@article {pmid40514640,
year = {2025},
author = {Almulla, AF and Maes, M},
title = {Peripheral Immune-Inflammatory Pathways in Major Depressive Disorder, Bipolar Disorder, and Schizophrenia: Exploring Their Potential as Treatment Targets.},
journal = {CNS drugs},
volume = {},
number = {},
pages = {},
pmid = {40514640},
issn = {1179-1934},
support = {RA66/016//FF66 grant and a Sompoch Endowment Fund (Faculty of Medicine), MDCU/ ; BG-RRP-2.004-0007-С01//Strategic Research and Innovation Program for the Development of MU - PLOVDIV-(SRIPD-MUP)", Creation of a network of research higher schools, National plan for recovery and sustainability, European Union - NextGenerationEU/ ; },
abstract = {Major depressive disorder (MDD), bipolar disorder (BD), and schizophrenia (SCZ) are major mental disorders linked to substantial morbidity. Traditional monoamine-based pharmacotherapies frequently produce inadequate outcomes for many patients. The elevated levels of treatment resistance require the exploration of new pharmacological targets. Evidence indicates that peripheral immune-inflammatory dysregulation, characterized by an imbalance between immunological responses and compensatory immune-regulatory systems (IRS/CIRS), together with increased oxidative and nitrosative stress (O&NS), significantly contributes to the pathogenesis of these disorders. This review examines IRS/CIRS/O&NS pathways as new drug targets and highlights novel pharmacological trials. Antiinflammatory drugs have been repurposed as augmentation strategies for the treatment of MDD/BD and SCZ, including nonsteroidal antiinflammatory medications, such as cyclooxygenase-2 (COX-2) inhibitors; cytokine-targeting biologics, such as tumor necrosis factor-α monoclonal antibodies; and minocycline, an antibiotic that attenuates neuroinflammation. N-acetylcysteine, curcumin, and omega-3 polyunsaturated fatty acids demonstrate some efficacy as augmentation therapies in MDD, likely by diminishing IRS activation and O&NS. Strategies aimed at the gut-brain axis and gut dysbiosis, including fecal microbiota transplantation, are under investigation for their capacity to restore immunological homeostasis by improving gut barrier integrity and microbiome composition. This review examines new potential therapeutic targets arising from recent discoveries in neuro-immune interactions and oxidative stress, including particular lymphocyte surface markers, the CIRS, and intracellular network molecules in both affective and psychotic disorders. The evidence underscores the clinical importance of immune-targeted augmentation treatments in psychiatric disorders and supports the ongoing development of these novel pharmacotherapies within a precision medicine paradigm.},
}

@article {pmid40513921,
year = {2025},
author = {Zhang, X and Sheng, N and Wang, Z and Cao, Y and Jiang, X and Yan, H and Cheng, F and Geng, T and Wei, K and Zhang, L and Gao, M and Zhou, G and Chen, P},
title = {Exploring the mechanism of Carbonized Typhae Pollen in treating blood stasis syndrome through metabolic profiling: the synergistic effect of hemostasis without blood stasis.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {120124},
doi = {10.1016/j.jep.2025.120124},
pmid = {40513921},
issn = {1872-7573},
abstract = {Removing blood stasis and stopping bleeding traditional Chinese medicines (RBSB-TCM) formed a unique class of TCM, characterized by vasodilating, removing stasis and hemostatic effects. Carbonized Typhae Pollen (CTP), derived from Typhae Pollen (TP) through carbonization, has emerged as a particularly valuable therapeutic agent. It has been widely used in clinical practice to treat hemorrhagic disorders caused by blood stasis syndrome (BSS). However, the potential mechanism for CTP to achieve the dual synergistic effect of promoting blood flow and hemostasis remains unclear.

AIM OF THE STUDY: From the standpoint of metabolite profiles, this study attempts to investigate the fundamental mechanism of CTP in the elimination of blood stasis and the cessation of bleeding.

MATERIALS AND METHODS: First, chemical constituents, absorbed constituents and metabolites in rats following oral administration of CTP were identified by ultra-high performance liquid chromatography coupled with the quadrupole time-of-flight mass spectrometry (UHPLC-Q-TOF-MS) method combined with MetabolitePilot 2.0.4 software. Subsequently, the pharmacological effects of CTP were systematically investigated using rat models with BSS and zebrafish with cerebral hemorrhage. Specifically, the impact on coagulation function and histopathology in rats, as well as the effect on cerebral hemorrhage in zebrafish, were thoroughly evaluated. Untargeted metabolomics based on rat plasma was applied to analyze the metabolic profile changes, revealing the potential action mechanism. The underlying mechanism was furtherly confirmed by gut microbiome analysis and systemic molecular biology experiments.

RESULTS: 34 prototype chemicals and 71 metabolites from the liver, heart, spleen, lung, kidney, small intestine, uterus, and serum were found. CTP improved the abnormal coagulation system, promoted blood circulation, and reduced pathological damage caused by BSS. Plasma metabolomics revealed that BSS significantly altered bile acid (BA) metabolism and arachidonic acid (AA) metabolism. Gut microbiome analysis and fecal microbiota transplantation (FMT) experiments further demonstrated that CTP modulated the gut microbiota. This modulation promoted BA production and activated endothelial nitric oxide synthase (eNOS), leading to increased nitric oxide (NO) levels. These changes contributed to the therapeutic effect of CTP in removing blood stasis. Systemic molecular biology experiments showed that CTP activated key components of the AA metabolic pathway. It promoted PLCγ1 phosphorylation, increased intracellular Ca[2+] levels, and upregulated COX-2 expression. In addition, CTP enhanced the production of AA-related metabolites, including 6-keto-prostaglandin F1α (6-keto-PGF1α), prostaglandin E2 (PGE2), and thromboxane B2 (TXB2). It also increased the transcription of AA metabolism-related genes, such as PLCγ1, PTGS2a, PTGS2b, PTGIS, PTGES, TXBAS, and vWF.

CONCLUSIONS: CTP could promote the generation of AA metabolites through PLCγ1/Ca[2+]/COX-2 to stop bleeding, while also enhancing eNOS activity and NO synthesis through gut microbiota-bile acid axis to remove blood stasis. These two effect were balanced to achieve hemostasis without blood stasis.},
}

@article {pmid40511533,
year = {2025},
author = {Mo, X and Shen, L and Wang, X and Ni, W and Li, L and Xia, L and Liu, H and Cheng, R and Wen, L and Xu, J and Liu, L},
title = {Melatonin Mitigates Sarcopenic Obesity via Microbiota and Short-Chain Fatty Acids: Evidence From Epidemiologic and In Vivo Studies.},
journal = {Journal of cachexia, sarcopenia and muscle},
volume = {16},
number = {3},
pages = {e13869},
pmid = {40511533},
issn = {2190-6009},
support = {82230112//National Natural Science Foundation of China/ ; 82273631//National Natural Science Foundation of China/ ; 2024M761026//China Postdoctoral Science Foundation/ ; 2022YFA0806100//National Key Research and Development Program of China/ ; },
mesh = {Animals ; *Melatonin/pharmacology/therapeutic use ; *Sarcopenia/drug therapy/epidemiology/etiology ; *Obesity/drug therapy/epidemiology ; *Fatty Acids, Volatile/metabolism ; *Gastrointestinal Microbiome/drug effects ; Humans ; Male ; Rats ; Middle Aged ; Female ; Case-Control Studies ; Aged ; },
abstract = {INTRODUCTION: Gut dysbiosis is closely related to the development of sarcopenic obesity (SO). Melatonin (MLT) regulates gut microbiota and promotes the production of short-chain fatty acids (SCFAs). However, whether MLT affects SO through the gut microbiota and SCFAs remains unclear. This study aimed to investigate the effect and mechanism of MLT in SO induced by a high-fat diet (HFD).

METHODS: First, a case-control study was conducted to explore the potential association between serum MLT levels and SO-related parameters in 31 patients. Next, rats fed with a HFD were orally administered with MLT for 16 weeks, and obesity-related metabolic disorders and muscle atrophy were measured. 16S rRNA gene sequencing and gas chromatography-mass spectrometry were used to detect gut microbiota and SCFAs, respectively. Gut barrier integrity was assessed by the expression of the Muc-2 protein and tight junction proteins. Finally, faecal microbiota transplantation and SCFAs administration were performed to confirm the causal role of the gut microbiota and SCFAs in the effect of MLT on SO.

RESULTS: The serum levels of MLT decreased in patients with SO (29.87 ± 6.71 vs. 24.94 ± 5.68, p < 0.01) and were closely associated with appendicular skeletal muscle mass index (r = 0.3514, p < 0.01) and handgrip strength (r = 0.2824, p < 0.05). MLT ameliorated obesity-related metabolic disorders (p < 0.05), poor muscle mass (p < 0.05), strength (p < 0.05) and function (p < 0.05) and muscle atrophy (p < 0.05) in HFD-fed rats. MLT regulated HFD-induced gut dysbiosis, which was mainly characterized by increases in SCFAs-related bacteria and SCFAs (p < 0.05). MLT recovered HFD-induced impairment of gut barrier integrity by promoting the expression levels of Muc-2, claudin-1, occludin and zonula occluden-1 proteins in the colon (p < 0.05). Correlation analysis showed that SCFAs-related bacteria and SCFAs were negatively associated with SO. Faecal suspension from MLT-treated rats promoted the production of SCFAs in recipient rats (p < 0.05). In addition, faecal suspension from MLT-treated rats partially mitigated metabolic disorders (p < 0.05), poor muscle mass and function (p < 0.05) and muscle atrophy (p < 0.05) in recipient rats. SCFAs treatment alleviated the development of SO in HFD-fed rats by suppressing metabolic disorders (p < 0.05), reducing muscle oxidative stress and inflammation (p < 0.05) and promoting protein synthesis through the AKT/mTOR/p70S6k signalling pathway (p < 0.05).

CONCLUSIONS: MLT mitigated HFD-induced SO by regulating the gut microbiota and promoting the production of SCFAs. MLT might be a novel strategy for delaying the progression of SO.},
}

Animals
*Melatonin/pharmacology/therapeutic use
*Sarcopenia/drug therapy/epidemiology/etiology
*Obesity/drug therapy/epidemiology
*Fatty Acids, Volatile/metabolism
*Gastrointestinal Microbiome/drug effects
Humans
Male
Rats
Middle Aged
Female
Case-Control Studies
Aged

@article {pmid40510802,
year = {2025},
author = {Tan, S and Peng, C and Lin, X and Peng, C and Yang, Y and Liu, S and Huang, L and Bian, Y and Li, Y and Xu, C},
title = {Clinical efficacy of non-pharmacological treatment of functional constipation: a systematic review and network meta-analysis.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1565801},
pmid = {40510802},
issn = {2235-2988},
mesh = {Humans ; Acupuncture Therapy/methods ; *Constipation/therapy ; Fecal Microbiota Transplantation/methods ; Randomized Controlled Trials as Topic ; Treatment Outcome ; },
abstract = {INTRODUCTION: The purpose of this study is to compare the relative effectiveness and safety of non-pharmacological interventions for the treatment of functional constipation (FC).

