},
support = {82170769//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Kidney Transplantation ; *COVID-19/metabolism/microbiology/complications ; *Gastrointestinal Microbiome/physiology ; Female ; Male ; Middle Aged ; Adult ; *Metabolome ; SARS-CoV-2 ; Allografts ; Transplant Recipients ; Feces/microbiology ; Aged ; },
abstract = {BACKGROUND: The gut-lung-kidney axis is pivotal in immune-related kidney diseases, with gut dysbiosis potentially exacerbating the severity of Coronavirus disease 2019 (COVID-19) in recipients of kidney transplant. This study aimed to characterize the gut microbiome and metabolome in renal transplant recipients with COVID-19 pneumonia over a one-year follow-up period.

METHODS: A total of 30 renal transplant recipients were enrolled, comprising 17 with COVID-19 pneumonia, six with mild COVID-19, and seven without COVID-19. Fecal samples were collected at the onset of infection for gut microbiome and metabolome analysis. Generalized Estimating Equations (GEE) model and Latent Class Growth Mixed Model (LCGMM) were employed to dissect the relationships among clinical characteristics, laboratory tests, and gut microbiota and metabolites.

RESULTS: Four microbial phyla (Deferribacteres, TM7, Fusobacteria, and Gemmatimonadetes) and 13 genera were significantly enriched across three recipients groups, correlating with baseline inflammatory response and allograft function. Additionally, 52 differentially expressed metabolites were identified, with seven significantly correlating with eight altered microbiota genera. LCGMM revealed two distinct classes of recipients, with those suffering from COVID-19 pneumonia exhibiting significantly elevated serum creatinine (Scr) trajectories over the one-year period. GEE further identified 12 genera and 181 metabolites closely associated with these trajectories; a multivariable model incorporating gut metabolites of 1-Caffeoylquinic Acid and PMK was found to effectively predict one-year allograft function.

CONCLUSIONS: Our study indicates a possible interaction between the composition of the gut microbiota and metabolites community and COVID-19 in renal transplant recipients, particularly in relation to disease severity and the prediction of one-year allograft function.},
}

Humans
*Kidney Transplantation
*COVID-19/metabolism/microbiology/complications
*Gastrointestinal Microbiome/physiology
Female
Male
Middle Aged
Adult
*Metabolome
SARS-CoV-2
Allografts
Transplant Recipients
Feces/microbiology
Aged

@article {pmid40211191,
year = {2025},
author = {Li, A and Costello, SP and Bryant, RV and Haylock-Jacobs, S and Haifer, C and Lee, C and Yeung, D and Giri, P and Blunt, D and Bowen, JB and Ryan, FJ and Yong, A and Wardill, HR},
title = {A study protocol for a double-blinded, randomised, placebo-controlled trial on the use of encapsulated FMT for reducing the side effects of HSCT: the HSCT-BIOME study.},
journal = {BMC cancer},
volume = {25},
number = {1},
pages = {656},
pmid = {40211191},
issn = {1471-2407},
support = {#2021/81-QA25313//Hospital Research Foundation/ ; 2033529//National Health and Medical Research Council/ ; },
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/adverse effects/methods ; Double-Blind Method ; *Fecal Microbiota Transplantation/methods/adverse effects ; Gastrointestinal Microbiome ; Adult ; Female ; Male ; *Hematologic Neoplasms/therapy ; Randomized Controlled Trials as Topic ; Middle Aged ; Diarrhea/etiology/prevention & control ; Transplantation, Autologous ; Young Adult ; },
abstract = {BACKGROUND: The composition of the gut microbiota both prior to and after haematopoietic stem cell transplantation (HSCT) is increasingly implicated in the outcomes of HSCT, including infections, poor immune reconstitution and disease relapse. Faecal microbiota transplantation (FMT) offers a potential strategy of supporting the gut microbiota and improve HSCT outcomes. Although FMT has been investigated in HSCT recipients, it has largely been evaluated therapeutically for indications such as infection, or once immunocompetency is regained.

METHODS: Peri-HSCT FMT (i.e. before and after HSCT) will be administered to eligible participants (adults undergoing autologous HSCT for a haematological malignancy) over two courses, with the first delivered immediately prior to conditioning and the second starting when ANC > 0.8. Following an open-label, safety run in (N = 5), peri-HSCT FMT will be evaluated for its efficacy in 51 participants, randomised 2:1 to FMT or placebo. The primary outcome is the proportion of participants who develop severe gastrointestinal toxicity defined by 3 consecutive days of severe diarrhoea (Bristol Stool Chart 6+), at a frequency of 4 + bowel movements/day within 3 weeks of HSCT. Safety is defined as the incidence of treatment-emergent adverse events (TE-AEs). Tolerability is defined as the incidence of TE-AEs and adherence to FMT.

DISCUSSION: The HSCT-BIOME study is a multi-centre, double-blind, randomised placebo-controlled trial designed to determine the tolerability, safety and efficacy of orally-administered encapsulated FMT to promote the stability of the gastrointestinal microenvironment for HSCT recipients. Peri-HSCT delivered FMT is hypothesised to promote microbial composition both before and following HSCT. Thus, the study will determine if administration of FMT post-HSCT during the neutropenic phase will enhance efficacy.

TRIAL REGISTRATION: ACTRN12624001104549. Date of registration: September 19, 2024 (prospectively registered).},
}

Humans
*Hematopoietic Stem Cell Transplantation/adverse effects/methods
Double-Blind Method
*Fecal Microbiota Transplantation/methods/adverse effects
Gastrointestinal Microbiome
Adult
Female
Male
*Hematologic Neoplasms/therapy
Randomized Controlled Trials as Topic
Middle Aged
Diarrhea/etiology/prevention & control
Transplantation, Autologous
Young Adult

@article {pmid40210439,
year = {2025},
author = {Smith, BJ and Zhao, C and Dubinkina, V and Jin, X and Zahavi, L and Shoer, S and Moltzau-Anderson, J and Segal, E and Pollard, KS},
title = {Accurate estimation of intraspecific microbial gene content variation in metagenomic data with MIDAS v3 and StrainPGC.},
journal = {Genome research},
volume = {},
number = {},
pages = {},
doi = {10.1101/gr.279543.124},
pmid = {40210439},
issn = {1549-5469},
abstract = {Metagenomics has greatly expanded our understanding of the human gut microbiome by revealing a vast diversity of bacterial species within and across individuals. Even within a single species, different strains can have highly divergent gene content, affecting traits such as antibiotic resistance, metabolism, and virulence. Methods that harness metagenomic data to resolve strain-level differences in functional potential are crucial for understanding the causes and consequences of this intraspecific diversity. The enormous size of pangenome references, strain mixing within samples, and inconsistent sequencing depth present challenges for existing tools that analyze samples one at a time. To address this gap, we updated the MIDAS pangenome profiler, now released as version 3, and developed StrainPGC, an approach to strain-specific gene content estimation that combines strain tracking and correlations across multiple samples. We validate our integrated analysis using a complex synthetic community of strains from the human gut and find that StrainPGC outperforms existing approaches. Analyzing a large, publicly available metagenome collection from inflammatory bowel disease patients and healthy controls, we catalog the functional repertoires of thousands of strains across hundreds of species, capturing extensive diversity missing from reference databases. Finally, we apply StrainPGC to metagenomes from a clinical trial of fecal microbiota transplantation for the treatment of ulcerative colitis. We identify two Escherichia coli strains, from two different donors, that are both frequently transmitted to patients but have notable differences in functional potential. StrainPGC and MIDAS v3 together enable precise, intraspecific pangenomic investigations using large collections of metagenomic data without microbial isolation or de novo assembly.},
}

@article {pmid40210198,
year = {2025},
author = {Fu, M and Wang, QW and Liu, YR and Chen, SJ},
title = {The role of the three major intestinal barriers in ulcerative colitis in the elderly.},
journal = {Ageing research reviews},
volume = {108},
number = {},
pages = {102752},
doi = {10.1016/j.arr.2025.102752},
pmid = {40210198},
issn = {1872-9649},
abstract = {With the unprecedented pace of global population aging, there has been a parallel epidemiological shift marked by increasing incidence rates of ulcerative colitis (UC) in geriatric populations, imposing a substantial disease burden on healthcare systems globally. The etiopathogenesis of UC in the elderly remains poorly delineated, while current therapeutic strategies require further optimization to accommodate the unique pathophysiological characteristics of elderly patients. This review systematically elucidates the three barrier dysfunction - encompassing the gut microbiota ecosystem, mucosal epithelial integrity, and immunoregulatory network - that collectively drives UC pathogenesis during biological senescence. We emphasize the therapeutic potential of barrier-targeted interventions, particularly highlighting emerging modalities including fecal microbiota transplantation, intestinal organoid regeneration techniques, mesenchymal stem cell-mediated immunomodulation, and precision-engineered Chimeric Antigen Receptor T-cell therapies. Through this multidimensional analysis, we propose a paradigm-shifting approach to UC management in the elderly, advocating for the development of tailored and evidence-based therapeutic interventions that address the complex interplay between age-related biological changes and intestinal barrier homeostasis in elderly patients.},
}

@article {pmid40210031,
year = {2025},
author = {Zhao, M and Liu, Z and Geng, Y and Lv, X and Xu, J and Zhao, X and Yu, Z and Zhu, R and Li, M and Han, F and Ma, X and Gu, N},
title = {Role of a low-molecular-weight polysaccharide from Boletus edulis Bull: Fr. in modulating gut microbiota and metabolic disorders.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {142789},
doi = {10.1016/j.ijbiomac.2025.142789},
pmid = {40210031},
issn = {1879-0003},
abstract = {This study aimed to investigate the effects of Boletus edulis Bull: Fr. polysaccharide (BEP), extracted using a deep eutectic solvent based on l-lactic acid and glycine, on glucose and lipid metabolism in high-fat diet (HFD)-fed mice. The primary mechanism by which BEP improves symptoms of glucose and lipid imbalances involves the modulation of gut microbiota. Key beneficial bacteria, including S24-7, Lachnospiraceae, [Prevotella], and Lactobacillus, were significantly enriched in the intestines of BEP-treated mice, with abundances 2.48-, 1.62-, 6.33- and 2.60-fold higher, respectively, compared to the HFD group. In contrast, the abundance of harmful bacteria, particularly Desulfovibrio, was reduced by 1.81-fold. These microbial shifts contributed to the alleviation of intestinal mucus layer damage and a 50 % reduction in serum lipopolysaccharide (LPS) levels, a key driver of systemic inflammation, compared to the HFD group. As a result, BEP effectively inhibited LPS-induced activation of the hepatic TLR4/Myd88/MAPK signaling pathway, thereby normalizing the expression of proteins related to glucose and lipid metabolism. A fecal microbiota transplantation study further demonstrated that the gut microbiota changes induced by BEP were central to its anti-metabolic syndrome effects. Overall, BEP may serve as a dietary supplement for preventing and treating diet-induced metabolism disorders by targeting the gut microbiota.},
}

@article {pmid40209695,
year = {2025},
author = {Yamane, T and Masaoka, T and Ishii, C and Masuoka, H and Suda, W and Kurokawa, S and Kishimoto, T and Mikami, Y and Fukuda, S and Kanai, T},
title = {Factors contributing to the efficacy of fecal microbiota transplantation for diarrhea-dominant functional bowel disorders.},
journal = {Digestion},
volume = {},
number = {},
pages = {1-22},
doi = {10.1159/000545183},
pmid = {40209695},
issn = {1421-9867},
abstract = {INTRODUCTION: In cases of effective fecal microbiota transplantation (FMT) for irritable bowel syndrome (IBS), donor feces have been observed to be enriched in Bifidobacterium spp., and FMT for functional bowel disease improved psychiatric symptoms. Although intestinal dysbiosis has received attention as one of the pathophysiologies of IBS, the efficacy of FMT for IBS has not yet been established. In this study, we performed a post-hoc analysis of the efficacy of FMT, focusing on metabolites in donor feces.

METHODS: FMT was performed in 12 patients, 8 with refractory diarrhea-predominant IBS and 4 with functional diarrhea (FDr), who were refractory to medical therapy. The donors were family members within the second degree of kinship and were different for each transplant. Fecal characteristics were evaluated before and 12 weeks after transplantation using the Bristol stool scale (BS). BS scores of 3-5 at 12 weeks after transplantation were considered indicative of responders, while BS scores of 6 and 7 were indicative of non-responders. Metagenomic and metabolomic analyses of all 12 donor fecal samples were performed to compare the responder and non-responder groups.

RESULTS: Before transplantation, all 12 patients had BS scores of 6-7, but 12 weeks after transplantation, 6 were in the responder group and 6 were in the non-responder group. Metagenomic analysis showed that effective donor feces contained significantly higher levels of Prevotella than ineffective donor feces. Metabolomic analysis showed that effective donor feces contained significantly higher levels of propionate and butyrate and significantly lower lactate levels than ineffective donor feces.