METHODS: We searched Pubmed, Embase, Cochrane, and Web of Science databases for randomized controlled trials published from 2010 to November 2024. The quality of the included studies was evaluated using the Cochrane bias risk tool and Review Manager 5.4, and the evidence was graded using GRADEPro. A network meta-analysis (NMA) was conducted using R Studio, and the surface under the cumulative ranking curve (SUCRA) was used to rank the included drugs for each outcome measure to compare the clinical efficacy of different treatment methods for chronic functional constipation.

RESULTS: A total of 29 RCT studies were included, with a total of 4389 patients with functional constipation who were randomly assigned to receive placebo or one of the nine different non-pharmacological treatment methods. The assessment of bias risk showed that the bias risk of most included studies was low. The results showed that the first-ranked treatment method for clinical efficacy was acupuncture; the first-ranked treatment method for changes in spontaneous bowel movement (SBM) and complete spontaneous bowel movement (CSBM) was fecal microbiota transplantation (FMT); the first-ranked treatment method for changes in the Bristol Stool Form Scale (BSFS) score was FMT; the first-ranked treatment method for changes in the Patient Assessment of Constipation Quality of Life (PAC-QOL) score after treatment was the Vibration capsule; the first-ranked treatment method for changes in the Patient Assessment of Constipation Symptoms (PAC-SYM) score after treatment was percutaneous electrical stimulation; and the treatment method with the lowest incidence of adverse reactions was probiotics.

CONCLUSION: Based on the SUCRA values and NMA results, we found that FMT showed better effects and higher safety on BSFS scores, SBM, and CSBM. In addition, acupuncture showed a good clinical efficacy. We hypothesize that the combination of FMT and acupuncture may be an effective and safe treatment option for functional constipation, but further high-quality clinical studies are needed to confirm this.

https://www.crd.york.ac.uk/prospero/, identifier CRD42024625747.},
}

Humans
Acupuncture Therapy/methods
*Constipation/therapy
Fecal Microbiota Transplantation/methods
Randomized Controlled Trials as Topic
Treatment Outcome

@article {pmid40510588,
year = {2025},
author = {He, S and Chen, H and Xi, H and Sun, G and Du, B and Liu, X},
title = {Gut Microbiota-Derived Butyric Acid Alleviates Glucocorticoid-Associated Osteonecrosis of the Femoral Head via Modulating Inflammatory Cytokines in Bone Marrow Mesenchymal Stem Cells.},
journal = {Mediators of inflammation},
volume = {2025},
number = {},
pages = {8742817},
pmid = {40510588},
issn = {1466-1861},
mesh = {Animals ; *Butyric Acid/metabolism/therapeutic use/pharmacology ; *Gastrointestinal Microbiome/physiology/drug effects ; Rats, Sprague-Dawley ; Rats ; *Mesenchymal Stem Cells/metabolism/drug effects ; *Glucocorticoids/adverse effects ; *Cytokines/metabolism ; Male ; *Osteonecrosis/chemically induced/metabolism/drug therapy ; },
abstract = {Background: The role of gut microbiota and its metabolites in regulating bone metabolism has been well established, with inflammatory immune responses potentially playing a critical role. Glucocorticoid-associated osteonecrosis of the femoral head (GA-ONFH), caused by high-dose glucocorticoid use for inflammatory or immune-related diseases, is a prevalent condition of bone metabolic imbalance. However, the regulatory role and mechanisms of gut microbiota and its metabolites in the development and progression of GA-ONFH remain unclear. This study aims to investigate the intervention effects of gut microbiota and its metabolite butyric acid on GA-ONFH through a series of multi-omics in vitro and in vivo experiments. Methods: Sprague Dawley rats were randomly divided into four groups. The gut microbial composition of the groups was analyzed through 16S rDNA sequencing. Targeted metabolomics was employed to assess differences in short-chain fatty acids (SCFAs) among the groups. Butyric acid, identified as a key differential metabolite, was then selected for further exploration of its effects on bone marrow mesenchymal stem cells (BMSCs) and GA-ONFH rat models through in vitro and in vivo experiments. Results: 16S rDNA sequencing revealed alterations in gut microbiota structure in GA-ONFH rats. Micro-CT and HE staining demonstrated that depletion of gut microbiota with broad-spectrum antibiotics prior to GA-ONFH modeling exacerbated the disease's development. In contrast, fecal microbiota transplantation (FMT) was shown to alleviate GA-ONFH progression. Targeted metabolomics indicated that FMT mitigated the reduction in butyric acid levels induced by dexamethasone (DXM). Subsequent in vitro cell experiments confirmed that butyric acid promotes BMSC proliferation, migration, and osteogenic differentiation. RNA sequencing revealed that butyric acid regulates T cell-mediated inflammatory cytokine genes in BMSCs, while Western blot and immunofluorescence assays confirmed that butyric acid modulates the expression of TNF-α and IL-2/IL-4 in BMSCs. Finally, in vivo experiments demonstrated that butyric acid supplementation attenuated the progression of GA-ONFH and improved the expression of inflammation-related cytokines in femoral head tissue. Conclusions: Our study demonstrates that gut microbiota depletion exacerbates GA-ONFH, while FMT restores butyric acid levels and alleviates disease severity. Butyric acid reduced the expression of TNF-α and IL-2 while increasing the level of IL-4 in vivo and in vitro, thereby improving the local inflammatory environment of the femoral head and alleviating the progression of GA-ONFH. These findings highlight that reduction in butyric acid levels due to gut microbiota dysbiosis is a crucial factor in the progression of GA-ONFH.},
}

Animals
*Butyric Acid/metabolism/therapeutic use/pharmacology
*Gastrointestinal Microbiome/physiology/drug effects
Rats, Sprague-Dawley
Rats
*Mesenchymal Stem Cells/metabolism/drug effects
*Glucocorticoids/adverse effects
*Cytokines/metabolism
Male
*Osteonecrosis/chemically induced/metabolism/drug therapy

@article {pmid40509521,
year = {2025},
author = {Zhang, M and Wang, W and Li, W and Wang, Z and Bi, K and Li, Y and Wu, Y and Zhao, Y and Yang, R and Du, Q},
title = {Ultrasonic-Assisted Extraction of Polysaccharides from Brassica rapa L. and Its Effects on Gut Microbiota in Humanized Mice.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111994},
pmid = {40509521},
issn = {2304-8158},
support = {32260586//the National Natural Science Foundation of China - Regional Fund Project/ ; },
abstract = {This study optimized ultrasound-assisted extraction (UAE) for polysaccharide isolation from Brassica rapa L. using Box-Behnken design, achieving a maximum yield of 41.12% under conditions of 60 °C, 60 min, 175 W ultrasonic power, and 30 mL/g liquid-solid ratios. The crude polysaccharide (BRAP) was purified via DEAE-52 cellulose and Sephadex G-100 chromatography, yielding BRAP1-1 with the highest recovery rate. Structural analyses (FT-IR, HPGPC, SEM, SEC-MALLS-RI) identified BRAP1-1 as a β-glycosidic pyranose polysaccharide (32.55 kDa) composed of fucose, rhamnose, arabinose, galactose, and galacturonic acid (molar ratio 0.81:4.30:3.61:1.69:89.59). In a humanized mouse model via fecal microbiota transplantation (FMT), BRAP1-1 significantly increased α-diversity indices (ACE, Chao1; p < 0.05) and altered β-diversity, with PCA explaining 73% variance (PC1: 60.70%, PC2: 13.53%). BRAP1-1 elevated beneficial genera (Lysinibacillus, Solibacillus, Bacteroides, etc.) while suppressing pathogens (Treponema, Flavobacterium, etc.). Six genera, including [Eubacterium]_coprostanoligenes_group and Bacteroidales (p < 0.05), correlated with acetic/propionic acid production. These findings demonstrate BRAP1-1's potential to modulate gut microbiota composition and enhance intestinal homeostasis.},
}

@article {pmid40509464,
year = {2025},
author = {Gong, H and Zhao, H and Mao, X},
title = {Sea Cucumber Hydrolysates Alleviate Cognitive Deficits in D-Galactose-Induced C57BL/6J Aging Mice Associated with Modulation of Gut Microbiota.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111938},
pmid = {40509464},
issn = {2304-8158},
support = {2023YFF1104502//National Key R&D Program of China/ ; },
abstract = {As the global elderly population is rising, concerns about cognitive decline and memory loss are becoming urgent. This study evaluated the potential of sea cucumber hydrolysates (SCH) from Stichopus japonicus in alleviating cognitive deficits using a D-galactose-induced murine aging model. The effects of SCH on behavior, hippocampal morphology, gut microbiota, hippocampal cholinergic system, brain-derived neurotrophic factor (BDNF) signaling, and neuroinflammatory pathways were investigated. Results showed that SCH ameliorated learning and memory deficits and reduced neuronal damage in aging mice. SCH also modulated gut microbiota, along with increased fecal short-chain fatty acids levels. Functional prediction revealed that alterations in gut microbiota were related to signal transduction. Further, SCH enhanced hippocampal cholinergic function through elevating acetylcholine (ACh) levels and inhibiting acetylcholinesterase (AChE) activity and activated BDNF signaling, consistent with predictions of gut microbiota function. Restoration of cholinergic homeostasis and transmission of the BDNF pathway might contribute to the inhibition of hippocampal neuroinflammation via suppressing microglial activation and the nuclear factor kappa-B (NF-κB) pathway. In summary, SCH attenuated cognitive deficits through suppressing neuroinflammation, which might be correlated with the signal transduction caused by regulating gut microbiota. Further validation will be conducted through microbiota depletion and fecal microbiota transplantation. These findings suggest that SCH is a promising functional component for counteracting aging-related cognitive deficits.},
}

@article {pmid40509391,
year = {2025},
author = {Zang, R and Zhou, R and Li, Y and Liu, Z and Wu, H and Lu, L and Xu, H},
title = {Oleuropein Regulates Bile Acid Metabolism via Modulating the Gut Microbiota, Thereby Alleviating DSS-Induced Ulcerative Colitis in Mice.},
journal = {Foods (Basel, Switzerland)},
volume = {14},
number = {11},
pages = {},
doi = {10.3390/foods14111863},
pmid = {40509391},
issn = {2304-8158},
abstract = {The pathogenesis of ulcerative colitis (UC) involves genetic, immunological, and environmental factors as well as gut microbiota dysbiosis. As a natural antioxidant with various pharmacological activities widely present in Oleaceae plants, oleuropein (OLE) exhibits anti-inflammatory, anti-tumor, antiviral, hypoglycemic, and cardioprotective effects. It has been validated that OLE extracted from olive oil can ameliorate UC. However, it remains unclear if and how OLE modulates the gut microbiota in the alleviation of UC. Therefore, this study was conducted to explore the mechanisms for OLE to alleviate UC induced by dextran sulfate sodium (DSS), with the focus placed on its regulatory function in the gut microbiota. The results indicated that OLE mitigated DSS-induced UC by enhancing the intestinal barrier function, reshaping the gut microbiota, and modulating bile acid metabolism. The fecal microbiota transplantation (FMT) experiment results further confirmed that the protective effect of OLE against UC could be mediated by alterations in the gut microbiota and their metabolites induced by OLE. Additionally, OLE increased the abundance of Lactobacillus and certain bile acid metabolites in the colon, including hyodeoxycholic acid (HDCA). HDCA could upregulate the expression of ZO-1 and claudin-3, restoring intestinal barrier integrity. Simultaneously, HDCA could inhibit the activation of the nuclear factor kappa-B (NF-κB) signaling pathway in the colon and relieve colonic inflammation. Overall, it was corroborated that OLE alleviated DSS-induced UC by modulating the gut microbiota and altering bile acid metabolism.},
}

@article {pmid40508089,
year = {2025},
author = {Ai, P and Xu, S and Yuan, Y and Xu, Z and He, X and Mo, C and Zhang, Y and Yang, X and Xiao, Q},
title = {Targeted Gut Microbiota Modulation Enhances Levodopa Bioavailability and Motor Recovery in MPTP Parkinson's Disease Models.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115282},
pmid = {40508089},
issn = {1422-0067},
support = {82171246//National Natural Science Foundation of China/ ; 82371251//National Natural Science Foundation of China/ ; 2022YFE0210100//National Key R&D Program of China/ ; 22QA1405700//Shanghai Rising-Star Program/ ; },
mesh = {*Gastrointestinal Microbiome/drug effects ; Animals ; *Levodopa/pharmacokinetics/pharmacology/therapeutic use ; Mice ; Fecal Microbiota Transplantation ; Biological Availability ; Male ; Humans ; Disease Models, Animal ; *Parkinson Disease/drug therapy/metabolism ; Dopamine/metabolism ; Mice, Inbred C57BL ; Female ; },
abstract = {Emerging evidence highlights the gut microbiota as a pivotal determinant of pharmacological efficacy. While Enterococcus faecalis (E. faecalis)-derived tyrosine decarboxylases (tyrDCs) are known to decarboxylate levodopa (L-dopa), compromising systemic bioavailability, the causal mechanisms underlying microbiota-mediated pharmacodynamic variability remain unresolved. In our study, we employed antibiotic-induced microbiota depletion and fecal microbiota transplantation (FMT) to interrogate microbiota-L-dopa interactions in MPTP-induced Parkinson's disease (PD) mice. The study demonstrated that antibiotic-mediated microbiota depletion enhances L-dopa bioavailability and striatal dopamine (DA) level, correlating with improved motor function. To dissect clinical heterogeneity in the L-dopa response, PD patients were stratified into moderate responders and good responders following standardized L-dopa challenges. In vitro bioconversion assays revealed greater L-dopa-to-DA conversion in fecal samples from moderate responders versus good responders. FMT experiments confirmed mice receiving good-responder microbiota exhibited enhanced L-dopa bioavailability, higher striatal DA concentrations, and a heightened therapeutic effect of L-dopa relative to moderate-responder recipients. Collectively, our study provided evidence that the gut microbiota directly modulates L-dopa metabolism and microbial composition determines interindividual therapeutic heterogeneity. Targeted microbial modulation-through precision antibiotics or donor-matched FMT-is a viable strategy to optimize PD pharmacotherapy, supporting the potential for microbiota-targeted adjuvant therapies in PD management.},
}

*Gastrointestinal Microbiome/drug effects
Animals
*Levodopa/pharmacokinetics/pharmacology/therapeutic use
Mice
Fecal Microbiota Transplantation
Biological Availability
Male
Humans
Disease Models, Animal
*Parkinson Disease/drug therapy/metabolism
Dopamine/metabolism
Mice, Inbred C57BL
Female

@article {pmid40507919,
year = {2025},
author = {Belvončíková, P and Macáková, K and Tóthová, N and Babál, P and Tarabčáková, L and Gardlík, R},
title = {Investigating the Role of Gut Microbiota in the Pathogenesis and Progression of Rheumatoid Arthritis in a Collagen-Induced Arthritis Mouse Model.},
journal = {International journal of molecular sciences},
volume = {26},
number = {11},
pages = {},
doi = {10.3390/ijms26115099},
pmid = {40507919},
issn = {1422-0067},
support = {APVV-21-0370//Slovak Research and Development Agency/ ; VEGA 1/0706/25//Ministry of Education, Science, Research and Sport of the Slovak Republic/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome ; *Arthritis, Rheumatoid/microbiology/pathology/therapy/etiology ; *Arthritis, Experimental/microbiology/pathology/therapy ; Mice ; Disease Models, Animal ; RNA, Ribosomal, 16S/genetics ; Disease Progression ; Humans ; Mice, Inbred DBA ; Male ; Fecal Microbiota Transplantation ; Female ; },
abstract = {Rheumatoid arthritis (RA) is a chronic systemic autoimmune disorder whose precise etiology remains unclear, though growing evidence implicates gut microbiota in its pathogenesis. This study aimed to investigate the role of gut microbiota in the onset and progression of RA by employing fecal microbiota transplantation (FMT) in a collagen-induced arthritis (CIA) mouse model using DBA/1J and Aire[-]/[-] strains. Mice received FMT from healthy donors, treatment-naïve RA patients, or treated RA patients in relapse, followed by assessment of microbiota composition via 16S rRNA sequencing, arthritis severity scoring, histological evaluations, and systemic inflammatory markers. The findings revealed distinct microbiota clustering patterns post-FMT across experimental groups, highlighting strain-specific colonization effects. Notably, genera such as Bifidobacterium and Paraprevotella correlated positively with arthritis severity in DBA/1J mice, whereas Corynebacterium, Enterorhabdus, and Odoribacter exhibited negative correlations, suggesting potential protective roles. Despite these microbial differences, minor variations in arthritis scores, paw inflammation, or systemic inflammation were observed among FMT groups. This indicates that although gut microbiota alterations are associated with RA pathogenesis, further investigation with larger cohorts and comprehensive sequencing approaches is essential to elucidate the therapeutic potential of microbiome modulation in autoimmune diseases.},
}

Animals
*Gastrointestinal Microbiome
*Arthritis, Rheumatoid/microbiology/pathology/therapy/etiology
*Arthritis, Experimental/microbiology/pathology/therapy
Mice
Disease Models, Animal
RNA, Ribosomal, 16S/genetics
Disease Progression
Humans
Mice, Inbred DBA
Male
Fecal Microbiota Transplantation
Female

@article {pmid40506454,
year = {2025},
author = {Runge, S and von Zedtwitz, S and Maucher, AM and Bruno, P and Osbelt, L and Zhao, B and Gernand, AM and Lesker, TR and Gräwe, K and Rogg, M and Schell, C and Boerries, M and Strowig, T and Andrieux, G and Hild, B and Rosshart, SP},
title = {Laboratory mice engrafted with natural gut microbiota possess a wildling-like phenotype.},
journal = {Nature communications},
volume = {16},
number = {1},
pages = {5301},
pmid = {40506454},
issn = {2041-1723},
support = {491676693//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 256073931//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 446316360//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 431984000//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 241702976//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 438496892//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 501370692//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 256073931//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 256073931//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 491676693//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 259373024//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 431984000//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 441891347//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 471011418//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 493802833-P7//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 390874280//Deutsche Forschungsgemeinschaft (German Research Foundation)/ ; 2023.010.1//Wilhelm Sander-Stiftung (Wilhelm Sander Foundation)/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/immunology/physiology ; Mice ; Phenotype ; Specific Pathogen-Free Organisms ; Mice, Inbred C57BL ; Male ; Female ; *Fecal Microbiota Transplantation/methods ; Models, Animal ; },
abstract = {Conventional laboratory mice housed under specific pathogen-free (SPF) conditions are the standard model in biomedical research. However, in recent years, many rodent-based studies have been deemed irreproducible, raising questions about the suitability of mice as model organisms. Emerging evidence indicates that variability in SPF microbiota plays a significant role in data inconsistencies across laboratories. Although efforts have been made to standardize microbiota, existing microbial consortia lack the complexity and resilience necessary to replicate interactions in free-living mammals. We present a robust, feasible and standardizable approach for transplanting natural gut microbiota from wildlings into laboratory mice. Following engraftment, these TXwildlings adopt a structural and functional wildling-like microbiota and host physiology toward a more mature immune system, with characteristics similar to those of adult humans. We anticipate that adopting wild mouse-derived microbiota as standard for laboratory mouse models will improve the reproducibility and generalizability of basic and preclinical biomedical research.},
}

Animals
*Gastrointestinal Microbiome/immunology/physiology
Mice
Phenotype
Specific Pathogen-Free Organisms
Mice, Inbred C57BL
Male
Female
*Fecal Microbiota Transplantation/methods
Models, Animal

@article {pmid40500780,
year = {2025},
author = {Liu, J and Jing, C and Guo, Y and Shang, Z and Zhang, B and Zhou, X and Zhang, J and Lian, G and Tian, F and Li, L and Chen, Y},
title = {The central signaling pathways related to metabolism-regulating hormones of the gut-brain axis: a review.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {648},
pmid = {40500780},
issn = {1479-5876},
support = {ZR2022MH085//Natural Science Foundation of Shandong Province/ ; ZR2022MH070//Natural Science Foundation of Shandong Province/ ; 202134027//Jinan Science and Technology Bureau/ ; },
abstract = {Obesity is a widespread metabolic disorder linked to various conditions, including type 2 diabetes, hypertension, fatty liver disease, sleep apnea, and hyperuricemia. It significantly impacts quality of life and economic productivity. Traditional methods like diet and lifestyle changes often fail to produce substantial weight loss. Consequently, emerging treatments such as anti-obesity medications, bariatric surgery, and fecal microbiota transplantation are becoming more prominent. Recent research emphasizes the role of hormones that communicate with the hypothalamus through the gut-brain axis, affecting appetite, insulin secretion, and body weight via specific signaling pathways. This review explores the role of key gastrointestinal hormones (GLP-1, PYY, ghrelin, CCK, GIP, leptin, and bile acids) and their signaling pathways in metabolic regulation. The present research systematically evaluates the impact of bariatric surgery on appetite modulation and certain metabolic functions through key signaling pathways, including GLP-1R, GHS-R1a, and FXR/TGR5.},
}