CONCLUSION: Propionate-, butyrate-, or Prevotella-rich donor feces may contribute to successful FMT in patients with diarrhea-dominant functional gastrointestinal disorders.},
}

@article {pmid40208412,
year = {2025},
author = {Sandu, AM and Chifiriuc, MC and Vrancianu, CO and Cristian, RE and Alistar, CF and Constantin, M and Paun, M and Alistar, A and Popa, LG and Popa, MI and Tantu, AC and Sidoroff, ME and Mihai, MM and Marcu, A and Popescu, G and Tantu, MM},
title = {Healthcare-Associated Infections: The Role of Microbial and Environmental Factors in Infection Control-A Narrative Review.},
journal = {Infectious diseases and therapy},
volume = {},
number = {},
pages = {},
pmid = {40208412},
issn = {2193-8229},
support = {CNFIS-FDI-2024-F-0484 INOVEX//University of Bucharest/ ; Pillar III//Ministry of Research, Innovation and Digitalization through the National Recovery and Resilience Plan (PNRR) of Romania/ ; Component C9/Investment no. 8 (I8) - contract CF 68//Ministry of Research, Innovation and Digitalization through the National Recovery and Resilience Plan (PNRR) of Romania/ ; Project No. RO1567-IBB05/2023//Institute of Biology Bucharest of the Romanian Academy/ ; project no. 23020101//The core program within the National Research Development and Innovation Plan, 2022-2027', carried out with the support of the Ministry of Research, Innovation and Digitalization (MCID),/ ; Contract no. 7N from 3 January 2023//The core program within the National Research Development and Innovation Plan, 2022-2027', carried out with the support of the Ministry of Research, Innovation and Digitalization (MCID),/ ; Dezvoltarea cercetării genomice în România - ROGEN" (Development of genomic research in Romania -ROGEN).//ROGEN/ ; },
abstract = {Healthcare-associated infections (HAIs), previously known as nosocomial infections, represent a significant threat to healthcare systems worldwide, prolonging patient hospital stays and the duration of antimicrobial therapy. One of the most serious consequences of HAIs is the increase in the rate of antibiotic resistance (AR) generated by the prolonged, frequent, and sometimes incorrect use of antibiotics, which leads to the selection of resistant bacteria, making treatment difficult and expensive, with direct consequences for the safety of patients and healthcare personnel. Therefore, timely and accurate diagnosis of HAIs is mandatory to develop appropriate infection prevention and control practices (IPC) and new therapeutic strategies. This review aimed to present the prevalence, risk factors, current diagnosis, including artificial intelligence (AI) and machine learning approaches, future perspectives in combating HAIs causative bacteria (phage therapy, microbiome-based interventions, and vaccination), and HAIs surveillance strategies. Also, we discussed the latest findings regarding the relationships of AR with climate change and environmental pollution in the context of the One Health approach. Phage therapy is an emerging option that can offer an alternative to ineffective antibiotic treatments for antibiotic-resistant bacteria causing HAIs. Clinical trials dealing with vaccine development for resistant bacteria have yielded conflicting results. Two promising strategies, fecal microbiota transplantation and probiotic therapy, proved highly effective against recurrent Clostridium difficile infections and have been shown to reduce HAI incidence in hospitalized patients undergoing antibiotic therapy. Artificial intelligence and machine learning systems offer promising predictive capabilities in processing large volumes of clinical, microbiological, and patient data but require robust data integration. Our paper argues that HAIs are still a global challenge, requiring stringent IPC policies, computer vision, and AI-powered tools. Despite promising avenues like integrated One Health approaches, optimized phage therapy, microbiome-based interventions, and targeted vaccine development, several knowledge gaps in clinical efficacy, standardization, and pathogen complexity remain to be answered.},
}

@article {pmid40208053,
year = {2025},
author = {Xu, K and Motiwala, Z and Corona-Avila, I and Makhanasa, D and Alkahalifeh, L and Khan, MW},
title = {The Gut Microbiome and Its Multifaceted Role in Cancer Metabolism, Initiation, and Progression: Insights and Therapeutic Implications.},
journal = {Technology in cancer research & treatment},
volume = {24},
number = {},
pages = {15330338251331960},
doi = {10.1177/15330338251331960},
pmid = {40208053},
issn = {1533-0338},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Neoplasms/metabolism/therapy/etiology/pathology/microbiology ; Disease Progression ; Animals ; Dysbiosis/microbiology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {This review summarizes the intricate relationship between the microbiome and cancer initiation and development. Microbiome alterations impact metabolic pathways, immune responses, and gene expression, which can accelerate or mitigate cancer progression. We examine how dysbiosis affects tumor growth, metastasis, and treatment resistance. Additionally, we discuss the potential of microbiome-targeted therapies, such as probiotics and fecal microbiota transplants, to modulate cancer metabolism. These interventions offer the possibility of reversing or controlling cancer progression, enhancing the efficacy of traditional treatments like chemotherapy and immunotherapy. Despite promising developments, challenges remain in identifying key microbial species and pathways and validating microbiome-targeted therapies through large-scale clinical trials. Nonetheless, the intersection of microbiome research and cancer initiation and development presents an exciting frontier for innovative therapies. This review offers a fresh perspective on cancer initiation and development by integrating microbiome insights, highlighting the potential for interdisciplinary research to enhance our understanding of cancer progression and treatment strategies.},
}

Humans
*Gastrointestinal Microbiome
*Neoplasms/metabolism/therapy/etiology/pathology/microbiology
Disease Progression
Animals
Dysbiosis/microbiology
Probiotics/therapeutic use
Fecal Microbiota Transplantation

@article {pmid40207935,
year = {2025},
author = {Karra, DA and Suchodolski, JS and Newman, SJ and Flouraki, E and Lidbury, JA and Steiner, JM and Xenoulis, PG},
title = {Single Enema Fecal Microbiota Transplantation in Cats With Chronic Enteropathy.},
journal = {Journal of veterinary internal medicine},
volume = {39},
number = {3},
pages = {e70054},
pmid = {40207935},
issn = {1939-1676},
mesh = {Animals ; Cats ; *Cat Diseases/therapy ; *Fecal Microbiota Transplantation/veterinary ; Female ; Male ; *Enema/veterinary ; Chronic Disease ; Prospective Studies ; Dysbiosis/veterinary/therapy ; *Intestinal Diseases/veterinary/therapy ; },
abstract = {BACKGROUND: Chronic enteropathies (CE) are common in cats, and alterations of the intestinal microbiota might be involved in the pathogenesis.

HYPOTHESIS/OBJECTIVES: To evaluate the efficacy of a single enema fecal microbiota transplantation (FMT) in improving intestinal dysbiosis and clinical scores in cats with CE.

ANIMALS: Twenty-eight cats with either chronic inflammatory enteropathy (CIE; n = 19) or small cell gastrointestinal lymphoma (SCGL; n = 9) were prospectively enrolled.

METHODS: Eleven cats were randomly selected to receive a single enema FMT (FMT-group), and 17 cats were used as controls. Clinical activity was determined using the Feline Chronic Enteropathy Activity Index (FCEAI), and intestinal dysbiosis was determined using the feline dysbiosis index (DI) on the day of FMT (T0) and 30 days after FMT (T1).

RESULTS: At T0, 14/28 cats had an abnormal DI > 0. No significant difference was found in the DI from T0 to T1 in the FMT group (mean[SD]: 0.01[2.5] vs. 0.7[2.1]; p = 0.47). No significant difference was found in the DI between the FMT group and the control group at T1 (mean[SD]: -0.7[2.1] vs. 0.8[1.8]; p = 0.92). FCEAI significantly decreased at T1 compared to T0 in the FMT group (median[IQR] 10.0[7.7-11.3] vs. 4.5[4-5]; p = 0.002). No significant difference was found in the FCEAI between the FMT group and the control group at T1 (median[IQR] 4.5[4-5] vs. 4[3-5.75]; p = 0.64).

CONCLUSIONS: In this study, single enema FMT did not lead to a significant improvement in DI or FCEAI in cats with CE compared to controls.},
}

Animals
Cats
*Cat Diseases/therapy
*Fecal Microbiota Transplantation/veterinary
Female
Male
*Enema/veterinary
Chronic Disease
Prospective Studies
Dysbiosis/veterinary/therapy
*Intestinal Diseases/veterinary/therapy

@article {pmid40207915,
year = {2025},
author = {Moya Uribe, IA and Terauchi, H and Bell, JA and Zanetti, A and Jantre, S and Huebner, M and Arshad, SH and Ewart, SL and Mansfield, LS},
title = {Fecal microbiota transplants (FMT) of three distinct human communities to germ-free mice exacerbated inflammation and decreased lung function in their offspring.},
journal = {mBio},
volume = {},
number = {},
pages = {e0376424},
doi = {10.1128/mbio.03764-24},
pmid = {40207915},
issn = {2150-7511},
abstract = {UNLABELLED: Despite explosive rise in allergies, little is known about early life gut microbiota effects on postnatal respiratory function. We hypothesized that Enterobacteriaceae-dominant gut microbiota from eczemic infants increases Type 2 inflammation and decreases lung function in transplanted mice, while Bacteroidaceae-dominant gut microbiota from non-eczemic infants is protective. Fecal microbiota transplants (FMT) from eczemic infants "Infant A" and non-eczemic infants "Infant B" were successfully transplanted into germ-free C57BL/6 mice, passing to offspring unchanged. Infant A and B, Adult C-human-derived (positive control), and Mouse (negative control) microbiotas all in C57BL/6 mice were tested for effects on airway function in nonallergic (phosphate-buffered saline [PBS]) and allergic (house dust mite [HDM]) conditions. Baseline lung mechanics in mice with human microbiotas ([HU]microbiota) were significantly impaired compared to Mouse microbiota controls ([MO]microbiota) with or without HDM; respiratory system resistance (Rrs) was increased (P < 0.05-P < 0.01), and respiratory system compliance (Crs) was decreased (P < 0.05-P < 0.01). [HU]Microbiota mice showed a statistically significant impairment compared to [MO]microbiota mice in lung parameters Rrs, Ers, Rn, and G at baseline, and at multiple methacholine (MCh) doses with baseline removed. Impairment manifested as increased small airway resistance and tissue resistance. HDM significantly elevated IL-4, eosinophils, lung inflammation, and mucus cell metaplasia, and decreased macrophages and lung function (P < 0.05) in mice of all microbiotas, yet each [HU]microbiota produced distinct features. Infant B and Adult C mice had elevated basal levels of total IgE compared to [MO]microbiota and Infant A mice (P < 0.05). In [HU]microbiota mice given HDM, only Adult C had elevated IL-5 and IL-13 (P < 0.05), only Adult C and Infant B mice had elevated neutrophils (P < 0.05), and only Infant A had elevated lymphocytes (P < 0.01).

IMPORTANCE: Fecal microbiota transplants (FMT) of three distinct human communities to germ-free mice exacerbated inflammation and decreased lung function in their offspring. Taxa formerly described to induce an allergic response (agonists) and pro-inflammatory taxa were abundant in [HU]microbiotas compared to [MO]microbiota controls, while taxa formerly described to reduce allergic responses (antagonists) and anti-inflammatory taxa were numerous in [MO]microbiotas and low in [HU]microbiotas. Thus, we largely rejected our hypotheses because data supported multiple pro-inflammatory allergy agonists functioning in a community-wide fashion to impair lung function in the absence of antagonistic anti-inflammatory taxa. Structure of [HU]microbiotas played a key role in determining varied allergic responses and resulting lung impairment, yet, strikingly, all mice with [HU]microbiotas had impaired lung function even in the absence of allergens. Using a comparative approach, we showed that composition of gut microbiota can alter innate/immune regulation in the gut-lung axis to increase baseline lung function responses and the risk of allergic sensitization.},
}

@article {pmid40207909,
year = {2025},
author = {Spiegelhauer, MR and Offersen, SM and Mao, X and Gambino, M and Sandris Nielsen, D and Nguyen, DN and Brunse, A},
title = {Protection against experimental necrotizing enterocolitis by fecal filtrate transfer requires an active donor virome.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2486517},
pmid = {40207909},
issn = {1949-0984},
mesh = {Animals ; *Enterocolitis, Necrotizing/prevention & control/therapy/microbiology/pathology ; Swine ; Gastrointestinal Microbiome ; *Feces/virology ; *Virome/radiation effects ; *Fecal Microbiota Transplantation/methods ; Disease Models, Animal ; Animals, Newborn ; Virus Inactivation/radiation effects ; Ultraviolet Rays ; Clostridium perfringens ; Humans ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {Necrotizing enterocolitis (NEC) remains a frequent catastrophic disease in preterm infants, and fecal filtrate transfer (FFT) has emerged as a promising prophylactic therapy. This study explored the role of virome viability for the protective effect of FFT. Using ultraviolet (UV) irradiation, we established a viral inactivation protocol and administered FFT, UV-inactivated FFT (iFFT) or sterile saline orally to preterm piglets at risk for experimental NEC. The gut pathology and barrier properties were assessed, while the microbiome was explored by 16S rRNA amplicon and metavirome sequencing. Like in prior studies, FFT reduced NEC severity and intestinal inflammation, while these effects were absent in the iFFT group. Unexpectedly, piglets receiving FFT exhibited mild side effects in the form of early-onset diarrhea. The FFT also converged the gut colonization by increased viral heterogeneity and a reduced abundance of pathobionts like Clostridium perfringens and Escherichia. In contrast, the gut microbiome of iFFT recipients diverged from both FFT and the controls. These findings highlight the clear distinction between the ability of active and inactivate viromes to modulate gut microbiota and decrease pathology. The efficacy of FFT may be driven by active bacteriophages, and loss of virome activity could have consequences for the treatment efficacy.},
}

Animals
*Enterocolitis, Necrotizing/prevention & control/therapy/microbiology/pathology
Swine
Gastrointestinal Microbiome
*Feces/virology
*Virome/radiation effects
*Fecal Microbiota Transplantation/methods
Disease Models, Animal
Animals, Newborn
Virus Inactivation/radiation effects
Ultraviolet Rays
Clostridium perfringens
Humans
Bacteria/classification/genetics/isolation & purification