@article {pmid40505989,
year = {2025},
author = {Mehta, N and Little, K and Woodworth, MH and Goodenough, D and Dhonau, R and Fridkin, SK},
title = {Evaluating Disparities in Recurrent Clostridioides difficile Infection (CDI) and Fecal Microbiota Transplant (FMT) Treatment using Geospatial and Social Vulnerability Analytic Tools.},
journal = {Gastroenterology},
volume = {},
number = {},
pages = {},
doi = {10.1053/j.gastro.2025.05.028},
pmid = {40505989},
issn = {1528-0012},
}

@article {pmid40505847,
year = {2025},
author = {Yadav, A and Tadas, M and Kale, M and Wankhede, N and Umekar, M and Kotagale, N and Taksande, B},
title = {Gut Microbiota and Behavioral Ontogeny in Autism Spectrum Disorder: A Pathway to Therapeutic Innovations.},
journal = {Physiology & behavior},
volume = {},
number = {},
pages = {114989},
doi = {10.1016/j.physbeh.2025.114989},
pmid = {40505847},
issn = {1873-507X},
abstract = {Autism Spectrum Disorder (ASD) is a multifaceted neurodevelopmental condition characterized by deficits in social communication, repetitive behaviors, and restricted interests. Emerging evidence suggests that gut-brain axis a dynamic, bidirectional communication network between gut microbiota and central nervous system, is critical in shaping behavioral ontogeny in ASD. Dysbiosis of gut microbiota, commonly observed in individuals with ASD, has been associated with alterations in neurodevelopmental trajectories and symptom severity. Furthermore, disturbances in maternal microbiome during pregnancy are increasingly recognized as key factors influencing fetal brain development, potentially heightening risk of ASD and behavioral manifestations. Mechanistic research reveals that gut-derived metabolites modulate blood-brain barrier integrity, neuroinflammatory processes, and neuronal circuit formation, contributing to behavioral outcomes. These findings emphasize gut microbiota's profound influence on emergence and progression of ASD-related behaviors. Promising therapeutic strategies, including probiotics, prebiotics, fecal microbiota transplantation, and dietary interventions, have demonstrated potential in modulating the gut microbiome and improving behavioral symptoms in ASD. However, challenges such as individual variability in microbiome composition, limited clinical evidence, and an incomplete understanding of causative mechanisms remain significant barriers to clinical translation. This review explores the interplay between gut microbiota and ASD-associated behaviors, focusing on key mechanisms such as microbial regulation of neurotransmitter production, immune signaling, and neuroinflammation. It further highlights gut microbiota's potential as a modifiable factor influencing neurodevelopmental and behavioral outcomes in ASD. By advancing our understanding of gut-brain axis, we can pave the way for personalized and targeted interventions aimed at improving behavioral ontogeny and developmental trajectories in individuals with ASD.},
}

@article {pmid40505719,
year = {2025},
author = {Zhu, X and Xu, Y},
title = {Gut microbiome contributes to 6PPD-Quinone induced cognitive impairment through PI3K/Akt signaling.},
journal = {Toxicology},
volume = {},
number = {},
pages = {154217},
doi = {10.1016/j.tox.2025.154217},
pmid = {40505719},
issn = {1879-3185},
abstract = {Studies show that N-(1,3-dimethylbutyl)-N'-phenyl-p-phenylenediamine-quinone (6PPD-Q) accumulates in the central nervous system, but its role in cognitive impairment and underlying mechanisms remain unclear. Morris water maze assay revealed that 6-PPDQ significantly impairs cognitive function, particularly learning and memory. HE staining revealed alterations in the hippocampal DG and CA3 regions of exposed mice, including sparse cell arrangement, blurred boundaries, nuclear condensation, and a reduction in Nissl bodies. Fecal microbiota transplantation from 6-PPDQ-exposed mice to normal mice induced cognitive deficits and hippocampal pathological damage. Western Blot assay showed that 6-PPDQ exposure resulted in inhibition of PI3K/AKT signaling. Moreover, blunted PI3K/AKT signaling was observed in mice transplanted with 6-PPDQ-associated mice fecal microbiota. Further analysis of 16S rDNA assay identified a total of 30 differential bacteria at the genus level, including 8 upregulated bacteria such as g_Helicobacter and 22 downregulated bacteria such as g_Prevotellaceae_NK3B31_group. In conclusion, this study uncovers gut microbiome mediates 6PPD-Q-induced cognitive impairment through inhibiting of PI3K/Akt signaling, and provides a basis for further investigation into gut microbiome's protective effects on 6-PPDQ-induced nervous system injury.},
}

@article {pmid40502301,
year = {2025},
author = {Bhandari, P and Berezovskiy, R and Makhani, S and Gausman, V and Rastogi, N and Braude, S},
title = {Discordance in Clinical Indicators With Sequential Fecal Microbiota Transplantation: A Case of Fulminant Clostridioides Difficile Infection.},
journal = {ACG case reports journal},
volume = {12},
number = {6},
pages = {e01731},
pmid = {40502301},
issn = {2326-3253},
abstract = {Fulminant Clostridioides difficile infection (CDI) is a rare, severe type of CDI, often associated with extended hospitalizations, significant healthcare costs, and elevated mortality rates. Fecal microbiota transplantation remains an effective treatment modality for patients with fulminant CDI, with high cure rates reported after multiple treatments. Stool frequency, pseudomembrane resolution, and inflammatory markers are routinely monitored to evaluate disease severity and treatment responsiveness. Our case highlights a discordance in these indicators and demonstrates C-reactive protein as an important marker in assessing residual colitis and disease resolution. Comprehensive scoring systems should consider incorporating C-reactive protein and other biomarkers to optimize CDI management.},
}

@article {pmid40502184,
year = {2025},
author = {Verna, G and De Santis, S and Islam, B and Sommella, EM and Licastro, D and Zhang, L and De Almeida Celio, F and Merciai, F and Caponigro, V and Campiglia, P and Pizarro, TT and Chieppa, M and Cominelli, F},
title = {A missense mutation in Muc2 promotes gut microbiome- and metabolome-dependent colitis-associated tumorigenesis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.05.31.657160},
pmid = {40502184},
issn = {2692-8205},
abstract = {UNLABELLED: Colitis-associated cancer (CAC) arises from a complex interplay between host and environmental factors, including the gut microbiome. Since ulcerative colitis (UC), a significant risk factor for CAC, is rising in prevalence worldwide, an integrative approach is essential to identify potential triggers linking inflammation to cancer. In the present study, we investigated the role of the gut microbiome using Winnie mice, a UC-like model with a relevant missense mutation in the Muc2 gene. Upon transfer from a conventional (CONV) to a specific-pathogen-free (SPF) facility, Winnie mice exhibited a more severe colitis phenotype, and notably, spontaneous CAC as early as four weeks of age, which progressively worsened over time. In contrast, CONV Winnie developed only mild colitis but with no overt signs of tumorigenesis. Notably, when rederived into germ-free (GF) conditions, SPF Winnie mice were protected from colitis or colon tumor development, indicating an essential role for the gut microbiome in the initiation and progression of CAC in these mice. Using shotgun metagenomics, metabolomics, and lipidomics, we identified a distinct pro-inflammatory microbial and metabolic signature that potentially drives the transition from colitis to CAC. Fecal microbiota transplantation (FMT), using either SPF Winnie or WT (Bl/6) donors into GF Winnie recipients, demonstrated that while colitis developed regardless of donor, only FMT from SPF Winnie donors resulted in CAC, revealing a microbiota-driven, host-specific susceptibility to tumorigenesis in Winnie mice. Our studies present a novel and relevant model of CAC, providing further evidence that the microbiome plays a key role in the pathogenesis of CAC, thereby challenging the concept of colon cancer as a strictly non-transmissible disease.

LAY SUMMARY: This study reveals a distinct metagenomic, metabolomic, and lipidomic profile associated with tumorigenesis in a murine model of ulcerative colitis, highlighting the risks of specific intestinal dysbiosis in genetically predisposed subjects.

WHAT YOU NEED TO KNOW: Background and context: Colitis-associated colorectal cancer arises from complex host-environment interactions, including gut microbiome influences, driving chronic inflammation, with the intestinal lumen environment remaining a largely unexplored potential risk factor in cancer development.New findings: Winnie mice in specific pathogen-free conditions developed severe colitis, and a novel juvenile colon dysplasia and cancer, with gut microbiome changes driving colitis-associated cancer initiation and progression.Limitations: We identified a pro-inflammatory microbial/metabolic signature promoting colitis-to-CAC transition in Winnie mice, with FMT confirming microbiota-driven tumor susceptibility. However, further research is needed to pinpoint the key bacteria-metabolite-lipid combination driving CAC.Clinical research relevance: This newly characterized microbiota-metabolome-based model of CAC, challenges the dogma of cancer as a non-transmittable disease, providing a foundation for developing microbiota-based strategies for CAC prevention and treatment.Basic research relevance: Unlike genetic or chemically induced models, the Winnie mouse model uniquely serves as a dual model for spontaneous colitis and juvenile CAC, offering a fast, 100% penetrant phenotype that enhances reliability, accelerates research, and provides valuable insights into IBD and CAC.},
}

@article {pmid40501499,
year = {2025},
author = {Chen, L and Song, Y and Huang, Y and Hu, J and Meng, Y and Yuan, M and Zheng, G and Wang, X and Zhang, C and Qiu, Z},
title = {Cornus officinalis Extract Ameliorates Fructose-Induced Hepatic Steatosis in Mice by Sustaining the Homeostasis of Intestinal Microecology and Lipid Metabolism.},
journal = {Food science & nutrition},
volume = {13},
number = {6},
pages = {e70425},
pmid = {40501499},
issn = {2048-7177},
abstract = {Cornus officinalis Sieb. et Zucc. (Cornus officinalis), an edible natural plant fruit, has beneficial effects on a multitude of metabolic diseases, but the mechanism to improve hepatic steatosis remains elusive. In this study, the curative effect of Cornus officinalis extract (COE) is evaluated in a fructose-induced NAFLD mouse model using biochemical indicators monitoring, histological staining, 16S rRNA sequencing analysis, and fecal microbiota transplantation. Our results showed that COE attenuates hepatic steatosis in fructose-fed mice. Mechanistically, COE repairs intestinal barrier damage and gut flora dysbiosis to suppress proinflammatory microbe-derived metabolite transportation to the liver, thus inhibiting the hepatic inflammation and lipid metabolic dysfunction. Notably, transplantation of fecal microbiota isolated from the fructose-fed mice could reverse the beneficial effect of COE on attenuating NAFLD. Therefore, our study demonstrates that COE delays the progression of fructose-driven NAFLD by suppressing lipid metabolic dysfunction and gut microbiota-mediated liver inflammation, highlighting the potential of C. officinalis as a resource for the treatment of NAFLD drugs.},
}