@article {pmid40207766,
year = {2025},
author = {Kumar, M and Mehan, S and Sharma, T and Kumar, A and Khan, Z and Sharma, AK and Kumar, N and Gupta, GD},
title = {Integrating Gut-Brain Axis: Exploring the Neurogastrointestinal Interactions and Therapeutic Potentials in Autism Spectrum Disorder.},
journal = {Endocrine, metabolic & immune disorders drug targets},
volume = {},
number = {},
pages = {},
doi = {10.2174/0118715303369166250325110016},
pmid = {40207766},
issn = {2212-3873},
abstract = {This comprehensive review critically examines the gut-brain axis (GBA) and its implications in autism spectrum disorder (ASD). The GBA is a complex, bidirectional communication network that integrates the gastrointestinal tract, the central nervous system, and the gut microbiota. This axis is mediated through various physiological pathways, including the enteric nervous system (ENS), the vagus nerve, immune responses, and metabolic activities of gut microorganisms. ASD, a developmental disorder marked by social impairments and repetitive behaviors, presents with notable neurological irregularities. The review highlights the increased prevalence of gastrointestinal (GI) disturbances in individuals with ASD, suggesting a potential link between GI symptoms and the severity of ASD-related behaviors. This correlation is supported by evidence of altered gut microbiota composition in ASD, indicating significant interactions between the gut environment and neurological health. Moreover, the pathophysiology of ASD is explored with an emphasis on genetic and environmental contributions to neurodevelopmental impairments. Key topics include synaptic dysfunction, the roles of neurotransmitters like GABA and serotonin, and the impact of gut-brain interactions on ASD progression. Specifically, this review addresses how gut microbiota may influence metabolic alterations, immune dysregulation, oxidative stress, mitochondrial function, and neurotransmitter production in ASD. Emerging research on microbiome-based therapies for ASD is discussed, focusing on the potential of probiotics, prebiotics, and faecal microbiota transplantation (FMT) as novel interventions. Ethical considerations in this burgeoning field are also considered, highlighting the necessity for rigorous scientific inquiry and ethical oversight. The review advocates for a multidisciplinary approach to understanding and addressing the complexities of ASD. By integrating insights from genetics, neuroscience, psychology, and gastroenterology, a more comprehensive understanding of the role of GBA in ASD can be achieved. This interdisciplinary perspective is crucial for developing effective, individualized treatments and improving the quality of life for individuals with ASD.},
}

@article {pmid40207754,
year = {2025},
author = {V S, S and Prasad, C and Panicker, SP},
title = {Exploring the Role of Non-Coding RNAs in the Gut and Skin Microbiome: Implications for Colorectal Cancer and Healthy Longevity.},
journal = {MicroRNA (Shariqah, United Arab Emirates)},
volume = {},
number = {},
pages = {},
doi = {10.2174/0122115366342509250401043719},
pmid = {40207754},
issn = {2211-5374},
abstract = {In the last forty years, cancer mortality rates have risen by more than 40%, with colo-rectal cancer (CRC) ranking as the third most common kind worldwide, significantly affected by dietary factors. Restricted access to sophisticated medical treatment and insufficient comprehen-sion of colorectal cancer's biology contribute to its elevated occurrence. Researchers have recog-nized dysbiosis of the gut microbiome as a critical contributor to the development of colorectal cancer, as it influences the expression of non-coding RNAs (ncRNAs) and subsequent molecular pathways essential for tumor proliferation. Moreover, interactions between gut and skin microbi-ota can impact systemic health and ncRNA regulation, influencing CRC advancement. This study shows how important the gut-skin microbiome axis is in developing colorectal cancer. It suggests that targeting this axis may lead to new treatments, such as changing the microbiome through probiotics, prebiotics, or fecal microbiota transplantation. Nonetheless, we must address obstacles such as population heterogeneity and intricate microbiome-host interactions to facilitate the tran-sition of these medicines into clinical practice. This study seeks to elucidate the roles of dietary treatments, microbiomes, and ncRNAs in the etiology and prevention of colorectal cancer (CRC).},
}

@article {pmid40207229,
year = {2025},
author = {Chen, S and Yi, M and Yi, X and Zhou, Y and Song, H and Zeng, M},
title = {Unveiling the fungal frontier: mycological insights into inflammatory bowel disease.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1551289},
pmid = {40207229},
issn = {1664-3224},
mesh = {Humans ; *Inflammatory Bowel Diseases/microbiology/therapy/immunology/etiology/metabolism ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/immunology/microbiology ; *Fungi/immunology ; Animals ; *Mycoses/immunology/microbiology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; },
abstract = {Inflammatory bowel disease (IBD) is a chronic recurrent gastrointestinal disease that seriously affects the quality of life of patients around the world. It is characterized by recurrent abdominal pain, diarrhea, and mucous bloody stools. There is an urgent need for more accurate diagnosis and effective treatment of IBD. Accumulated evidence suggests that gut microbiota plays an important role in the occurrence and development of gut inflammation. However, most studies on the role of gut microbiota in IBD have focused on bacteria, while fungal microorganisms have been neglected. Fungal dysbiosis can activate the host protective immune pathway related to the integrity of the epithelial barrier and release a variety of pro-inflammatory cytokines to trigger the inflammatory response. Dectin-1, CARD9, and IL-17 signaling pathways may be immune drivers of fungal dysbacteriosis in the development of IBD. In addition, fungal-bacterial interactions and fungal-derived metabolites also play an important role. Based on this information, we explored new strategies for IBD treatment targeting the intestinal fungal group and its metabolites, such as fungal probiotics, antifungal drugs, diet therapy, and fecal microbiota transplantation (FMT). This review aims to summarize the fungal dysbiosis and pathogenesis of IBD, and provide new insights and directions for further research in this emerging field.},
}

Humans
*Inflammatory Bowel Diseases/microbiology/therapy/immunology/etiology/metabolism
*Gastrointestinal Microbiome/immunology
*Dysbiosis/immunology/microbiology
*Fungi/immunology
Animals
*Mycoses/immunology/microbiology
Fecal Microbiota Transplantation
Probiotics/therapeutic use

@article {pmid40206278,
year = {2025},
author = {Cresci, GAM and Liu, Q and Sangwan, N and Liu, D and Grove, D and Shapiro, D and Ali, K and Cazzaniga, B and Prete, LD and Miller, C and Hashimoto, K and Quintini, C},
title = {The Impact of Liver Graft Preservation Method on Longitudinal Gut Microbiome Changes Following Liver Transplant: A Proof-of-concept Study.},
journal = {Journal of clinical and translational hepatology},
volume = {13},
number = {4},
pages = {284-294},
pmid = {40206278},
issn = {2310-8819},
abstract = {BACKGROUND AND AIMS: End-stage liver disease is associated with disruptions in gut microbiota composition and function, which may facilitate gut-to-liver bacterial translocation, impacting liver graft integrity and clinical outcomes following liver transplantation. This study aimed to assess the impact of two liver graft preservation methods on fecal microbiota and changes in fecal and breath organic acids following liver transplantation.

METHODS: This single-center, non-randomized prospective pilot study enrolled liver transplant patients whose grafts were preserved using either static cold storage or ex situ normothermic machine perfusion (NMP). Fresh stool and breath samples were collected immediately before surgery and at postoperative months 3, 6, and 12. Stool microbiota was profiled via 16S rRNA gene sequencing, stool short-chain fatty acids were measured using gas chromatography/-mass spectrometry, and breath volatile organic compounds (VOCs) were analyzed with selected-ion flow-tube mass spectrometry.

RESULTS: Both cohorts experienced a loss of microbiota diversity and dominance by single taxa. The NMP cohort demonstrated enrichment of several beneficial gut taxa, while the static cold storage cohort showed depletion of such taxa. Various gut bacteria were found to correlate with stool short-chain fatty acids (e.g., lactic acid, butyric acid) and several VOCs.

CONCLUSIONS: Fecal microbiota alterations associated with end-stage liver disease do not fully normalize to a healthy control profile following liver transplantation. However, notable differences in microbiota composition and function were observed between liver graft preservation methods. Future research with larger randomized cohorts is needed to explore whether the NMP-associated shift in gut microbiota impacts clinical outcomes and if breath VOCs could serve as biomarkers of the clinical trajectory in liver transplant patients.},
}

@article {pmid40204291,
year = {2025},
author = {Li, S and Li, J and Chen, K and Wang, J and Wang, L and Feng, C and Wang, K and Xu, Y and Gao, Y and Yan, X and Zhao, Q and Li, B and Qiu, Y},
title = {Chronic Arsenic Exposure Causes Alzheimer's Disease Characteristic Effects and the Intervention of Fecal Microbiota Transplantation in Rats.},
journal = {Journal of applied toxicology : JAT},
volume = {},
number = {},
pages = {},
doi = {10.1002/jat.4782},
pmid = {40204291},
issn = {1099-1263},
support = {202203021211246//Shanxi Natural Science Foundation of China/ ; 20240017//Fund Program for the Scientific Activities of Selected Returned Overseas Professionals in Shanxi Province/ ; },
abstract = {Arsenic exposure and intestinal microbiota disorders may be related with Alzheimer's disease (AD), but the mechanism has not been elucidated. This study conducted chronic arsenic exposure from rat's maternal body to adult offspring to investigate the mechanisms of the characteristic effects of chronic arsenic exposure on AD, and further explored the intervention effect of fecal microbiota transplantation (FMT) on arsenic-mediated neurotoxicity. Transmission electron microscopy, HE staining, and related indicators were measured in the control group, the exposed group, and the FMT intervention group. Western blot was used to determine microtubule-associated proteins Tau and p-Tau396, intestinal-brain barrier-related proteins Claudin-1 and Occludin, ELISA was used to detect the content of Aβ1-42, and 16S rRNA sequencing was used to detect the intestinal flora of feces. Results showed that chronic arsenic exposure could lead to neurobehavioral defects in rats, increase the expression levels of Tau, p-Tau396, and Aβ1-42 in hippocampus (p < 0.05), increase the abundance of Clostridium _ UCG-014, decrease the abundance of Roseburia, and decrease the expression levels of Claudin-1 and Occludin in colon and hippocampus (p < 0.05). After FMT intervention, the expression levels of Tau and p-Tau396 were decreased (p < 0.05), and the abundance of Roseburia was increased. In summary, chronic arsenic exposure caused intestinal flora disorder by changing the abundance of inflammation-related flora, thereby destroying the gut-brain barrier and causing AD characteristic effects in rats. Although the bacterial specific genus was improved and the expression of AD-related proteins was reduced after transplantation, it could not alleviate the neurobehavioral defects and neurotoxicity caused by arsenic exposure.},
}

@article {pmid40203217,
year = {2025},
author = {Randolph, NK and Salerno, M and Klein, H and Diaz-Campos, D and van Balen, JC and Winston, JA},
title = {Preparation of Fecal Microbiota Transplantation Products for Companion Animals.},
journal = {PloS one},
volume = {20},
number = {4},
pages = {e0319161},
pmid = {40203217},
issn = {1932-6203},
support = {T35 OD010977/OD/NIH HHS/United States ; },
mesh = {Animals ; Dogs ; Cats ; *Fecal Microbiota Transplantation/methods/veterinary ; *Feces/microbiology ; *Pets/microbiology ; Microbial Viability ; },
abstract = {Fecal microbiota transplantation (FMT) is increasingly utilized in small animal medicine for the treatment of a variety of gastrointestinal and non-gastrointestinal disorders. Despite proven clinical efficacy, there is no detailed protocol available for the preparation and storage of FMT products for veterinarians in a variety of clinical settings. Herein, the effect of processing technique on the microbial community structure was assessed with amplicon sequence analysis. Microbial viability was assessed with standard culture techniques using selective media. Given the fastidious nature of many intestinal microbes, colony forming units are considered surrogate viable microbes, representing a portion of potentially viable microbes. FMT products from four screened canine fecal donors and six screened feline fecal donors were processed aerobically according to a double centrifugation protocol adapted from the human medical literature. Fresh feces from an additional three screened canine fecal donors were used to evaluate the effect of cryopreservative, centrifugation, and short-term storage on microbial community structure and in vitro surrogate bacterial viability. Finally, fresh feces from a third group of three screened canine and three screened feline fecal donors were used to evaluate the long-term in vitro surrogate bacterial viability of three frozen and lyophilized FMT products. Microbiota analysis revealed that each canine fecal donor has a unique microbial profile. Processing of canine and feline feces for FMT does not significantly alter the overall microbial community structure. The addition of cryopreservatives and lyopreservatives significantly improved long-term viability, up to 6 months, for frozen and lyophilized FMT products compared to unprocessed raw feces with no cryopreservative. These results prove the practicality of this approach for FMT preparation in veterinary medicine and provide a detailed protocol for researchers and companion animal practitioners. Future in vivo research is needed to evaluate how the preparation and microbial viability of FMT impacts the recipient's microbial community and clinical outcomes across multiple disease phenotypes.},
}

Animals
Dogs
Cats
*Fecal Microbiota Transplantation/methods/veterinary
*Feces/microbiology
*Pets/microbiology
Microbial Viability

@article {pmid40202719,
year = {2025},
author = {Huang, Z and Liu, C and Zhao, X and Guo, Y},
title = {The effect of elevated levels of the gut metabolite TMAO on glucose metabolism after sleeve gastrectomy.},
journal = {Archives of physiology and biochemistry},
volume = {},
number = {},
pages = {1-10},
doi = {10.1080/13813455.2025.2489721},
pmid = {40202719},
issn = {1744-4160},
abstract = {Purpose：Bariatric surgery can effectively alleviate obesity and diabetes by regulation of the gut microbiota. This study aimed to investigate the change in the gut microbiota metabolite TMAO and to explore its effect on glucose metabolism after sleeve gastrectomy (SG). Materials and methods：Diet-induced obesity mouse models were established, and the mice were randomly divided into four groups: an SG group, a sham-operated group pair-fed with the SG group (PF), a sham-operated group fed ad libitum (AL), and a lean control group (C). At 10 weeks post-surgery, the changes in glycogen content of liver, gut microbiota and the level of FMO3 in the liver were evaluated, and their correlation with TMAO production was analysed. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured. Results：At 10 weeks post-surgery, hepatocyte glycogen levels were restored, and serum TMA and TMAO levels were significantly increased. Faecal metagenomic sequencing results showed that the abundances of Ruminococcaceae and Lachnospiraceae, which were positively correlated with TMAO production, were significantly increased after surgery. While the changes in FMO3, the key enzyme producing TMAO in the liver was found decreased significantly after SG. The expression levels of the TMAO/PERK/FOXO1 pathway and the gluconeogenic genes G6PC and PCK1 were measured. Inconsistent with the changing trend of TMAO, the expression of PERK, FOXO1, PCK, and G6PC significantly decreased after SG. Conclusions：SG can significantly reduce obesity and restore glucose metabolism. After surgery, TMAO metabolites increased in a microbiota-dependent manner.},
}

@article {pmid40202676,
year = {2025},
author = {Sharma, S and Tiwari, N and Tanwar, SS},
title = {The current findings on the gut-liver axis and the molecular basis of NAFLD/NASH associated with gut microbiome dysbiosis.},
journal = {Naunyn-Schmiedeberg's archives of pharmacology},
volume = {},
number = {},
pages = {},
pmid = {40202676},
issn = {1432-1912},
abstract = {Recent research has highlighted the complex relationship between gut microbiota, metabolic pathways, and nonalcoholic fatty liver disease (NAFLD) progression. Gut dysbiosis, commonly observed in NAFLD patients, impairs intestinal permeability, leading to the translocation of bacterial products like lipopolysaccharides, short-chain fatty acids, and ethanol to the liver. These microbiome-associated mechanisms contribute to intestinal and hepatic inflammation, potentially advancing NAFLD to NASH. Dietary habits, particularly those rich in saturated fats and fructose, can modify the microbiome composition, leading to dysbiosis and fatty liver development. Metabolomic approaches have identified unique profiles in NASH patients, with specific metabolites like ethanol linked to disease progression. While bariatric surgery has shown promise in preventing NAFLD progression, the role of gut microbiome and metabolites in this improvement remains to be proven. Understanding these microbiome-related pathways may provide new diagnostic and therapeutic targets for NAFLD and NASH. A comprehensive review of current literature was conducted using multiple medical research databases, including PubMed, Scopus, Web of Science, Embase, Cochrane Library, ClinicalTrials.gov, ScienceDirect, Medline, ProQuest, and Google Scholar. The review focused on studies that examine the relationship between gut microbiota composition, metabolic pathways, and NAFLD progression. Key areas of interest included microbial dysbiosis, endotoxin production, and the influence of diet on gut microbiota. The analysis revealed that gut dysbiosis contributes to NAFLD through several mechanisms, diet significantly influences gut microbiota composition, which in turn affects liver function through the gut-liver axis. High-fat diets can lead to dysbiosis, altering microbial metabolic activities and promoting liver inflammation. Specifically, gut microbiota-mediated generation of saturated fatty acids, such as palmitic acid, can activate liver macrophages and increase TNF-α expression, contributing to NASH development. Different dietary components, including cholesterol, fiber, fat, and carbohydrates, can modulate the gut microbiome and influence NAFLD progression. This gut-liver axis plays a crucial role in maintaining immune homeostasis, with the liver responding to gut-derived bacteria by activating innate and adaptive immune responses. Microbial metabolites, such as bile acids, tryptophan catabolites, and branched-chain amino acids, regulate adipose tissue and intestinal homeostasis, contributing to NASH pathogenesis. Additionally, the microbiome of NASH patients shows an elevated capacity for alcohol production, suggesting similarities between alcoholic steatohepatitis and NASH. These findings indicate that targeting the gut microbiota may be a promising approach for NASH treatment and prevention. Recent research highlights the potential of targeting gut microbiota for managing nonalcoholic fatty liver disease (NAFLD). The gut-liver axis plays a crucial role in NAFLD pathophysiology, with dysbiosis contributing to disease progression. Various therapeutic approaches aimed at modulating gut microbiota have shown promise, including probiotics, prebiotics, synbiotics, fecal microbiota transplantation, and dietary interventions. Probiotics have demonstrated efficacy in human randomized controlled trials, while other interventions require further investigation in clinical settings. These microbiota-targeted therapies may improve NAFLD outcomes through multiple mechanisms, such as reducing inflammation and enhancing metabolic function. Although lifestyle modifications remain the primary recommendation for NAFLD management, microbiota-focused interventions offer a promising alternative for patients struggling to achieve weight loss targets.},
}

@article {pmid39851236,
year = {2025},
author = {Golob, JL and Hou, G and Swanson, BJ and Berinstein, JA and Bishu, S and Grasberger, H and Zataari, ME and Lee, A and Kao, JY and Kamada, N and Bishu, S},
title = {Inflammation-Induced Th17 Cells Synergize with the Inflammation-Trained Microbiota to Mediate Host Resiliency Against Intestinal Injury.},
journal = {Inflammatory bowel diseases},
volume = {31},
number = {4},
pages = {1082-1094},
doi = {10.1093/ibd/izae293},
pmid = {39851236},
issn = {1536-4844},
support = {K08DK123403//the NIDDK/ ; },
mesh = {Animals ; *Th17 Cells/immunology ; Mice ; Mice, Inbred C57BL ; Citrobacter rodentium ; *Colitis/immunology/chemically induced/microbiology/pathology ; *Inflammation/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; Dextran Sulfate/toxicity ; *Intestinal Mucosa/immunology/pathology/microbiology ; Disease Models, Animal ; Mice, Knockout ; Fecal Microbiota Transplantation ; *Enterobacteriaceae Infections/immunology ; *Dysbiosis/immunology/microbiology ; },
abstract = {BACKGROUND AND AIMS: Inflammation can generate pathogenic Th17 cells and cause an inflammatory dysbiosis. In the context of inflammatory bowel disease (IBD), these inflammatory Th17 cells and dysbiotic microbiota may perpetuate injury to intestinal epithelial cells. However, many models of IBD like T-cell transfer colitis and IL-10-/- mice rely on the absence of regulatory pathways, so it is difficult to tell if inflammation can also induce protective Th17 cells.

METHODS: We subjected C57BL6, RAG1-/-, or JH-/- mice to systemic or gastrointestinal (GI) Citrobacter rodentium (Cr). Mice were then subjected to 2.5% dextran sodium sulfate (DSS) to cause epithelial injury. Fecal microbiota transfer was performed by bedding transfer and co-housing. Flow cytometry, qPCR, and histology were used to assess mucosal and systemic immune responses, cytokines, and tissue inflammation. 16s sequencing was used to assess gut bacterial taxonomy.

RESULTS: Transient inflammation with GI but not systemic Cr was protective against subsequent intestinal injury. This was replicated with sequential DSS collectively indicating that transient inflammation provides tissue-specific protection. Inflammatory Th17 cells that have a tissue-resident memory (TRM) signature expanded in the intestine. Experiments with reconstituted RAG1-/-, JH-/- mice, and cell trafficking inhibitors showed that inflammation-induced Th17 cells were required for protection. Fecal microbiota transfer showed that the inflammation-trained microbiota was necessary for protection, likely by maintaining protective Th17 cells in situ.

CONCLUSION: Inflammation can generate protective Th17 cells that synergize with the inflammation-trained microbiota to provide host resiliency against subsequent injury, indicating that inflammation-induced Th17 TRM T cells are heterogenous and contain protective subsets.},
}

Animals
*Th17 Cells/immunology
Mice
Mice, Inbred C57BL
Citrobacter rodentium
*Colitis/immunology/chemically induced/microbiology/pathology
*Inflammation/immunology/microbiology
*Gastrointestinal Microbiome/immunology
Dextran Sulfate/toxicity
*Intestinal Mucosa/immunology/pathology/microbiology
Disease Models, Animal
Mice, Knockout
Fecal Microbiota Transplantation
*Enterobacteriaceae Infections/immunology
*Dysbiosis/immunology/microbiology

@article {pmid40201970,
year = {2025},
author = {Chen, Y and Zeng, Y and Zhang, Y and Chen, J and Qian, Y and Huang, J and Chen, G and Xia, G and Wang, C and Feng, A and Nie, X},
title = {Differential gut microbiota and inflammatory cytokines contribute to IgA vasculitis.},
journal = {Clinical and experimental rheumatology},
volume = {43},
number = {4},
pages = {563-574},
doi = {10.55563/clinexprheumatol/ff61t7},
pmid = {40201970},
issn = {0392-856X},
mesh = {*Gastrointestinal Microbiome/immunology ; Humans ; Animals ; Male ; Female ; Child ; *Immunoglobulin A/immunology/blood ; *Cytokines/blood/immunology ; *Dysbiosis/immunology ; *IgA Vasculitis/microbiology/immunology/blood/diagnosis ; Case-Control Studies ; Mice ; *Inflammation Mediators/blood ; Disease Models, Animal ; *Bacteria/immunology/genetics ; Adolescent ; Child, Preschool ; Fecal Microbiota Transplantation ; },
abstract = {OBJECTIVES: Immunoglobulin A vasculitis (IgAV) is the most common form of vasculitis in childhood. Emerging evidence indicates that gut microbiota plays a key role in the pathogenesis of IgAV. However, the factors linking gut microbiota to the onset and progression of IgAV are poorly understood. We aimed to demonstrate that the presence of a specific dysbiosis in patients with IgAV contributes to the onset of IgAV.

METHODS: We transplanted gut microbiota from human donors with IgAV or healthy controls (HCs). The changes in gut microbiota and serum indexes of the recipient mice were detected, and the IgAV-associated bacteria were determined by integrating the results from the mouse sequence data analysis with the human sequence results.

RESULTS: 55 amplicon sequence variants (ASVs) specific to IgAV children were detected in the recipient IgAV microbiota (rIMb) mice, and 35 ASVs specific to healthy children were detected in the recipient healthy microbiota (rHMb) mice. Gut microbiota in rIMb mice differs from that in rHMb mice. Alcaligenaceae could discriminate rIMb from rHMb mice, while its abundance was decreased in rIMb compared to rHMb (p<0.05). In children with IgAV, the abundance of Burkholderiaceae (Alcaligenaceae accounted for 99.7%) at the family level was significantly lower compared to HCs, which can be used to distinguish children with IgAV from HCs, and the constructed receiver operating characteristic (ROC) curve had an area under the curve (AUC) value of 0.766. In addition, the rIMb group had a markedly higher interleukin (IL)-17A and IL-21 level than those in the rHMb group. The Spearman correlation analysis indicated significant correlations between the relative levels of these pro-inflammatory cytokines, IgA and alterations of gut microbiota.

CONCLUSIONS: IgAV is characterised by disturbances of gut microbiota composition and an imbalance in inflammatory cytokines. The manipulation of gut microbiota could be a possible way to prevent and manage IgAV.},
}

*Gastrointestinal Microbiome/immunology
Humans
Animals
Male
Female
Child
*Immunoglobulin A/immunology/blood
*Cytokines/blood/immunology
*Dysbiosis/immunology
*IgA Vasculitis/microbiology/immunology/blood/diagnosis
Case-Control Studies
Mice
*Inflammation Mediators/blood
Disease Models, Animal
*Bacteria/immunology/genetics
Adolescent
Child, Preschool
Fecal Microbiota Transplantation

@article {pmid40201831,
year = {2025},
author = {Dewey, CW},
title = {Poop for thought: Can fecal microbiome transplantation improve cognitive function in aging dogs?.},
journal = {Open veterinary journal},
volume = {15},
number = {2},
pages = {556-564},
pmid = {40201831},
issn = {2218-6050},
mesh = {Dogs ; Animals ; *Fecal Microbiota Transplantation/veterinary ; *Dog Diseases/therapy/microbiology ; Dysbiosis/therapy/veterinary ; Gastrointestinal Microbiome ; *Aging ; *Cognitive Dysfunction/therapy ; Cognition ; *Alzheimer Disease/therapy/veterinary ; Humans ; },
abstract = {Canine cognitive dysfunction (CCD) is the dog version of human Alzheimer's disease (AD), and it has strikingly similar pathological features to those of this neurodegenerative disorder. The gastrointestinal system is in constant communication with the brain via several conduits collectively termed the gut-brain axis. The microbial population of the gut, referred to as the microbiota, has a profound effect on the interactions that occur along this communication route. Recent evidence suggests that dysbiosis, an abnormal gastrointestinal microbial population, is linked to cognitive impairment in rodent AD models and human AD. There is also evidence from rodent AD models that correcting dysbiosis by transferring fecal material from healthy donors to the gastrointestinal tracts of cognitively impaired recipients [fecal microbiome transplantation (FMT)] reverses AD-associated brain pathology and improves cognitive function. Although limited, some clinical reports have described the improvement of cognitive function with FMT in human AD. The goals of this review article are to provide an overview of the mechanisms involved in dysbiosis- associated cognitive decline and the role of FMT in therapy for such decline. The potential role of FMT in CCD is also discussed.},
}

Dogs
Animals
*Fecal Microbiota Transplantation/veterinary
*Dog Diseases/therapy/microbiology
Dysbiosis/therapy/veterinary
Gastrointestinal Microbiome
*Aging
*Cognitive Dysfunction/therapy
Cognition
*Alzheimer Disease/therapy/veterinary
Humans

@article {pmid40201444,
year = {2025},
author = {Liu, Y and Li, X and Chen, Y and Yao, Q and Zhou, J and Wang, X and Meng, Q and Ji, J and Yu, Z and Chen, X},
title = {Fecal microbiota transplantation: application scenarios, efficacy prediction, and factors impacting donor-recipient interplay.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1556827},
pmid = {40201444},
issn = {1664-302X},
abstract = {Fecal microbiota transplantation (FMT) represents a therapeutic approach that directly regulates the gut microbiota of recipients, normalizes its composition and reaping therapeutic rewards. Currently, in addition to its general application in treating Clostridium difficile (C. difficile) infection (CDI), FMT treatment has also been extended to the fields of other gastrointestinal diseases, infections, gut-liver or gut-brain axis disorders, metabolic diseases and cancer, etc. Prior to FMT, rigorous donor screening is essential to reduce the occurrence of adverse events. In addition, it is imperative to evaluate whether the recipient can safely and effectively undergo FMT treatment. However, the efficacy of FMT is influenced by the complex interactions between the gut microbiota of donor and recipient, the degree of donor microbiota engraftment is not necessarily positively related with the success rate of FMT. Furthermore, an increasing number of novel factors affecting FMT outcomes are being identified in recent clinical trials and animal experiments, broadening our understanding of FMT treatment. This article provides a comprehensive review of the application scenarios of FMT, the factors influencing the safety and efficacy of FMT from the aspects of both the donors and the recipients, and summarizes how these emerging novel regulatory factors can be combined to predict the clinical outcomes of patients undergoing FMT.},
}

@article {pmid40200137,
year = {2025},
author = {Wang, X and Geng, Q and Jiang, H and Yue, J and Qi, C and Qin, L},
title = {Fecal microbiota transplantation enhanced the effect of chemoimmunotherapy by restoring intestinal microbiota in LLC tumor-bearing mice.},
journal = {BMC immunology},
volume = {26},
number = {1},
pages = {30},
pmid = {40200137},
issn = {1471-2172},
support = {CJ20220086//Changzhou 8th Batch of Science and Technology Project (Applied Basic Research)/ ; CMCC202201//Clinical Research Project of Changzhou Medical Center, Nanjing Medical University/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/immunology ; *Fecal Microbiota Transplantation/methods ; Mice ; *Carcinoma, Lewis Lung/therapy/immunology/microbiology ; Mice, Inbred C57BL ; *Immunotherapy/methods ; RNA, Ribosomal, 16S/genetics ; Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology ; },
abstract = {OBJECTIVE: To assess the effect of half-dose chemotherapy (HDC) and standard-dose chemotherapy (SDC) on the intestinal microbiota and to investigate whether fecal microbiota transplantation (FMT) can restore the intestinal microecology to enhance the efficacy of chemoimmunotherapy containing an anti-PD- 1 antibody (PD1).