@article {pmid40501442,
year = {2025},
author = {Maor, M and Levy Barazany, H and Kolodkin-Gal, I},
title = {The ladder of regulatory stringency and balance: an application to the US FDA's regulation of bacterial live therapeutics.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2517377},
doi = {10.1080/19490976.2025.2517377},
pmid = {40501442},
issn = {1949-0984},
mesh = {Humans ; United States ; United States Food and Drug Administration/legislation & jurisprudence ; *Probiotics/therapeutic use ; *Fecal Microbiota Transplantation ; Bacteria/genetics ; Gastrointestinal Microbiome ; },
abstract = {The three main types of live bacterial therapies - probiotics, fecal/microbiome transplants, and engineered bacterial therapies - hold immense potential to revolutionize medicine. While offering targeted and personalized treatments for various diseases, these therapies also carry risks such as adverse immune reactions, antibiotic resistance, and the potential for unintended consequences. Therefore, developing and deploying these therapies necessitates a robust regulatory framework to protect public health while fostering innovation. In this paper, we propose a novel conceptual tool - the Ladder of Regulatory Stringency and Balance-which can assist in the design of robust regulatory regimes which encompass medicine practices based not only on definitive Randomized Controlled Trials (RCTs), but also on meta-analyses, observational studies, and clinicians experience. Regulatory stringency refers to the strictness of regulations, while regulatory balance concerns the degree of alignment between the regulatory framework governing a technology and the actual risks posed by specific products within that technology. Focusing on the US regulatory environment, we subsequently position the three types of live bacterial therapies on the Ladder. The insight gained from this exercise demonstrates that probiotics are generally positioned at the bottom of the Ladder, corresponding to low-stringency regulation, with a proportionate regulatory balance. However, probiotics intended for high-risk populations are currently subject to low-stringency regulations, resulting in under-regulation. Our analysis also supports the conclusion that fecal microbiota transplants (FMT) for recurrent Clostridium difficile infection should be positioned close to but below the threshold for under regulation by the U.S. Food and Drug Administration (FDA), and we recommend improved donor screening procedures, preservation and processing, storage, and distribution. Our framework can serve as a scale to assess regulatory gaps for live bacterial therapies and to identify potential solutions where such gaps exist.},
}

Humans
United States
United States Food and Drug Administration/legislation & jurisprudence
*Probiotics/therapeutic use
*Fecal Microbiota Transplantation
Bacteria/genetics
Gastrointestinal Microbiome

@article {pmid40500750,
year = {2025},
author = {Yang, B and Li, X and Wang, J and Xu, Y and Wang, L and Wu, Z and Zhao, D and Huang, L and Li, N and Chen, Q and Liu, Z},
title = {The efficacy and safety of fecal microbiota transplantation in the treatment of sarcopenia: a retrospective study.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {645},
pmid = {40500750},
issn = {1479-5876},
support = {2022YFA1304100//National Key R&D Program of China/ ; 2022YFC2010101//National Key R&D Program of China/ ; 82470701//National Natural Science Foundation of China/ ; },
mesh = {Humans ; *Sarcopenia/therapy/physiopathology/microbiology ; *Fecal Microbiota Transplantation/adverse effects ; Male ; Female ; Aged ; Retrospective Studies ; Treatment Outcome ; Middle Aged ; Resistance Training ; Inflammation ; },
abstract = {BACKGROUND: Sarcopenia, a prevalent geriatric syndrome, is influenced by factors such as inflammation, immune deficiency, and oxidative stress. In elderly individuals, alterations in the microbiome, including reduced biodiversity and functional changes, significantly contribute to the progression of the disease. Targeting the gut-muscle axis has emerged as a promising therapeutic strategy to mitigate age-related muscle atrophy and dysfunction.

METHODS: This study employed fecal microbiota transplantation (FMT) to restore intestinal homeostasis in patients with sarcopenia. Muscle mass was measured using bioelectrical impedance analysis, while muscle function was assessed through grip strength and the five-time sit-to-stand test. Inflammatory markers, including tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP), were also analyzed. Eighty-seven patients received resistance training (RT) treatment, while eighty-five patients received FMT combined with RT treatment, with a follow-up period of 24 weeks.

RESULTS: After 24 weeks, the resistance training (RT) group showed a partial remission (PR) rate of 54.7% and a complete remission (CR) rate of 32.4%. The FMT plus RT group demonstrated a PR rate of 66.5% and a CR rate of 46.7%. Significant improvements induced by FMT treatment were observed in clinical markers of muscle mass, function, and inflammation.

CONCLUSIONS: These results underscore the promise of microbial-based therapies, including fecal microbiota transplantation (FMT), as groundbreaking strategies for addressing sarcopenia. The research indicates that integrating FMT with resistance training could improve muscle mass and function while alleviating inflammation in sarcopenia patients, presenting a hopeful avenue for effective management of the condition.},
}

Humans
*Sarcopenia/therapy/physiopathology/microbiology
*Fecal Microbiota Transplantation/adverse effects
Male
Female
Aged
Retrospective Studies
Treatment Outcome
Middle Aged
Resistance Training
Inflammation

@article {pmid40503501,
year = {2023},
author = {Kim, SY},
title = {[Gut Microbiota and Obesity].},
journal = {The Korean journal of helicobacter and upper gastrointestinal research},
volume = {23},
number = {4},
pages = {240-246},
pmid = {40503501},
issn = {2671-826X},
abstract = {Obesity is a global health concern associated with a wide range of diseases, including diabetes, metabolic syndrome, fatty liver, and cardiovascular conditions. Recent studies highlight the significant role of gut microbiota in obesity. Research indicates notable changes in the composition and diversity of gut microbiota in individuals diagnosed with obesity. The gut microbiota participate in energy metabolism, lipid synthesis, and regulation of inflammation and therefore play a key role in the pathogenesis of obesity. Therapeutic approaches based on the use of probiotics, prebiotics, Akkermansia muciniphila, and fecal microbiota transplantation have shown promise in animal studies as useful strategies against obesity and metabolic syndrome. However, further research is warranted to conclusively establish the specific strains, dosages, and mechanisms underlying the effectiveness of these novel strategies against obesity in humans.},
}

@article {pmid40497058,
year = {2025},
author = {Zhang, Q and Gao, Z and Deng, Y and Xu, X and Sun, W and Liu, R and Zhang, T and Sun, X},
title = {Current status and trends in the study of intestinal flora in cognitive disorders: a bibliometric and visual analysis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1577597},
pmid = {40497058},
issn = {1664-302X},
abstract = {BACKGROUND: Cognitive impairment is a decline in people's ability to think, learn, and remember, which has some impact on an individual's daily activities or social functioning. Microbial toxins and metabolites from dysregulated gut microbiota directly interact with the intestinal epithelium. This interaction triggers neuroinflammation and neurodegeneration in the central nervous system, ultimately impairing cognitive function. It has been found that modulation of gut flora can be an effective intervention to improve cognitive dysfunction. This study is the first to summarize and outline the global research status and trends in this field from a bibliometric perspective, providing reference and guidance for future research in this field.

METHODS: Based on the Web of Science Core Collection (WoSCC) database, Literature on gut flora and cognitive impairment published between 1999-2025 was searched. Bibliometric analysis was performed using VOSviewer and CiteSpace software to analyze the data on countries, institutions, authors, journals, keywords, citations, and to generate visual maps.

RESULTS: A total of 1,702 pieces of related literature were retrieved. The overall trend of publication is increasing. China has published the largest number of papers, and Huazhong University of Science & Technology and Kim, Dong-Hyun were the institutions and individuals with more publications. The most frequently cited journal is SCI REP-UK. The most frequent keywords are gut microbiota, followed by Alzheimer's disease, cognitive impairment, Brain, oxidative stress and Inflammation.

CONCLUSION: In recent years, the research application of gut flora in the treatment of cognitive impairment has made remarkable progress. Oxidative stress and inflammatory response have become the main research hotspots for gut flora to improve cognitive impairment in patients. The gut-brain axis plays an important role in the study of the mechanism of action. Short-chain fatty acids are the focus of research on gut microbial metabolism. Fecal microbial transplantation technology is increasingly being used as an emerging method for the application of intestinal flora. Modifying the gut flora by modifying diet and exercise may be an effective strategy to prevent and improve cognitive dysfunction in the future. Future studies may focus more on gender differences in the role of gut flora in the modulation of cognitive function.},
}

@article {pmid40497049,
year = {2025},
author = {Ren, X and Zheng, L and Huang, L and Zhao, J},
title = {The role of the gut microbiota in shaping the tumor microenvironment and immunotherapy of breast cancer.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1591745},
pmid = {40497049},
issn = {1664-302X},
abstract = {Breast cancer is the most prevalent malignancy among women worldwide and is a major contributor to cancer-related mortality. The tumor microenvironment (TME), composed of tumor cells, immune infiltrates, fibroblasts, and vascular components, is critically involved in tumor initiation, metastatic progression, and therapeutic response. In recent years, therapies targeting the TME have undergone rapid advancements, with the objective of enhancing antitumor immunity. Concurrently, mounting evidence underscores the pivotal role of the gut microbiota and its metabolites in modulating host immunity, influencing metabolic homeostasis, inflammation, and immune equilibrium. The composition and diversity of the gut microbiome influence breast cancer progression and patients' responses to immunotherapy. Therefore, modulating the gut microbiota is a promising strategy to enhance the clinical outcomes of TME-targeted immunotherapies. In this review, we discuss the influence of gut microbiota and its derived metabolites on breast cancer progression and immunotherapy prognosis and explore potential strategies to optimize immunotherapy through gut microbiota modulation.},
}

@article {pmid40497047,
year = {2025},
author = {Rivero, MR and Vissio, C and Feliziani, C and De Angelo, C and Touz, MC and Tiranti, K and Lombardelli, JA and Duartez, FJ and Curletto, L},
title = {Cryptosporidium spp. in Argentina: epidemiology and research advances in human, animal, and environmental settings during the 21st century.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1592564},
pmid = {40497047},
issn = {1664-302X},
abstract = {INTRODUCTION: Cryptosporidium spp. is an intestinal protozoan causing cryptosporidiosis, a diarrheal disease affecting humans and animals, with zoonotic potential. In immunocompromised individuals, infections can be severe or fatal. It is a major waterborne parasite and a leading cause of neonatal diarrhea in calves. This study systematically reviews Cryptosporidium spp. research in Argentina during the 21st century, highlighting its epidemiological significance and research gaps.