METHODS: Lewis lung cancer (LLC) tumor-bearing mice were divided into six groups, including Control, HDC, SDC, SDC + FMT, SDC + PD1, and SDC + PD1 + FMT. After the treatment, analyses were conducted on intestinal microbiota using 16S rRNA sequencing, immune cells through flow cytometry, cytokines and chemokines via polymerase chain reaction (PCR), and programmed death-ligand 1 (PD-L1) expression in tumor tissues by immunohistochemistry.

RESULTS: Alpha and beta diversity of intestinal flora were not significantly different between HDC and SDC groups, nor was there a significant difference in the abundance of the top 10 species at the phylum, class, order, family, genus, or species levels. FMT increased both alpha and beta diversity and led to an increase in the abundance of Ruminococcus_callidus and Alistipes_finegoldii at the species level in mice receiving SDC + FMT. Besides, tumor growth was significantly slowed in SDC + PD1 + FMT compared to SDC + PD1 group, accompanied by an up-regulated Bacteroidetes/Firmicutes ratio, down-regulated abundance of Proteobacteria species (including Pseudolabrys, Comamonas, Alcaligenaceae, Xanthobacteraceae and Comamonadaceae), as well as Faecalicoccus of Firmicutes, the increased number of cDC1 cells, cDC2 cells, CD4[+] T cells and CD8[+] T cells in the peripheral blood, and IFN-γ[+]CD8[+] T cells, IFN-γ, granzyme B, TNF-α, CXCL9 and CXCL10 in intestinal tissues.

CONCLUSIONS: There were no significant differences between HDC and SDC in their effects on the intestinal microbiota. FMT exhibited a beneficial impact on gut microbiota and improved the efficacy of chemoimmunotherapy, possibly associated with the increase of immune cells and the modulation of related cytokines and chemokines.},
}

Animals
*Gastrointestinal Microbiome/immunology
*Fecal Microbiota Transplantation/methods
Mice
*Carcinoma, Lewis Lung/therapy/immunology/microbiology
Mice, Inbred C57BL
*Immunotherapy/methods
RNA, Ribosomal, 16S/genetics
Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology

@article {pmid40199985,
year = {2025},
author = {Vecchiato, CG and Sabetti, MC and Sung, CH and Sportelli, F and Delsante, C and Pinna, C and Alonzo, M and Erba, D and Suchodolski, JS and Pilla, R and Pietra, M and Biagi, G and Procoli, F},
title = {Effect of faecal microbial transplantation on clinical outcome, faecal microbiota and metabolome in dogs with chronic enteropathy refractory to diet.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {11957},
pmid = {40199985},
issn = {2045-2322},
mesh = {Animals ; Dogs ; *Fecal Microbiota Transplantation/methods ; *Metabolome ; Male ; Female ; *Feces/microbiology ; *Dog Diseases/therapy/microbiology/metabolism ; Treatment Outcome ; Gastrointestinal Microbiome ; *Intestinal Diseases/therapy/veterinary/microbiology ; Chronic Disease ; Diet ; Bile Acids and Salts/metabolism ; Dysbiosis/therapy ; },
abstract = {Chronic enteropathy (CE) is a common complaint in canine gastroenterology. Recently, faecal microbiota transplantation (FMT) gained attention as a treatment strategy. However, the efficacy and long-term impact of FMT is still unclear. Clinical index (CIBDAI), faecal microbiota and metabolome were monitored in 20 CE dogs refractory to diet before (T0) and 3 months (T3) after FMT. Further data were retrospectively collected up to 1-year after FMT. Significant improvements were observed in CIBDAI, Dysbiosis Index (DI), and primary (PBAs) and secondary (SBAs) faecal bile acids and propionate one month (T1) after FMT (CIBDAI (median and range): T0 5 (1-9) vs. T1 1 (0-5), p < 0.0001; DI (median and range): T0 -0.1 (-5.6 to 3.8) vs. T1 -2.1 (-5.7 to 4.7), p < 0.05; PBAs decreased by 57%, SBAa increased by 41%; propionate increased by 20%). According to CIBDAI, 17 dogs clinically improved up to T3, and 10 dogs remained clinically stable up to one year after FMT. Alpha- and beta-diversity of the faecal microbiota of CE dogs did not differ, neither before nor after FMT, from that of 17 healthy controls. The results highlight that CE dogs refractory to diet with mild clinical signs and dysbiosis may benefit long-term from treatment with FMT.},
}

Animals
Dogs
*Fecal Microbiota Transplantation/methods
*Metabolome
Male
Female
*Feces/microbiology
*Dog Diseases/therapy/microbiology/metabolism
Treatment Outcome
Gastrointestinal Microbiome
*Intestinal Diseases/therapy/veterinary/microbiology
Chronic Disease
Diet
Bile Acids and Salts/metabolism
Dysbiosis/therapy

@article {pmid40199868,
year = {2025},
author = {Liu, C and Zheng, X and Ji, J and Zhu, X and Liu, X and Liu, H and Guo, L and Ye, K and Zhang, S and Xu, YJ and Sun, X and Zhou, W and Wong, HLX and Tian, Y and Qian, H},
title = {The carotenoid torularhodin alleviates NAFLD by promoting Akkermanisa muniniphila-mediated adenosylcobalamin metabolism.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {3338},
pmid = {40199868},
issn = {2041-1723},
mesh = {Animals ; *Carotenoids/pharmacology ; Male ; *Non-alcoholic Fatty Liver Disease/drug therapy/metabolism/microbiology ; Mice ; Humans ; Gastrointestinal Microbiome/drug effects ; Mice, Inbred C57BL ; *Akkermansia/metabolism/drug effects ; Liver/metabolism/drug effects/pathology ; Disease Models, Animal ; *Vitamin B 12/metabolism/analogs & derivatives ; Colon/metabolism/drug effects ; },
abstract = {Torularhodin, a unique carotenoid, confers beneficial effects on nonalcoholic fatty liver disease (NAFLD). However, the precise mechanism underlying its therapeutic effects remains unknown. Here, we report that torularhodin alleviates NAFLD in male mice by modulating the gut microbiota. Additionally, transplanting fecal microbiota from torularhodin-treated mice to germ-free mice also improves NAFLD. Mechanistically, torularhodin specifically enriches the abundance of Akkermansia muciniphila, which alleviates NAFLD by promoting the synthesis of adenosylcobalamin. Utilizing a human gastrointestinal system and a colonic organoid model, we further demonstrate that adenosylcobalamin confers protective effects against NAFLD through reducing ceramides, a well-known liver damaging compound, and this effect is mediated by inhibition of the hypoxia-inducible factor 2α pathway. Notably, we construct electrospun microsphere-encapsulated torularhodin, which facilitates the slow release of torularhodin in the colon. Together, our findings indicate the therapeutic potential of microbial utilization of carotenoids, such as torularhodin, for treating NAFLD.},
}

Animals
*Carotenoids/pharmacology
Male
*Non-alcoholic Fatty Liver Disease/drug therapy/metabolism/microbiology
Mice
Humans
Gastrointestinal Microbiome/drug effects
Mice, Inbred C57BL
*Akkermansia/metabolism/drug effects
Liver/metabolism/drug effects/pathology
Disease Models, Animal
*Vitamin B 12/metabolism/analogs & derivatives
Colon/metabolism/drug effects

@article {pmid40198451,
year = {2025},
author = {Duo, R and Wang, Y and Ma, Q and Wang, X and Zhang, Y and Shen, H},
title = {MTX-induced gastrointestinal reactions in RA: Prevotella enrichment, gut dysbiosis, and PI3K/Akt/Ras/AMPK pathways.},
journal = {Clinical rheumatology},
volume = {},
number = {},
pages = {},
pmid = {40198451},
issn = {1434-9949},
support = {No. CY2023-MS-A13//CuiYing Technology Project of Lanzhou University/ ; No. 2023-4-27//Science and Technology Planning Project of Lanzhou/ ; No. 2018-3-49//Science and Technology Planning Project of Lanzhou/ ; No. CYXZ2022-13//Cuiying Scientific Training Program for Undergraduates of The Second Hospital & Clinical Medical School/ ; 25JRRA617//Natural Science Foundation of Gansu Province/ ; 2025B-020//Gansu Province Higher Education Institution Teachers' Innovation Fund Project/ ; },
abstract = {OBJECTIVES: To investigate the role of gut microbiota in methotrexate (MTX)-induced gastrointestinal reactions (MRGR) in patients with rheumatoid arthritis (RA).

METHODS: As a prospective, single-center, convenience sampling study, stool samples were obtained from 28 RA patients (male: female = 10:18) at Lanzhou University Second Hospital who were undergoing MTX treatment for analysis of their gut microbiota using 16S rRNA gene sequencing. Clinical disease activity (CDAI) and MRGR were assessed after two months of MTX therapy. All data collection periods exceeded one year. Intestinal germ-free mice, generated through antibiotic treatment, received fecal microbiota transplantation (FMT) from the patients, followed by varying doses of MTX to observe MRGR. Intestinal transcriptomics and markers related to intestinal barrier function were subsequently examined.

RESULTS: Females (84.6%) and high disease activity (CDAI scores, 39.6 ± 11.2 vs 26.3 ± 9.2) were prone to have MRGR in RA patients. Patients with MRGR (PT-GR) showed lower gut microbial diversity versus non-MRGR (PT-noGR). Prevotella abundance, positively correlated with CDAI and MRGR (p < 0.05), was elevated in PT-GR. Administering 10 mg/kg MTX to mice caused intestinal damage. FMT-GR-MTX mice exhibited weight loss (95.2%), morphological deterioration (86.4%), and reduced tight junction proteins (Claudin-1:72.4%; ZO-1:81.2%). Transcriptomics linked upregulated Gβγ/CREB/Atp4b to PI3K/Akt/Ras pathways and downregulated PFK2/PP2 to AMPK signaling in MRGR.

CONCLUSION: Our study identified notable gut microbiota alterations in RA patients prone to MRGR, with changes in intestinal gene expression and reduced intestinal barrier function potentially contributing to MRGR. These findings suggest potential strategies to mitigate MRGR in RA patients undergoing MTX treatment. Key Points • The RA-related MRGR is correlated with the intestinal microbiota. • Females, low gut diversity, and Prevotella enrichment are MRGR risks in RA. • Upregulated DEGs in MRGR linked to PI3K/Akt, Ras pathways. • Downregulated DEGs in MRGR focus on the AMPK pathway.},
}

@article {pmid40198007,
year = {2025},
author = {Attauabi, M and Madsen, GR and Holm, JP and Bendtsen, F and Møller, S and Seidelin, JB and Burisch, J},
title = {Incidence of Osteoporosis and Osteopenia in Newly Diagnosed Inflammatory Bowel Disease: A Population-Based Cohort Study.},
journal = {Inflammatory bowel diseases},
volume = {},
number = {},
pages = {},
doi = {10.1093/ibd/izaf063},
pmid = {40198007},
issn = {1536-4844},
support = {//Novo Nordisk Fonden/ ; 101095470//EU Horizon Europe Program/ ; },
abstract = {BACKGROUND: Individuals with Crohn's disease (CD) and ulcerative colitis (UC) are at risk of developing osteoporosis. In Denmark, osteoporosis has been observed in 12.0% of postmenopausal women and 2.6% in men aged ≥ 50 years in the general population. We aimed to conduct a population-based analysis determining bone mineral density (BMD) at diagnosis of UC and CD.

METHODS: All adult patients diagnosed with UC or CD between May 2021 and May 2023 in an area covering 20% (1.2 million inhabitants) of the Danish population were invited for dual-energy X-ray absorptiometry at inflammatory bowel disease (IBD) diagnosis.

RESULTS: In total, 209 and 141 patients with UC and CD, respectively, were included. Among postmenopausal women (age ≥ 52 years) with UC, 15/42 (35.7%) had osteoporosis and 17/42 (40.5%) had osteopenia, while rates among patients with CD were 6/21 (28.6%, P = .57) and 8/21 (38.1%, P = .86), respectively. Among males aged ≥ 50 years, the rates were 5/38 (13.2%) and 17/38 (44.7%) in UC, respectively, and 3/24 (12.5%, P = 1.00) and 12/24 (50.0%, P = .69) in CD, respectively. Among younger patients, BMD below the expected range for age was observed in 3/69 (4.3%) and 3/60 (5.0%) of females and males with UC, and in 1/42 (2.4%) and 8/54 (14.8%) with CD, respectively. No nutritional or inflammatory marker, including C-reactive protein, fecal calprotectin, Mayo Endoscopic Score, or Simple Endoscopic Score for CD correlated with the T-score.