METHODS: A systematic review following PRISMA guidelines was conducted using LILACS, PubMed, Scopus, and SciELO Argentina. Eligible studies (2001-2024) included human (community and hospital-based), animal (domestic, wild, and captive), and environmental (water, soil and vegetable) surveys. The review analyzed epidemiology, diagnosis, treatment, genetic diversity, distribution, and risk factors.

RESULTS: Of 277 articles reviewed, 66 met eligibility criteria. Cryptosporidium spp. was detected in 17 of Argentina's 23 provinces, mainly in the Pampean region. Five species were identified (C. hominis, C. parvum, C. suis, C. scrofarum, and C. varanii), though genetic diversity studies remain limited. Human cryptosporidiosis primarily affects immunocompromised individuals (HIV/AIDS, transplant recipients, hematologic cancer patients). The parasite was found in feces, duodenal biopsies, blood, sputum, and cerebrospinal fluid, with complications such as cholangiopathy and pulmonary cryptosporidiosis. Infections with C. hominis and C. parvum (including co-infections) were observed, with multiple subtypes documented. In animals, C. parvum was prevalent in Pampean calves, while C. suis and C. scrofarum were found in domestic pigs. Wildlife, including non-human primates and coypu, also tested positive. Cryptosporidium was detected in recreational and drinking water samples. No Cryptosporidium spp. oocysts were detected in soil. Risk factors included socio-economic conditions and animal management practices.

CONCLUSION: Cryptosporidium spp. is widely distributed in Argentina, yet eco-epidemiological transmission factors remain poorly understood, hindering control strategies. Limited research on genetic diversity and distribution highlights the need for further studies, particularly in vulnerable populations and areas of close human-animal interaction, such as productive systems. The presence of Cryptosporidium spp. in water underscores the importance of improving public health policies and water treatment standards. From a One Health perspective, these findings emphasize the need for enhanced epidemiological surveillance and research to strengthen prevention and control in Argentina.},
}

@article {pmid40495848,
year = {2025},
author = {Iqbal, A and Bokhari, SFH and Rehman, MU and Faizan Sattar, SM and Bakht, D and Dost, W and Basit, A},
title = {Gut-brain connection in schizophrenia: A narrative review.},
journal = {World journal of psychiatry},
volume = {15},
number = {5},
pages = {103751},
pmid = {40495848},
issn = {2220-3206},
abstract = {Schizophrenia is a complex neuropsychiatric disorder characterized by cognitive, emotional, and behavioral impairments. The microbiota-gut-brain axis is crucial in its pathophysiology, mediating communication between the gut and brain through neural, immune, endocrine, and metabolic pathways. Dysbiosis, or an imbalance in gut microbiota, is linked to neuroinflammation, systemic inflammation, and neurotransmitter disruptions, all of which contribute to the symptoms of schizophrenia. Gut microbiota-derived metabolites, such as short-chain fatty acids, influence brain function, including immune responses and neurotransmitter synthesis. These findings suggest that microbial imbalances exacerbate schizophrenia, providing a novel perspective on the disorder's underlying mechanisms. Emerging microbiota-targeted therapies-such as probiotics, prebiotics, dietary interventions, and fecal microbiota transplantation-show promise as adjunctive treatments, aiming to restore microbial balance and improve clinical outcomes. While further research is needed, targeting the microbiota-gut-brain axis offers an innovative approach to schizophrenia management, with the potential to enhance patient outcomes and quality of life.},
}

@article {pmid40495179,
year = {2025},
author = {Liu, W and Zhou, X and Xiao, L and Huang, X and Chang, D and Zhong, X and Zeng, M and Xian, Y and Zheng, Y and Huang, W and Huang, R and Huang, M},
title = {The gut microbiota-mediated ferroptosis pathway: a key mechanism of ginsenoside Rd against metabolism-associated fatty liver disease.},
journal = {Chinese medicine},
volume = {20},
number = {1},
pages = {83},
pmid = {40495179},
issn = {1749-8546},
support = {2022YFC3501200//National Key Research and Development Program of China/ ; 82274080//National Natural Science Foundation of China Projects/ ; X2024019//School Management Project of Fujian University of Traditional Chinese Medicine/ ; X2024035//School Management Project of Fujian University of Traditional Chinese Medicine/ ; 2024Y9511//Fujian Provincial Science and Technology Innovation Joint Fund Project/ ; },
abstract = {BACKGROUND: Ginsenoside Rd (G-Rd), found in Panax species, has shown therapeutic potential against metabolism-associated fatty liver disease (MAFLD), but its mechanism has not been well elucidated. This study investigated the key mechanisms of G-Rd in modulating the gut microbiome and lipid peroxidation-mediated ferroptosis pathway in MAFLD.

METHODS: A high-fat diet-induced MAFLD model was established. Ultrastructural changes in liver tissue were observed using transmission electron microscopy. Metagenomics were employed to detect alterations in gut microbiota and their metabolites. Biochemical analysis and immunohistochemistry were used to examine liver injury, blood lipids, lipid peroxidation-related indicators, and tissue iron content.

RESULTS: G-Rd significantly reduced liver injury and steatosis in MAFLD mice and downregulated the elevated relative abundance of Firmicutes and the Firmicutes/Bacteroidetes ratio. It also significantly reduced the abundances of Faecalibaculum rodentium while increasing Muribaculum intestinale, with its functional role being relevant to lipid metabolism regulation. Moreover, G-Rd ameliorated mitochondrial damage and inhibited the ferroptosis pathway in the liver, which was associated with antioxidant-related factors mediated by Nrf2 signaling. The liver protective effect of G-Rd was driven by the regulation of gut microbiota, as demonstrated by antibiotic cocktail treatment and fecal microbiota transplantation.

CONCLUSIONS: G-Rd attenuated HFD-induced MAFLD by alleviating liver oxidative stress, lipid peroxidation, and ferroptosis through modulation of the gut microbiota. The antioxidant and anti-ferroptotic actions of G-Rd, mediated via the Nrf2 pathway, were found to contribute to the amelioration of liver injury and hepatic steatosis in MAFLD.},
}

@article {pmid40494686,
year = {2025},
author = {von Muhlenbrock, C and Núñez, P and Herrera, K and Pacheco, N and Quera, R},
title = {Fecal microbiota transplantation through colonoscopy for the management of severe refractory irritable bowel syndrome: Preliminary results.},
journal = {Revista de gastroenterologia de Mexico (English)},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.rgmxen.2025.03.001},
pmid = {40494686},
issn = {2255-534X},
abstract = {Recent studies have explored the role of the microbiota in disorders of gut-brain interaction, opening pathways for therapies, such as dietary adjustments, probiotics, and fecal microbiota transplantation (FMT). We present herein a pilot study on 4 patients with severe irritable bowel syndrome (IBS), refractory to conventional treatment, in which FMT through colonoscopy showed improvement in pain, bloating, and stool consistency that was maintained during the 6-month follow-up. To establish the broader clinical application of FMT, more research on its efficacy according to instillation site and patient results is needed.},
}

@article {pmid40494661,
year = {2025},
author = {Laura, R and Fariha, B and Claire, R and Christopher, B and Lewindon, P},
title = {Oral vancomycin solution is superior to capsule in inducing clinical biomarker and endoscopic remission in children with atypical ulcerative colitis.},
journal = {British journal of clinical pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1002/bcp.70121},
pmid = {40494661},
issn = {1365-2125},
support = {240050//Lastentautien Tutkimussäätiö/ ; //Orionin Tutkimussäätiö/ ; T63344/50621//State funding for university-level health research, Tampere University Hospital, Wellbeing services county of Pirkanmaa/ ; },
abstract = {AIMS: Atypical colitis (presenting reverse gradient colitis, backwash ileitis or rectal sparing) is associated with primary sclerosing cholangitis-ulcerative colitis (PSC). Oral vancomycin has been used to manage paediatric atypical colitis with/without confirmed PSC. Different preparations had shown different efficacy. We compared oral vancomycin solution to capsules in inducing remission in children with atypical colitis, while assessing other potential confounders.

METHODS: Children using oral vancomycin for at least 3 months to manage atypical colitis were retrospectively identified. Factors associated with colitis remission (Paediatric Ulcerative Colitis Activity Index [PUCAI], faecal calprotectin, colonoscopy and histology) were explored.

RESULTS: Of 32/48 children with elevated PUCAI, 27/32 achieved PUCAI < 10 (20/23 after solution vs. 7/9 after capsules, P = .520). Faecal calprotectin <100 μg/g was achieved in 35/48 (28/35 after solution vs. 6/13 after capsules, P = .022). Follow-up colonoscopy during treatment (n = 25) showed reduced Mayo from median 2 to 0 (P < .001) after solution vs. from 2 to 1 (P = .257) after capsules. Pan-colonic histological remission was seen in 14/25 (12/20 after solution vs. 1/5 after capsules, P = .109). In adjusted analysis, use of oral vancomycin solution was a significant predictor for biomarker (adjusted odds ratio 23.1, 95% confidence interval 2.11-253) and pan-colonic histological remission (adjusted odds ratio 900, 95% confidence interval 1.61-504 929). No other predictors were identified. Within 12 months after ceasing oral vancomycin in children who achieved remission, 52% relapsed. No clinical predictors, including vancomycin preparation, were established.

CONCLUSION: Oral vancomycin solution was superior to capsules for inducing biomarker and colonoscopic remission in children with atypical colitis with/without confirmed PSC. This finding warrants further investigation to ensure optimal use.},
}

@article {pmid40491765,
year = {2025},
author = {Tang, Y and Xie, X and Guo, Y and Chen, Y and Huang, X and Dai, D and Wu, X},
title = {Exploring correlation between preoperative gut microbiota and PONV using 16S absolute quantitative sequencing: a prospective observational study.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1563329},
pmid = {40491765},
issn = {2296-858X},
abstract = {BACKGROUND: Postoperative nausea and vomiting (PONV) is a common complication following surgery. Despite various preventive measures, satisfactory outcomes have not been achieved. This study explores the potential of gut microbiota interactions with the host in understanding and preventing PONV, using 16S absolute quantitative sequencing technology to uncover new insights.

METHODS: Patients who experienced nausea and vomiting within 24 h after surgery were divided into a PONV group (n = 22) and a non-PONV group (n = 22). Microbial communities linked to PONV were assessed through bioinformatics analysis. Fecal samples from both groups were transplanted into rats, which were then anesthetized with isoflurane for 100 min. Pica behavior was monitored over the next 24 h to assess nausea and vomiting in the rats.