CONCLUSIONS: This population-based study demonstrated high rates of osteoporosis among postmenopausal women and males aged ≥ 50 years at IBD diagnosis, highlighting the need for systematic evaluation in these patients.},
}

@article {pmid40197991,
year = {2025},
author = {Malard, F and Thepot, S and Cluzeau, T and Carre, M and Lebon, D and Bories, P and Legrand, O and Schwarz, M and Loschi, M and Meunier, M and Joris, M and Gasc, C and Jouve, J and Levast, B and Plantamura, E and Prestat, E and Sabourin, A and Gaugler, B and Dore, J and Récher, C and Mohty, M},
title = {Gut microbiota restoration with oral pooled fecal microbiotherapy after intensive chemotherapy: the phase Ib CIMON trial.},
journal = {Blood advances},
volume = {},
number = {},
pages = {},
doi = {10.1182/bloodadvances.2024015571},
pmid = {40197991},
issn = {2473-9537},
abstract = {Intensive chemotherapy (IC) combined with broad-spectrum antibiotics for acute myeloid leukemia (AML) leads to gut microbiota dysbiosis, promoting pathological conditions and an increased incidence of complications, possibly limiting eligibility to allogenic hematopoietic cell transplantation (alloHCT). The purpose of this dose-ranging phase I study (CIMON) was to evaluate the first-in-man use of MaaT033, a pooled, allogeneic, lyophilized, and standardized fecal microbiotherapeutic product, formulated as a delayed-release capsule for oral administration. Primary objectives of the study were to evaluate the maximum tolerable dose of MaaT033 in 21 AML patients having undergone IC and antibiotics. Secondary objectives were to assess MaaT033 safety, its efficacy in restoring the patients' gut microbiome using shotgun sequencing in order to evaluate the recommended dose regimen, and patient compliance (ClinicalTrials.gov number: NCT04150393). MaaT033 was shown to be safe and effective for gut microbiota restoration in AML patients receiving IC and antibiotics, with an excellent gut microbiota reconstruction based on diversity indices at the species level, and restoration of microbial communities close to the composition of the drug product. Moreover, inflammatory markers (C-reactive protein, interleukin-6) decrease with treatment, while short-chain fatty acids increase over time. A randomized, placebo-controlled phase IIb trial, in recipients of alloHCT patients in ongoing.},
}

@article {pmid40196486,
year = {2025},
author = {Shealy, NG and Baltagulov, M and de Brito, C and McGovern, A and Castro, P and Schrimpe-Rutledge, AC and Malekshahi, C and Condreanu, SG and Sherrod, SD and Jana, S and Jones, K and Machado Ribeiro, T and McLean, JA and Beiting, DP and Byndloss, MX},
title = {Short-term alterations in dietary amino acids override host genetic susceptibility and reveal mechanisms of Salmonella Typhimurium small intestine colonization.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.03.25.645332},
pmid = {40196486},
issn = {2692-8205},
abstract = {In addition to individual genetics, environmental factors (e.g., dietary changes) may influence host susceptibility to gastrointestinal infection through unknown mechanisms. Herein, we developed a model in which CBA/J mice, a genetically resistant strain that tolerates intestinal colonization by the enteric pathogen Salmonella Typhimurium (S. Tm), rapidly succumb to infection after exposure to a diet rich in L-amino acids (AA). In mice, S. Tm-gastroenteritis is restricted to the large intestine (cecum), limiting their use to understand S . Tm small intestine (ileum) colonization, a feature of human Salmonellosis. Surprisingly, CBA mice fed AA diet developed ileitis with enhanced S . Tm ileal colonization. Using germ-free mice and ileal-fecal slurry transplant, we found diet-mediated S . Tm ileal expansion to be microbiota-dependent. Mechanistically, S . Tm relied on Fructosyl-asparagine utilization to expand in the ileum during infection. We demonstrate how AA diet overrides host genetics by altering the gut microbiota's ability to prevent S. Tm ileal colonization.},
}

@article {pmid40195995,
year = {2025},
author = {Larsen, T and Ayayee, P and Cluster, G and Clayton, J and Price, J and Ramer-Tait, A},
title = {Assessing gut microbial provisioning of essential amino acids to host in a murine model with reconstituted gut microbiomes.},
journal = {Research square},
volume = {},
number = {},
pages = {},
doi = {10.21203/rs.3.rs-6255159/v1},
pmid = {40195995},
issn = {2693-5015},
abstract = {Gut microbial essential amino acid (EAA) provisioning to mammalian hosts remains a critical yet poorly understood aspect of host-microbe nutritional interactions, with significant implications for human and animal health. To investigate microbial EAA contributions in mice with reconstituted gut microbiomes, we analyzed stable carbon isotopes ([13]C) of six EAAs across multiple organs. Germ-free (GF) mice fed a high-protein diet (18%) were compared to conventionalized (CVZ) mice fed a low-protein diet (10%) following fecal microbiota transplantation 30 days prior and a 20-day dietary intervention. We found no evidence for microbial EAA contributions to host tissues, with [13]C-EAA fingerprinting revealing nearly identical patterns between GF and CVZ organs. Both groups maintained their expected microbiome statuses, with CVZ gut microbiota dominated by Firmicutes and Bacteroidetes phyla. These findings raise important questions about the functional capacities of reconstituted gut microbiomes. Future studies should investigate longer adaptation periods, varied dietary protein levels, and complementary analytical techniques to better understand the context-dependent nature of microbial EAA provisioning in mammalian hosts.},
}

@article {pmid40195644,
year = {2025},
author = {Barrios Steed, D and Koundakjian, D and Harris, AD and Rosato, AE and Konstantinidis, KT and Woodworth, MH},
title = {Leveraging strain competition to address antimicrobial resistance with microbiota therapies.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2488046},
doi = {10.1080/19490976.2025.2488046},
pmid = {40195644},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Anti-Bacterial Agents/pharmacology ; *Bacteria/drug effects/genetics/growth & development ; Fecal Microbiota Transplantation ; *Drug Resistance, Bacterial ; Animals ; Probiotics ; },
abstract = {The enteric microbiota is an established reservoir for multidrug-resistant organisms that present urgent clinical and public health threats. Observational data and small interventional studies suggest that microbiome interventions, such as fecal microbiota products and characterized live biotherapeutic bacterial strains, could be an effective antibiotic-sparing prevention approach to address these threats. However, bacterial colonization is a complex ecological phenomenon that remains understudied in the context of the human gut. Antibiotic resistance is one among many adaptative strategies that impact long-term colonization. Here we review and synthesize evidence of how bacterial competition and differential fitness in the context of the gut present opportunities to improve mechanistic understanding of colonization resistance, therapeutic development, patient care, and ultimately public health.},
}

Humans
*Gastrointestinal Microbiome/drug effects
Anti-Bacterial Agents/pharmacology
*Bacteria/drug effects/genetics/growth & development
Fecal Microbiota Transplantation
*Drug Resistance, Bacterial
Animals
Probiotics

@article {pmid40192235,
year = {2025},
author = {Jiao, Y and Ren, J and Xie, S and Yuan, N and Shen, J and Yin, H and Wang, J and Guo, H and Cao, J and Wang, X and Wu, D and Zhou, Z and Qi, X},
title = {Raffinose-metabolizing bacteria impair radiation-associated hematopoietic recovery via the bile acid/FXR/NF-κB signaling pathway.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2488105},
doi = {10.1080/19490976.2025.2488105},
pmid = {40192235},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/radiation effects ; *Bile Acids and Salts/metabolism ; Mice ; *NF-kappa B/metabolism/genetics ; Signal Transduction/radiation effects ; *Raffinose/metabolism ; Mice, Inbred C57BL ; Whole-Body Irradiation/adverse effects ; *Receptors, Cytoplasmic and Nuclear/metabolism/genetics ; Fecal Microbiota Transplantation ; Male ; *Acute Radiation Syndrome/microbiology/metabolism ; *Hematopoiesis/radiation effects ; *Bacteria/metabolism/genetics/classification/isolation & purification ; Dysbiosis/microbiology ; },
abstract = {Radiation-associated hematopoietic recovery (RAHR) is critical for mitigating lethal complications of acute radiation syndrome (ARS), yet therapeutic strategies remain limited. Through integrated multi-omics analysis of a total body irradiation (TBI) mouse model, we identify Bacteroides acidifaciens-dominated gut microbiota as key mediators of RAHR impairment. 16S ribosomal rRNA sequencing revealed TBI-induced dysbiosis characterized by Bacteroidaceae enrichment, while functional metagenomics identified raffinose metabolism as the most significantly perturbed pathway. Notably, raffinose supplementation (10% w/v) recapitulated radiation-induced microbiota shifts and delayed bone marrow recovery. Fecal microbiota transplantation (FMT) revealed a causative role for raffinose-metabolizing microbiota, particularly Bacteroides acidifaciens, in delaying RAHR progression. Mechanistically, B. acidifaciens-mediated bile acid deconjugation activated FXR, subsequently suppressing NF-κB-dependent hematopoietic recovery. Therapeutic FXR inhibition via ursodeoxycholic acid (UDCA) had been shown to be a viable method for rescuing RAHR. Our results delineated a microbiome-bile acid-FXR axis as a master regulator of post-irradiation hematopoiesis. Targeting B. acidifaciens or its metabolic derivatives could represent a translatable strategy to mitigate radiation-induced hematopoietic injury.},
}

Animals
*Gastrointestinal Microbiome/radiation effects
*Bile Acids and Salts/metabolism
Mice
*NF-kappa B/metabolism/genetics
Signal Transduction/radiation effects
*Raffinose/metabolism
Mice, Inbred C57BL
Whole-Body Irradiation/adverse effects
*Receptors, Cytoplasmic and Nuclear/metabolism/genetics
Fecal Microbiota Transplantation
Male
*Acute Radiation Syndrome/microbiology/metabolism
*Hematopoiesis/radiation effects
*Bacteria/metabolism/genetics/classification/isolation & purification
Dysbiosis/microbiology

@article {pmid40192143,
year = {2025},
author = {Feuerstadt, P and Allegretti, J and Khanna, S},
title = {Treatment of Clostridioides difficile: The Times They are a Changing.},
journal = {The American journal of gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.14309/ajg.0000000000003445},
pmid = {40192143},
issn = {1572-0241},
}

@article {pmid40192074,
year = {2025},
author = {Geng, L and Yang, X and Sun, J and Ran, X and Zhou, D and Ye, M and Wen, L and Wang, R and Chen, M},
title = {Gut Microbiota Modulation by Inulin Improves Metabolism and Ovarian Function in Polycystic Ovary Syndrome.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e2412558},
doi = {10.1002/advs.202412558},
pmid = {40192074},
issn = {2198-3844},
support = {23Y11909600//Science and Technology Commission of Shanghai Municipality/ ; 1365//Talent reservoir program of Shanghai First Maternity and Infant Hospital/ ; 81871213//National Natural Science Foundation of China/ ; 81671468//National Natural Science Foundation of China/ ; SHDC2020CR4080//Shanghai Municipal Hospital Development Center/ ; 2021ScienceandTechnology02-37//Shanghai Collaborative Innovation Center for Chronic Disease Prevention and Health Services/ ; },
abstract = {The management of metabolic disorder associated with polycystic ovary syndrome (PCOS) has been suggested as an effective approach to improve PCOS which is highly involved with gut microbiota, while the underlying mechanism is unclear. Here, we investigated the role of inulin, a gut microbiota regulator, in the alleviation of PCOS. Our findings showed that inulin treatment significantly improved hyperandrogenism and glucolipid metabolism in both PCOS cohort and mice. Consistent with the cohort, inulin increased the abundance of microbial co-abundance group (CAG) 12 in PCOS mice, including Bifidobacterium species and other short-chain fatty acids (SCFAs)-producers. We further verified the enhancement of SCFAs biosynthesis capacity and fecal SCFAs content by inulin. Moreover, inulin decreased lipopolysaccharide-binding protein (LBP) and ameliorated ovarian inflammation in PCOS mice, whereas intraperitoneal lipopolysaccharide (LPS) administration reversed the protective effects of inulin. Furthermore, fecal microbiota transplantation (FMT) from inulin-treated patients with PCOS enhanced insulin sensitivity, improved lipid accumulation and thermogenesis, reduced hyperandrogenism and ovarian inflammatory response in antibiotic-treated mice. Collectively, these findings revealed that gut microbiota mediates the beneficial effects of inulin on metabolic disorder and ovarian dysfunction in PCOS. Therefore, modulating gut microbiota represents a promising therapeutic strategy for PCOS.},
}

@article {pmid40191185,
year = {2025},
author = {Chen, L and Ruan, G and Zhao, X and Yi, A and Xiao, Z and Tian, Y and Cheng, Y and Chen, D and Wei, Y},
title = {Pseudomonas aeruginosa enhances anti-PD-1 efficacy in colorectal cancer by activating cytotoxic CD8[+] T cells.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1553757},
pmid = {40191185},
issn = {1664-3224},
mesh = {Animals ; *Colorectal Neoplasms/immunology/therapy/microbiology ; *Pseudomonas aeruginosa/immunology ; Mice ; *Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology ; *Immune Checkpoint Inhibitors/pharmacology/therapeutic use ; Gastrointestinal Microbiome/immunology ; Humans ; *CD8-Positive T-Lymphocytes/immunology ; Fecal Microbiota Transplantation ; Female ; Lymphocyte Activation/immunology ; *T-Lymphocytes, Cytotoxic/immunology ; Cell Line, Tumor ; Male ; },
abstract = {BACKGROUND: Immune checkpoint therapy for colorectal cancer (CRC) has been found to be unsatisfactory for clinical treatment. Fecal microbiota transplantation (FMT) has been shown to remodel the intestinal flora, which may improve the therapeutic effect of αPD-1. Further exploration of key genera that can sensitize cells to αPD-1 for CRC treatment and preliminary exploration of immunological mechanisms may provide effective guidance for the clinical treatment of CRC.

METHODS: In this study, 16S rRNA gene sequencing was analyzed in the fecal flora of both responders and no-responders to αPD-1 treatment, and the therapeutic effect was experimentally verified.

RESULTS: Pseudomonas aeruginosa was found to be highly abundant in the fecal flora of treated mice, and Pseudomonas aeruginosa mannose-sensitive hemagglutinin (PA-MSHA) in combination with αPD-1 was effective in the treatment of CRC through the induction of CD8[+] T-cell immunological effects.

CONCLUSION: The clinical drug PA-MSHA can be used in combination with αPD-1 for the treatment of CRC as a potential clinical therapeutic option.},
}

Animals
*Colorectal Neoplasms/immunology/therapy/microbiology
*Pseudomonas aeruginosa/immunology
Mice
*Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology
*Immune Checkpoint Inhibitors/pharmacology/therapeutic use
Gastrointestinal Microbiome/immunology
Humans
*CD8-Positive T-Lymphocytes/immunology
Fecal Microbiota Transplantation
Female
Lymphocyte Activation/immunology
*T-Lymphocytes, Cytotoxic/immunology
Cell Line, Tumor
Male

@article {pmid40190259,
year = {2025},
author = {Nagayama, M and Gogokhia, L and Longman, RS},
title = {Precision microbiota therapy for IBD: premise and promise.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2489067},
doi = {10.1080/19490976.2025.2489067},
pmid = {40190259},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation/methods ; *Inflammatory Bowel Diseases/therapy/microbiology ; Animals ; *Precision Medicine/methods ; },
abstract = {Inflammatory Bowel Disease (IBD) is a spectrum of chronic inflammatory diseases of the intestine that includes subtypes of ulcerative colitis (UC) and Crohn's Disease (CD) and currently has no cure. While IBD results from a complex interplay between genetic, environmental, and immunological factors, sequencing advances over the last 10-15 years revealed signature changes in gut microbiota that contribute to the pathogenesis of IBD. These findings highlight IBD as a disease target for microbiome-based therapies, with the potential to treat the underlying microbial pathogenesis and provide adjuvant therapy to the emerging spectrum of advanced therapies for IBD. Building on the success of fecal microbiota transplantation (FMT) for Clostridioides difficile infection, therapies targeting gut microbiota have emerged as promising approaches for treating IBD; however, unique aspects of IBD pathogenesis highlight the need for more precision in the approach to microbiome therapeutics that leverage aspects of recipient and donor selection, diet and xenobiotics, and strain-specific interactions to enhance the efficacy and safety of IBD therapy. This review focuses on both pre-clinical and clinical studies that support the premise for microbial therapeutics for IBD and aims to provide a framework for the development of precision microbiome therapeutics to optimize clinical outcomes for patients with IBD.},
}

Humans
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation/methods
*Inflammatory Bowel Diseases/therapy/microbiology
Animals
*Precision Medicine/methods

@article {pmid40189556,
year = {2025},
author = {Zhang, Y and Si, L and Shu, X and Qiu, C and Wan, X and Li, H and Ma, S and Jin, X and Wei, Z and Hu, H},
title = {Gut microbiota contributes to protection against porcine deltacoronavirus infection in piglets by modulating intestinal barrier and microbiome.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {93},
pmid = {40189556},
issn = {2049-2618},
mesh = {Animals ; Swine ; *Gastrointestinal Microbiome ; *Deltacoronavirus/physiology ; *Swine Diseases/microbiology/virology/prevention & control ; *Coronavirus Infections/veterinary/microbiology/virology ; Fecal Microbiota Transplantation ; *Intestinal Mucosa/microbiology ; Feces/microbiology ; Diarrhea ; Intestines/microbiology/virology ; },
abstract = {BACKGROUND: Gut microbiota plays a critical role in counteracting enteric viral infection. Our previous study demonstrated that infection of porcine deltacoronavirus (PDCoV) disturbs gut microbiota and causes intestinal damage and inflammation in piglets. However, the influence of gut microbiota on PDCoV infection remains unclear.

RESULTS: Firstly, the relationship between gut microbiota and disease severity of PDCoV infection was evaluated using 8-day-old and 90-day-old pigs. The composition of gut microbiota was significantly altered in 8-day-old piglets after PDCoV infection, leading to severe diarrhea and intestinal damage. In contrast, PDCoV infection barely affected the 90-day-old pigs. Moreover, the diversity (richness and evenness) of microbiota in 90-day-old pigs was much higher compared to the 8-day-old piglets, suggesting the gut microbiota is possibly associated with the severity of PDCoV infection. Subsequently, transplanting the fecal microbiota from the 90-day-old pigs to the 3-day-old piglets alleviated clinical signs of PDCoV infection, modulated the diversity and composition of gut microbiota, and maintained the physical and chemical barrier of intestines. Additionally, metabolomic analysis revealed that the fecal microbiota transplantation (FMT) treatment upregulated the swine intestinal arginine biosynthesis, FMT significantly inhibited the inflammatory response in piglet intestine by modulating the TLR4/MyD88/NF-κB signaling pathway.

CONCLUSIONS: PDCoV infection altered the structure and composition of the gut microbiota in neonatal pigs. FMT treatment mitigated the clinical signs of PDCoV infection in the piglets by modulating the gut microbiota composition and intestinal barrier, downregulating the inflammatory response. The preventive effect of FMT provides novel targets for the development of therapeutics against enteropathogenic coronaviruses. Video Abstract.},
}

Animals
Swine
*Gastrointestinal Microbiome
*Deltacoronavirus/physiology
*Swine Diseases/microbiology/virology/prevention & control
*Coronavirus Infections/veterinary/microbiology/virology
Fecal Microbiota Transplantation
*Intestinal Mucosa/microbiology
Feces/microbiology
Diarrhea
Intestines/microbiology/virology

@article {pmid40189555,
year = {2025},
author = {Zhou, J and Lu, P and He, H and Zhang, R and Yang, D and Liu, Q and Liu, Q and Liu, M and Zhang, G},
title = {The metabolites of gut microbiota: their role in ferroptosis in inflammatory bowel disease.},
journal = {European journal of medical research},
volume = {30},
number = {1},
pages = {248},
pmid = {40189555},
issn = {2047-783X},
support = {No.82474662//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Ferroptosis ; *Gastrointestinal Microbiome/physiology ; *Inflammatory Bowel Diseases/microbiology/metabolism/therapy/pathology ; Oxidative Stress ; Animals ; Fatty Acids, Volatile/metabolism ; Bile Acids and Salts/metabolism ; },
abstract = {Inflammatory bowel disease (IBD) includes chronic inflammatory conditions, such as Crohn's disease and ulcerative colitis, characterized by impaired function of the intestinal mucosal epithelial barrier. In recent years, ferroptosis, a novel form of cell death, has been confirmed to be involved in the pathological process of IBD and is related to various pathological changes, such as oxidative stress and inflammation. Recent studies have further revealed the complex interactions between the microbiome and ferroptosis, indicating that ferroptosis is an important target for the regulation of IBD by the gut microbiota and its metabolites. This article reviews the significant roles of gut microbial metabolites, such as short-chain fatty acids, tryptophan, and bile acids, in ferroptosis in IBD. These metabolites participate in the regulation of ferroptosis by influencing the intestinal microenvironment, modulating immune responses, and altering oxidative stress levels, thereby exerting an impact on the pathological development of IBD. Treatments based on the gut microbiota for IBD are gradually becoming a research hotspot. Finally, we discuss the potential of current therapeutic approaches, including antibiotics, probiotics, prebiotics, and fecal microbiota transplantation, in modulating the gut microbiota, affecting ferroptosis, and improving IBD symptoms. With a deeper understanding of the interaction mechanisms between the gut microbiota and ferroptosis, it is expected that more precise and effective treatment strategies for IBD will be developed in the future.},
}

Humans
*Ferroptosis
*Gastrointestinal Microbiome/physiology
*Inflammatory Bowel Diseases/microbiology/metabolism/therapy/pathology
Oxidative Stress
Animals
Fatty Acids, Volatile/metabolism
Bile Acids and Salts/metabolism

@article {pmid40189523,
year = {2025},
author = {Yu, X and Chen, Y and Lei, L and Li, P and Lin, D and Shen, Y and Hou, C and Chen, J and Fan, Y and Jin, Y and Lu, H and Wu, D and Xu, Y},
title = {Mendelian randomization analysis of blood metabolites and immune cell mediators in relation to GVHD and relapse.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {201},
pmid = {40189523},
issn = {1741-7015},
support = {QNXM2024010//Suzhou Science and Education Strengthening Health Youth ProjectSuzhou Science and Education Strengthening Health Youth Project/ ; MQ2024022//Medical research project of Jiangsu Provincial Health Commission/ ; BXQN2023032//Boxi cultivation program project of the First Affiliated Hospital of Suzhou University/ ; KYCX23_3270//Postgraduate Research & Practice Innovation Program of Jiangsu Province/ ; SKJY2021049//Suzhou Science and Technology Program Project/ ; SKY2022043//Suzhou Science and Technology Program Project/ ; SLT201911//Suzhou Science and Technology Program Project/ ; 82100231//National Natural Science Foundation of China/ ; 82020108003//National Natural Science Foundation of China/ ; 82070187//National Natural Science Foundation of China/ ; CXZX202201//Jiangsu Provincial Medical Innovation Center/ ; 2022YFC2502700//National Key Research and Development Program/ ; },
mesh = {*Graft vs Host Disease/genetics/blood/immunology ; Humans ; *Mendelian Randomization Analysis ; *Hematopoietic Stem Cell Transplantation/adverse effects ; Recurrence ; Genome-Wide Association Study ; Male ; Female ; },
abstract = {BACKGROUND: Graft-versus-host disease (GVHD) and relapse are major complications following allogeneic hematopoietic stem cell transplantation (allo-HSCT). Metabolites play crucial roles in immune regulation, but their causal relationships with GVHD and relapse remain unclear.

METHODS: We utilized genetic variants from genome-wide association studies (GWAS) of 309 known metabolites as instrumental variables to evaluate their causal effects on acute GVHD (aGVHD), gut GVHD, chronic GVHD (cGVHD), and relapse in different populations. Multiple causal inference methods, heterogeneity assessments, and pleiotropy tests were conducted to ensure result robustness. Multivariable MR analysis was performed to adjust for potential confounders, and validation MR analysis further confirmed key findings. Mediation MR analysis was employed to explore indirect causal pathways.

RESULTS: After correction for multiple testing, we identified elevated pyridoxate and proline levels as protective factors against grade 3-4 aGVHD (aGVHD3) and relapse, respectively. Conversely, glycochenodeoxycholate increased the risk of aGVHD3, whereas 1-stearoylglycerophosphoethanolamine had a protective effect. The robustness and stability of these findings were confirmed by multiple causal inference approaches, heterogeneity, and horizontal pleiotropy analyses. Multivariable MR analysis further excluded potential confounding pleiotropic effects. Validation MR analyses supported the causal roles of pyridoxate and 1-stearoylglycerophosphoethanolamine, while mediation MR revealed that pyridoxate influences GVHD directly and indirectly via CD39[ +] Tregs. Pathway analyses highlighted critical biochemical alterations, including disruptions in bile acid metabolism and the regulatory roles of vitamin B6 derivatives. Finally, clinical metabolic analyses, including direct fecal metabolite measurements, confirmed the protective role of pyridoxate against aGVHD.

CONCLUSIONS: Our findings provide novel insights into the metabolic mechanisms underlying GVHD and relapse after allo-HSCT. Identified metabolites, particularly pyridoxate, may serve as potential therapeutic targets for GVHD prevention and management.},
}

*Graft vs Host Disease/genetics/blood/immunology
Humans
*Mendelian Randomization Analysis
*Hematopoietic Stem Cell Transplantation/adverse effects
Recurrence
Genome-Wide Association Study
Male
Female

@article {pmid40189067,
year = {2025},
author = {Jiang, ST and Wang, MQ and Gao, L and Zhang, QC and Tang, C and Dong, YF},
title = {Adjusting the composition of gut microbiota prevents the development of post-stroke depression by regulating the gut-brain axis in mice.},
journal = {Journal of affective disorders},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jad.2025.03.195},
pmid = {40189067},
issn = {1573-2517},
abstract = {Disturbances in gut microbiota contribute to an imbalanced gut-brain axis, which is critical for post-stroke depression (PSD), while the underlying mechanisms remain unclear. The objective of this study was to examine the effects of modifying gut microbiota through antibiotic treatment (ABX) and fecal microbiota transplantation (FMT) on the progression of PSD. The PSD model was established by occluding the middle cerebral artery (MCAO), followed by a four-week isolated housing and restraint stress initiated three days after MCAO. For ABX, the PSD mice received antibiotic water for four weeks. While another group of PSD mice underwent FMT or fluoxetine (FLX) for four weeks. At day 35 post-MCAO, behavioral tests were conducted. Results indicated ABX and FMT significantly altered the composition of intestinal flora caused by PSD, all the treatments markedly attenuated anxiety- and depressive-like behaviors and inflammation in the gut and brain. ABX obviously alleviated PSD-induced disorder of intestinal barrier, decreased mRNA levels of TNF-α, IL-1β and IL-6, and decreased CD4[+] cells in the colon. While FMT significantly decreased CD8[+] cells and increased the goblet cells in colon. Furthermore, both ABX and FMT could reduce activated microglia and pro-inflammatory cytokines in the brain, alleviate decreased Nissl's bodies in the hippocampus, and reverse the decreases in 5-HT, Glu and DA in the striatum caused by PSD. Unlike ABX, FMT was similar to FLX. These findings suggest homeostasis of gut microbiota is indispensable for the development of PSD; adjusting the gut microbiota significantly improves PSD with enhanced functions of gut-brain axis.},
}

@article {pmid40188410,
year = {2025},
author = {Oyovwi, MO and Ben-Azu, B and Babawale, KH},
title = {Therapeutic potential of microbiome modulation in reproductive cancers.},
journal = {Medical oncology (Northwood, London, England)},
volume = {42},
number = {5},
pages = {152},
pmid = {40188410},
issn = {1559-131X},
mesh = {Humans ; *Microbiota ; Probiotics/therapeutic use ; Female ; Dysbiosis/microbiology/therapy ; *Genital Neoplasms, Female/microbiology/therapy ; Fecal Microbiota Transplantation/methods ; Animals ; Gastrointestinal Microbiome ; },
abstract = {The human microbiome, a complex ecosystem of microbial communities, plays a crucial role in physiological processes, and emerging research indicates a potential link between it and reproductive cancers. This connection highlights the significance of understanding the microbiome's influence on cancer development and treatment. A comprehensive review of current literature was conducted, focusing on studies that investigate the relationship between microbiome composition, reproductive cancer progression, and potential therapeutic approaches to modulate the microbiome. Evidence suggests that imbalances in the microbiome, known as dysbiosis, may contribute to the development and progression of reproductive cancers. Specific microbial populations have been associated with inflammatory responses, immune modulation, and even resistance to conventional therapies. Interventions such as probiotics, dietary modifications, and fecal microbiota transplantation have shown promise in restoring healthy microbiome function and improving cancer outcomes in pre-clinical models, with pilot studies in humans indicating potential benefits. This review explores the therapeutic potential of microbiome modulation in the management of reproductive cancers, discussing the mechanisms involved and the evidence supporting microbiome-targeted therapies. Future research is warranted to unravel the complex interactions between the microbiome and reproductive cancer pathophysiology, paving the way for innovative approaches.},
}