RESULTS: Significant differences in α- and β-diversity were observed between the PONV and non-PONV groups. Six key microorganisms were identified, with Bifidobacterium, Bilophila, and Oscillibacter showing a negative correlation with PONV severity. Receiver operating characteristic (ROC) analysis demonstrated that Bifidobacterium could reliably predict PONV. Rats receiving feces from the PONV group exhibited significantly higher kaolin consumption within 24 h post-anesthesia compared to those receiving feces from the non-PONV group.

CONCLUSION: These results suggest a potential new mechanism for PONV involving gut microbiota, offering a theoretical basis for preoperative prediction of PONV based on gut microbial composition.},
}

@article {pmid40491530,
year = {2025},
author = {Jian, S and Jian, X and Ye, L and Yang, K and Zhang, L and Xie, Y and Deng, J and Yin, Y and Deng, B},
title = {Gallic acid prevents obesity in mice on a high-fat diet via the gut microbiota-adipose tissue axis.},
journal = {Current research in food science},
volume = {10},
number = {},
pages = {101084},
pmid = {40491530},
issn = {2665-9271},
abstract = {Obesity is closely related to the gut microbiota, and gallic acid (GA) has anti-obesity properties, but its relationship with the gut microbiota is unclear. The aim of this study was to investigate the role of gut microbiota in the anti-obesity mechanism of GA by fecal microbiota transplantation (FMT). Here, we found that high-fat diet (HFD) promoted lipid deposition and gut microbiota dysbiosis in mice, whereas GA slowed down lipid deposition and restored gut microbiota dysbiosis and its functional profile, as evidenced by the reduction of the obesity-causing bacterium Desulfovibrio and the enrichment of the beneficial bacterium Lachnospiraceae_NK4A136_group, Clostridiales_unclassified, Oscillospira and Adlercreutzia. These gut microbiota and metabolites produced positive feedback effects on body weight, glucose tolerance, insulin resistance, as well as glycemic and lipid parameters. Mechanistically, GA significantly enhanced lipid and energy metabolism in obese mice by promoting the expression of uncoupling protein 1 (UCP1), adiponectin, and adiponectin receptor 2 in white adipose tissue of the epididymal white adipose tissue, as well as promoting thermogenesis in interscapular brown adipose tissue by stimulating UCP1 expression. Interestingly, GA failed to alleviate lipid accumulation in HFD of antibiotic-treated mice. In contrast, after FMT treatment, the fecal microbiota of GA-treated donor mice significantly alleviated lipid metabolism in HFD-fed mice, which is mechanistically consistent with direct addition of GA. Collectively, GA can alleviate HFD-induced obesity by modulating the gut microbiota, and the specific mechanism may be through the gut microbiota-adipose tissue axis.},
}

@article {pmid40488649,
year = {2025},
author = {Park, JH and Lee, YK and Lee, CK and Lee, HS and Kim, JH and Lee, MH and Seo, YJ and Cho, H and Park, CS},
title = {The preventive effect of solubilized sturgeon oil on dextran sulfate sodium-induced ulcerative colitis via inflammation attenuation and intestinal microbiota regulation.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo01038a},
pmid = {40488649},
issn = {2042-650X},
abstract = {Ulcerative colitis (UC), an inflammatory bowel disease, causes inflammation in the colonic mucosa. The pathogenesis of UC is closely linked to abnormalities in the gastrointestinal microbiota and immune response. Current treatments for UC primarily alleviate symptoms but are associated with several drawbacks, particularly with prolonged use. Therefore, there is a crucial need to explore novel treatment strategies. Solubilized sturgeon oil (SSO) has gained prominence for its anti-inflammatory effects in various contexts; however, its efficacy in UC has not yet been investigated. In this study, we investigated the preventive effects and underlying mechanisms of SSO in a dextran sulfate sodium-induced UC model. Oral administration of SSO significantly alleviated colitis severity by improving weight, disease activity index, and colon length. Moreover, SSO significantly downregulated the expression of interleukin (IL)-1β, IL-6, tumor necrosis factor-alpha, cyclooxygenase-2, and nitric oxide synthase, while enhancing the expression of tight junction-related proteins such as occludin and ZO-1 in colonic tissues. Additionally, SSO inhibited the activation of lipopolysaccharide-stimulated dendritic cells and macrophages and induced alterations in the gut microbiota, with increased Firmicutes and decreased Bacteroidetes abundances. Furthermore, colitis and gastrointestinal inflammation were alleviated in recipient mice that received fecal transplants from SSO-treated mice. These findings indicate that SSO is a promising natural therapeutic agent for preventing colitis by regulating the gastrointestinal microbiota and suppressing the hyperactivation of myeloid cells.},
}

@article {pmid40487274,
year = {2025},
author = {Roy, K and Moncada, E and Reddivari, L},
title = {Ulcerative Colitis but Not Dextran Sodium Sulfate-Induced Colitis-Associated Microbiota Promotes Early Biomarkers of Colitis in Interleukin-10 -/- Mice.},
journal = {Gastro hep advances},
volume = {4},
number = {6},
pages = {100636},
pmid = {40487274},
issn = {2772-5723},
abstract = {BACKGROUND AND AIMS: Inflammatory bowel diseases, including Crohn's disease and ulcerative colitis (UC), are inflammatory gastrointestinal conditions in which the pathogenesis is influenced by immune dysfunction, genetics, and environmental factors. Of the 2 conditions, UC is more prevalent, and there is a positive correlation between bacterial dysbiosis and colitis severity and incidence. Therefore, we hypothesize that mice that are genetically predisposed to colitis when colonized with colitic associated bacteria will exhibit an early onset of colitis biomarkers.

METHODS: Four sets of germ-free interleukin-10 -/- mice were gavaged orally with pooled fecal samples from 2 healthy individuals or an individual with severe colitis or healthy mice or dextran sodium sulfate (DSS)-induced colitis mice. The disease activity index was used to rank colitis severity weekly in transplanted mice for eight weeks.

RESULTS: There were significant differences in alpha (Shannon Index) and beta diversity (Bray-Curtis) between healthy and colitic-associated microbiota recipients, indicating dysbiosis (human fecal microbial transplantation P = 8.09∗10[-6], P = .001); (Mice fecal microbiota transplant P = .0197, P = .025). Despite the lack of colitis development, UC-associated microbiota recipients had reduced mucus thickness and increased expression of proinflammatory cytokines in the distal colon compared to healthy-associated microbiota recipients. However, DSS-induced colitis associated microbiota recipients did not show an increase in colitis biomarkers compared to healthy associated microbiota recipients.

CONCLUSION: This study demonstrates that UC-associated bacterial dysbiosis induces colonic inflammation and mucus thinning, biomarkers of early colitis onset, in interleukin-10 -/- mice compared to mice with healthy human associated bacteria.Colitis induction depends on bacterial community stability as DSS-induced colitis associated microbiota recipients did not show an increase in colitis or colitis biomarkers in the absence of DSS.},
}

@article {pmid40486846,
year = {2025},
author = {Shang, M and Ning, J and Zang, C and Ma, J and Yang, Y and Wan, Z and Zhao, J and Jiang, Y and Chen, Q and Dong, Y and Wang, J and Li, F and Bao, X and Zhang, D},
title = {Microbial metabolite 3-indolepropionic acid alleviated PD pathologies by decreasing enteric glia cell gliosis via suppressing IL-13Rα1 related signaling pathways.},
journal = {Acta pharmaceutica Sinica. B},
volume = {15},
number = {4},
pages = {2024-2038},
pmid = {40486846},
issn = {2211-3835},
abstract = {Although enteric glial cell (EGC) abnormal activation is reported to be involved in the pathogenesis of Parkinson's disease (PD), and inhibition of EGC gliosis alleviated gut and dopaminergic neuronal dysfunction was verified in our previous study, the potential role of gut microbiota on EGC function in PD still need to be addressed. In the present study, fecal microbiota transplantation revealed that EGC function was regulated by gut microbiota. By employing 16S rRNA and metabolomic analysis, we identified that 3-indolepropionic acid (IPA) was the most affected differential microbial metabolite that regulated EGC gliosis. The protective effects of IPA on PD were validated in rotenone-stimulated EGCs and rotenone (30 mg/kg i.g. for 4 weeks)-induced PD mice, as indicated by decreased inflammation, improved intestinal and brain barrier as well as dopaminergic neuronal function. Mechanistic study showed that IPA targeted pregnane X receptor (PXR) in EGCs, and inhibition of IL-13Rα1 involved cytokine-cytokine receptor interaction pathway, leading to inactivation of downstream JAK1-STAT6 pathway. Our data not only provided evidence that EGC gliosis was critical in spreading intestinal damage to brain, but also highlighted the potential role of microbial metabolite IPA in alleviating PD pathological damages through gut-brain axis.},
}

@article {pmid40486731,
year = {2025},
author = {Zhou, C and Feng, X and Liu, H and Cai, T and Li, Y and Fan, H},
title = {Bidirectional modulation of Alzheimer's disease via gut microbiota: rescue by fecal transplantation from healthy donors and aggravation by colitis-associated dysbiosis.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1593854},
pmid = {40486731},
issn = {1662-4548},
abstract = {INTRODUCTION: Emerging evidence implicates gut microbiota dysbiosis as a key modulator for the pathogenesis of Alzheimer's disease (AD) via the gut-brain axis. To investigate the causal role of microbial communities in AD progression, we performed fecal microbiota transplantation (FMT) in APP/PS1 transgenic mice using donor microbiota from healthy wild-type mice or dextran sulfate sodium (DSS)-induced colitis mice.

METHODS: Cognitive function, amyloid-beta (Aβ) pathology, and pro-inflammatory cytokine levels were assessed in mice. 16S ribosomal RNA sequencing of gut microbiota and bioinformatic functional analyses were applied to identify the specific microbial communities potentially involved in AD progression.

RESULTS: FMT-WT mice (fecal microbiota transplantation from healthy wild-type mice) exhibited significant improvements in spatial memory (Morris Water Maze), exploratory behavior (Y-maze), and locomotor activity (Open Field Test), alongside reduced Aβ plaque burden and normalized expression of pro-inflammatory cytokines (IL-6, IL-1β, TNF-α) in both gut and brain tissues. Conversely, FMT-DSS mice (fecal microbiota transplantation from DSS-treated donors) displayed exacerbated cognitive deficits, heightened Aβ deposition, and elevated pro-inflammatory cytokine levels. Microbial profiling revealed stark contrasts: FMT-WT mice harbored beneficial taxa (Bacteroides, Lachnospiraceae) linked to anti-inflammatory products like short-chain fatty acid, while FMT-DSS mice showed blooms of pathogenic genera (Erysipelatoclostridium, Enterobacteriaceae) associated with neurotoxic metabolites. Functional analyses predicted enrichment of neuroprotective pathways (e.g., lysine metabolism) in FMT-WT and pro-inflammatory pathways (e.g., carbon metabolism) in FMT-DSS. Crucially, neuroinflammation occurred independently of gut barrier disruption, implicating circulating microbial metabolites as key mediators.