Humans
*Microbiota
Probiotics/therapeutic use
Female
Dysbiosis/microbiology/therapy
*Genital Neoplasms, Female/microbiology/therapy
Fecal Microbiota Transplantation/methods
Animals
Gastrointestinal Microbiome

@article {pmid40187666,
year = {2025},
author = {Moreno-Sabater, A and Sintes, R and Truong, S and Lemoine, K and Camou, O and Kapel, N and Magne, D and Joly, AC and Quelven-Bertin, I and Alric, L and Hennequin, C and Sokol, H and , },
title = {Assessment of Dientamoeba fragilis interhuman transmission by fecal microbiota transplantation.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107504},
doi = {10.1016/j.ijantimicag.2025.107504},
pmid = {40187666},
issn = {1872-7913},
abstract = {Fecal microbiota transplantation (FMT) for recurrent Clostridioides difficile infection (rCDI) requires careful selection of stool donors to avoid transmitting pathogens. Dientamoeba fragilis detection remains an exclusion criterion based on its uncertain pathogenicity. The aim of this study was to assess D. fragilis interhuman transmission by FMT and its impact on the clinical success of rCDI. A retrospective study was conducted in rCDI patients from the COSMIC cohort undergoing FMT to investigate the potential transfer of D. fragilis from donor to recipient. The impact of FMT involving D. fragilis was also evaluated on the clinical outcomes of rCDI and adverse effects. This protist was found to be present in 15 out of 86 healthy donors screened (18.7%) who voluntarily took part in an FMT program. Examination of D. fragilis presence in stool samples from 17 patients both before and after FMT with D. fragilis-positive donations revealed no evidence of interhuman transmission through this process. Analysis of clinical outcomes and adverse events in 124 rCDI patients who underwent FMT (with 45 receiving D. fragilis-positive donations) showed no significant differences in success rates between patients receiving positive or negative D. fragilis transplants, 95.5% and 93.6%, respectively. No significant variances were observed in other side effects analyzed. These findings underscore the safety of using fecal transplant from D. fragilis positive donors in the FMT process. D. fragilis should be removed from the donor screening, which will represent a major improvement in the donor selection process from financial and practical standpoints.},
}

@article {pmid40187461,
year = {2025},
author = {Yang, J and Ren, H and Cao, J and Fu, J and Wang, J and Su, Z and Lu, S and Sheng, K and Wang, Y},
title = {Gut commensal Lachnospiraceae bacteria contribute to anti-colitis effects of Lactiplantibacillus plantarum exopolysaccharides.},
journal = {International journal of biological macromolecules},
volume = {309},
number = {Pt 1},
pages = {142815},
doi = {10.1016/j.ijbiomac.2025.142815},
pmid = {40187461},
issn = {1879-0003},
abstract = {The probiotic Lactiplantibacillus plantarum (L. plantarum) could ameliorate colitis. Alterations in the composition of gut microbiota (GM) have been proved in cases of colitis. The exopolysaccharides from L. plantarum HMPM2111 (LPE) could be effective in colitis through altering the composition of the GM. These effects were linked to inhibiting intestinal inflammation, regulating the TXNIP/NLRP3 inflammasome axis, and attenuating colonic barrier dysfunction. The combination of fecal microbiota transplantation (FMT) and antibiotic inducement showed that gut bacteria susceptible to vancomycin were inversely associated with colitis features and were necessary for the anti-inflammatory effects of LPE. The elevated abundances of gut commensal Lachnospiraceae bacteria were associated with the restoration of colitis treated by LPE. Metabolomics analysis showed that colitis mice treated with LPE had higher levels of propionate and tryptophan metabolites generated from gut bacteria. The administration of these metabolites protected colitis and resulted in a reduction in inflammatory responses. The outcomes of our investigation emerge the significance of the GM in controlling the protective implications of LPE against colitis. Lachnospiraceae bacteria, together with downstream metabolites, contribute substantially to protection. This work elucidates the essential function of the GM-metabolite axis in producing comprehensive protection versus colitis and identifies prospective treatment targets.},
}

@article {pmid40187430,
year = {2025},
author = {Cai, M and Xue, SS and Zhou, CH and Feng, YC and Liu, JZ and Liu, R and Wang, P and Wang, HN and Peng, ZW},
title = {Effects of fecal microbiota transplantation from patients with generalized anxiety on anxiety-like behaviors: The role of the gut-microbiota-endocannabinoid-brain Axis.},
journal = {Journal of affective disorders},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jad.2025.04.018},
pmid = {40187430},
issn = {1573-2517},
abstract = {BACKGROUND: Intestinal dysbacteriosis is frequently implicated in generalized anxiety disorder (GAD). However, the molecular mechanisms and functional changes of the gut-brain axis in GAD remain largely unexplored.

METHODS: We investigated anxiety-like behaviors, gut microbiota changes, brain region-specific endocannabinoid (eCB) system alterations, including the expression of cannabinoid type 1 (CB1R), monoacylglycerol lipase (MAGL), and fatty acid amide hydrolase (FAAH) in the hippocampus (Hip), prefrontal cortex (PFC), and amygdala (Amy), as well as plasma medium- and long-chain fatty acids (MLCFAs) in a mouse model of chronic restraint stress (CRS) and antibiotic-treated mice receiving fecal microbiota transplantation from GAD patients (FMT-GAD). Additionally, we assessed the impact of FMT-GAD on anxiety-like behavior in systemic CB1R/FAAH/MAGL knockout mice.

RESULTS: CRS induced anxiety-like behaviors, suppressed eCB signaling in the brain, and altered the gut microbiota and plasma MLCFA composition in mice. FMT-GAD-treated mice exhibited anxiety-like behaviors, increased FAAH expression in the Hip and Amy, and MAGL expression in the Hip, while reducing CB1R expression in the Hip. FMT-GAD was associated with decreased plasma polyunsaturated fatty acids (PUFAs) and reduced microbiome function for fatty acid biosynthesis. Notably, FMT-GAD intensified anxiety-like behaviors in CB1R-KO mice but failed to induce anxiety-like behaviors in MAGL-KO and FAAH-KO mice.

CONCLUSIONS: This study demonstrates that the interplay between the gut microbiota and the eCB system modulates GAD-related anxiety-like behaviors.},
}

@article {pmid40185558,
year = {2025},
author = {Shin, JH and Jackson-Akers, JY and Hoang, SC and Behm, BW and Warren, CA},
title = {Fulminant Clostridioides difficile Infection: A Journey into the Unknown!.},
journal = {The Medical clinics of North America},
volume = {109},
number = {3},
pages = {721-734},
doi = {10.1016/j.mcna.2025.01.001},
pmid = {40185558},
issn = {1557-9859},
support = {R01 AI145322/AI/NIAID NIH HHS/United States ; },
mesh = {Humans ; *Clostridium Infections/diagnosis/therapy ; *Anti-Bacterial Agents/therapeutic use ; *Clostridioides difficile/isolation & purification ; Colectomy ; Fecal Microbiota Transplantation ; Ileostomy ; Immunoglobulins, Intravenous/therapeutic use ; },
abstract = {Clostridioides difficile is 1 of the 5 urgent antibiotic resistance threats in the United States as reported by the Centers for Disease Control and Prevention. Fulminant C difficile infection (CDI), characterized by hallmarks of critical illness such as hypotension, shock, or megacolon, has been difficult to define and treat. In this article, we describe the diagnostic criteria for fulminant CDI, clinical factors and inflammatory markers. We review the currently recommended treatment modalities including antibiotics and surgical interventions, colectomy, and diverting loop ileostomy. We also included treatment approaches that are still investigational such as intestinal microbiota transplant, tigecycline, and intravenous immunoglobulin.},
}

Humans
*Clostridium Infections/diagnosis/therapy
*Anti-Bacterial Agents/therapeutic use
*Clostridioides difficile/isolation & purification
Colectomy
Fecal Microbiota Transplantation
Ileostomy
Immunoglobulins, Intravenous/therapeutic use

@article {pmid40185194,
year = {2025},
author = {Docherty, J},
title = {Therapeutic potential of faecal microbiota transplantation for alcohol use disorder, a narrative synthesis.},
journal = {Progress in neuro-psychopharmacology & biological psychiatry},
volume = {},
number = {},
pages = {111354},
doi = {10.1016/j.pnpbp.2025.111354},
pmid = {40185194},
issn = {1878-4216},
abstract = {BACKGROUND: Faecal microbiota transplantation is proposed as an alternative therapy to treat alcohol use disorder and has completed a Phase 1 clinical trial, with a Phase 2 clinical trial underway. Alcohol, a modifiable risk factor for noncommunicable diseases, resulted in approximately 3 million global deaths (5 %) in 2016 according to the World Health Organization.

AIMS: A narrative synthesis examines the effects of alcohol and faecal microbiota transplantation on gut microbiota and how gut microbiota impacts the gut-brain axis, leading to certain behavioural symptoms of alcohol use disorder. These behavioural symptoms are alcohol craving and relapse in humans; and preference for alcohol, anxiety and depression in rodents.

SEARCH METHODS AND RESULTS: Electronic databases PubMed, Embase, and Scopus were searched in January 2024 using the terms: faecal microbiota trans* AND alcohol AND microbio*. Ten studies out of 964 met the inclusion criteria of published primary studies with faecal microbiota transplantation as an intervention to study the gut-brain axis in alcohol use disorder.

RESULTS: The gut microbiota is altered in alcohol use disorder, which can be modified with faecal microbiota transplantation. Behavioural symptoms such as alcohol craving and relapse are associated with inflammation due to a loss of intestinal barrier function. Beneficial microbiota produce short-chain fatty acids that maintain intestinal barrier function and reduce inflammation. Studies also reported anxiety and depression-like behaviours, in addition to a preference for alcohol in alcohol-naïve rodents after faecal microbiota transplantation from patients with alcohol use disorder.

CONCLUSIONS: Faecal microbiota transplantation may moderate the behavioural symptoms of alcohol use disorder by altering gut microbiota, affecting intestinal permeability and inflammation, however, specific gut microbiota composition and long-term treatment outcomes require further clinical studies.},
}

@article {pmid40185172,
year = {2025},
author = {Liu, C and Fan, P and Dai, J and Ding, Z and Yi, Y and Zhan, X and Wang, CC and Liang, R},
title = {Integrated microbiome and metabolome analysis reveals that Zishen Qingre Lishi Huayu recipe regulates gut microbiota and butyrate metabolism to ameliorate polycystic ovary syndrome.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {107533},
doi = {10.1016/j.micpath.2025.107533},
pmid = {40185172},
issn = {1096-1208},
abstract = {BACKGROUND: s: Polycystic ovary syndrome (PCOS) is a metabolic disorder disease strongly associated with gut microbiota (GM). Zishen Qingre Lishi Huayu recipe (ZQLHR), a traditional Chinese medicinal compound, has patented and shown therapeutic effects in treating PCOS in clinical trials without clear pharmacological mechanisms. This study aimed to disclose the potential therapeutic mechanism of ZQLHR on PCOS.

METHODS: We firstly confirmed the therapeutic effects of ZQLHR treatment in PCOS patients. 16S rRNA sequencing, untargeted metabolomics, fecal microbiota transplantation (FMT), high performance liquid chromatography (HPLC) and Person's correlation analysis were conducted to elucidate the potential therapeutic mechanism.

RESULTS: These results showed that PCOS symptoms in ZQLHR patients were significantly ameliorated. ZQLHR could increase the levels of butyrate-producing Lachnospira and Faecalibacterium and decrease the abundance of Escherichia-Shigella. Untargeted metabolomics showed that ZQLHR significantly improved host metabolic function, particularly butyrate metabolism and citrate cycle (TCA cycle) metabolism. The combined Faecalibacterium and butyrate metabolism datasets were correlated. Stool samples from ZQLHR patients could ameliorate ovarian architecture, significantly reduce testosterone (T), estradiol (E2) and luteinizing hormone (LH) levels and increased follicle-stimulating hormone (FSH) levels and increase the content of butyric acid in PCOS mice (P < 0.01). Moreover, the correlation analysis showed that some biochemical parameters (T, E2, LH levels and FSH) and butyric acid were correlated.

CONCLUSION: We firstly depicted that ZQLHR could alleviate the series of symptom in women with PCOS by regulating gut microbiota and butyrate metabolism. This study provides a scientific basis and new ideas for the therapy of PCOS.},
}

@article {pmid40184763,
year = {2025},
author = {Huang, M and Zhang, Y and Chen, Z and Yu, X and Luo, S and Peng, X and Li, X},
title = {Gut microbiota reshapes the TNBC immune microenvironment: Emerging immunotherapeutic strategies.},
journal = {Pharmacological research},
volume = {215},
number = {},
pages = {107726},
doi = {10.1016/j.phrs.2025.107726},
pmid = {40184763},
issn = {1096-1186},
abstract = {Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer with limited treatment options and poor prognosis. The gut microbiota, a diverse community of microorganisms in the gastrointestinal tract, plays a crucial role in regulating immune responses through the gut-immune axis. Recent studies have highlighted its significant impact on TNBC progression and the efficacy of immunotherapies. This review examines the interactions between gut microbiota and the immune system in TNBC, focusing on key immune cells and pathways involved in tumor immunity. It also explores microbiota modulation strategies, including probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation, as potential methods to enhance immunotherapeutic outcomes. Understanding these mechanisms offers promising avenues for improving treatment efficacy and patient prognosis in TNBC.},
}