DISCUSSION: Our findings demonstrate that gut microbiota composition bidirectionally influences AD progression, with FMT from healthy donors attenuating neuroinflammation and pathology, while colitis-associated dysbiosis exacerbates disease hallmarks. Our study positions microbiota-targeted therapies as a promising strategy to modulate AD progression through the gut-brain axis.},
}

@article {pmid40485937,
year = {2025},
author = {Liu, Y and Zhang, P and Sun, H},
title = {A narrative review of research advances in gut microbiota and microecological agents in children with attention deficit hyperactivity disorder (ADHD).},
journal = {Frontiers in psychiatry},
volume = {16},
number = {},
pages = {1588135},
pmid = {40485937},
issn = {1664-0640},
abstract = {The role of gut microecology in attention deficit hyperactivity disorder (ADHD) has garnered growing attention. Studies have suggested a potential link between ADHD development and an imbalance in gut microbiota composition. This review aims to analyze the characteristics of the gut microbiota in children with ADHD, explore how changes in the gut microbiota affect ADHD through nervous, neuroendocrine, and immune pathways, and discuss the potential application of microecological agents and fecal microbiota transplantation in the prevention and treatment of ADHD in children. Pubmed, Google Scholar, EBSCO, Scopus and Medline were utilized to conduct searches using the following key terms:Attention Deficit Hyperactivity Disorder OR ADHD AND gut microbiota OR probiotics OR prebiotics OR synbiotics OR fecal microbiota transplantation OR FMT. Studies published in English from all years were included. A thorough review of numerous papers and their references was conducted to identify relevant articles. Sorting and analysis revealed that the gut microbiota of children with ADHD has changed to some extent, and targeting the gut microbiota, using microecological agents or fecal microbiota transplantation, especially in combination with central nervous system stimulants, may provide additional benefits for children with ADHD.},
}

@article {pmid40485663,
year = {2025},
author = {Radford-Smith, DE and Oke, K and Costa, CFFA and Anthony, DC},
title = {Systematic review and meta-analysis of microbiota-gut-astrocyte axis perturbation in neurodegeneration, brain injury, and mood disorders.},
journal = {Brain, behavior, & immunity - health},
volume = {46},
number = {},
pages = {101013},
pmid = {40485663},
issn = {2666-3546},
abstract = {BACKGROUND: Astrocytes are essential for preserving homeostasis, maintaining the blood-brain barrier, and they are a key element of the tripartite neuronal synapse. Despite such multifaceted roles, their importance as contributors to the microbiota-gut-brain axis studies, which typically focus on microglia and neurons, has been largely overlooked. This meta-analysis provides the first systematic review of the microbiota-gut-astrocyte (MGA) axis in vivo, integrating findings across distinct neurological diseases.

METHODS: A systematic narrative review was conducted per PRISMA guidelines. The search term employed for PubMed was "Microbiota"[MeSH] AND (astrocyte OR glial) NOT (Review[Publication Type]) and for Web of Science, Embase, and Scopus, "Microbio∗ AND (astrocyte OR glial)" with filters applied to exclude review articles. Searches were completed by May 9th[,] 2024. Data extracted included study models, interventions, and outcomes related to astrocyte biology and rodent behaviour. SYRCLE's risk of bias tool was used to assess individual study designs.

RESULTS: 53 studies met the inclusion criteria, covering rodent models of stroke and traumatic (acute) brain injury, chronic neurodegenerative diseases including Alzheimer's and Parkinson's disease and other heterogeneous models of cognitive impairment and affective disorders. Significant heterogeneity in methodology was observed between studies. Five studies had a high risk of bias, and 15 were low risk. Astrocyte biology, typically measured by GFAP expression, was increased in neurodegeneration and acute brain injury models but varied significantly in mood disorder models, depending on the source of stress. Common findings across diseases included altered gut microbiota, particularly an increased Bacteroidetes/Firmicutes ratio and compromised gut barrier integrity, linked to increased GFAP expression. Faecal microbiota transplants and microbial metabolite analyses suggested a direct impact of the gut microbiota on astrocyte biology and markers of neuroinflammation.

CONCLUSIONS: This review and meta-analysis describes the impact of the gut microbiota on astrocyte biology, and argues that the MGA axis is a promising therapeutic target for neurological disorders. However, it is clear that our understanding of the relationship between the gut microbiota and astrocyte behaviour is incomplete, including how different subtypes of astrocytes may be affected. Future studies must adopt new, multi-dimensional studies of astrocyte function and dysfunction, to elucidate their role in disease and explore the therapeutic potential of gut microbiota modulation.},
}

@article {pmid40484955,
year = {2025},
author = {Lin, A and Huang, L and Jiang, A and Zhu, L and Mou, W and Li, Y and Zhang, C and Liu, Z and Zhang, J and Cheng, Q and Wei, T and Luo, P},
title = {Microbiota boost immunotherapy? A meta-analysis dives into fecal microbiota transplantation and immune checkpoint inhibitors.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {341},
pmid = {40484955},
issn = {1741-7015},
support = {2021A1515012593//Natural Science Foundation of Guangdong Province/ ; 82373129//National Natural Science Foundation of China/ ; 82172750//National Natural Science Foundation of China/ ; 2022A1515111212//Basic and Applied Basic Research Foundation of Guangdong Province/ ; 2023A04J1257//Science and Technology Program of Guangzhou/ ; NO.2023RC3074//Hunan Youth Science and Technology Talent Project/ ; },
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Immune Checkpoint Inhibitors/therapeutic use ; *Neoplasms/therapy ; *Gastrointestinal Microbiome ; *Immunotherapy/methods ; Treatment Outcome ; },
abstract = {BACKGROUND: Immune checkpoint inhibitors (ICIs) are a cornerstone of modern cancer treatment, but their effectiveness is limited. Fecal microbiota transplantation (FMT), which alters the gut microbiome, has shown promise in enhancing ICIs' therapeutic effects.

METHODS: We conducted a comprehensive search of relevant studies available up to September 30, 2024, to analyze the clinical efficacy and safety of combining FMT with ICIs in cancer treatment. The primary endpoint was the objective response rate (ORR), with secondary evaluations of survival outcomes and safety.

RESULTS: A total of 10 studies involving 164 patients with solid tumors were included. The pooled ORR was 43% (95% CI: 0.35-0.51). Subgroup analysis revealed that the combination of anti-PD-1 and anti-CTLA-4 therapies was associated with a significantly higher ORR (60%) compared to anti-PD-1 monotherapy (37%; P = 0.01). The incidence of grade 1-2 adverse events (AEs) was 42% (95% CI: 0.32-0.52), while grade 3-4 AEs occurred in 37% of patients (95% CI: 0.28-0.46).

CONCLUSIONS: This meta-analysis provides preliminary evidence supporting the use of FMT as a strategy to enhance the efficacy of ICIs in patients with advanced or refractory solid tumors. However, larger-scale randomized controlled trials with long-term follow-up are required to confirm and optimize treatment protocols.},
}

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

@article {pmid40484558,
year = {2025},
author = {Liu, W and Yu, L and Chen, Q and Zhang, C and Wang, L and Yu, N and Peng, D and Ou, J and Chen, W and Zhang, Y and Wang, Y},
title = {Poria cocos polysaccharides alleviate obesity-related adipose tissue insulin resistance via gut microbiota-derived short-chain fatty acids activation of FGF21/PI3K/AKT signaling.},
journal = {Food research international (Ottawa, Ont.)},
volume = {215},
number = {},
pages = {116671},
doi = {10.1016/j.foodres.2025.116671},
pmid = {40484558},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Insulin Resistance ; *Obesity/metabolism ; *Polysaccharides/pharmacology ; Mice ; Proto-Oncogene Proteins c-akt/metabolism ; Male ; *Fatty Acids, Volatile/metabolism ; Fibroblast Growth Factors/metabolism ; Signal Transduction/drug effects ; Diet, High-Fat/adverse effects ; *Adipose Tissue/metabolism/drug effects ; Mice, Inbred C57BL ; Phosphatidylinositol 3-Kinases/metabolism ; *Wolfiporia/chemistry ; },
abstract = {Obesity is a chronic condition that increases the risk of metabolic disorders, with intestinal dysbiosis and adipose tissue insulin resistance (Adipose-IR) playing key roles in its pathogenesis. Poria cocos polysaccharides (PCP), derived from traditional Chinese medicine, have shown potential in improving glucose metabolism and modulating gut microbiota. However, whether PCP can alleviate obesity-induced Adipose-IR and its dependence on gut microbiota remain unclear. This study investigated the effects of PCP on Adipose-IR in high-fat diet (HFD)-induced obese mice. PCP supplementation reduced body weight, adipose tissue mass, and improved glucose tolerance and lipid metabolism. Histological analysis showed alleviation of adipocyte hypertrophy and colonic barrier damage. PCP also modulated gut microbiota, enhancing the abundance of Lactobacillus, Allobaculum, and Phascolarctobacterium, and increased fecal short-chain fatty acids (SCFAs). These changes activated fibroblast growth factor 21 (FGF21), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and glucose transporter 4 (GLUT4) expression, improving insulin sensitivity. Antibiotic treatment and fecal microbiota transplantation (FMT) further confirmed that PCP's effects on glucose and lipid metabolism are gut microbiota-dependent. Our findings suggest that PCP may serve as a prebiotic agent to alleviate obesity-induced Adipose-IR and metabolic disorders, supporting its potential for functional food development.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Insulin Resistance
*Obesity/metabolism
*Polysaccharides/pharmacology
Mice
Proto-Oncogene Proteins c-akt/metabolism
Male
*Fatty Acids, Volatile/metabolism
Fibroblast Growth Factors/metabolism
Signal Transduction/drug effects
Diet, High-Fat/adverse effects
*Adipose Tissue/metabolism/drug effects
Mice, Inbred C57BL
Phosphatidylinositol 3-Kinases/metabolism
*Wolfiporia/chemistry

@article {pmid40482880,
year = {2025},
author = {Conrad, MA and Kaplan, AL and Weinbrom, S and Nastasio, S and Jo, D and Conover, K and Lo, K and Liu, E and Crawford, M and Michail, S and Nicholson, M and Hourigan, SK and Kelsen, JR and Kahn, SA},
title = {Fidaxomicin Treatment of Clostridioides difficile Infections and Recurrences in Children and Adolescents: A Retrospective Multicenter Study.},
journal = {The Journal of pediatrics},
volume = {},
number = {},
pages = {114681},
doi = {10.1016/j.jpeds.2025.114681},
pmid = {40482880},
issn = {1097-6833},
abstract = {OBJECTIVE: To report the effectiveness and tolerability of treating children with primary and recurrent Clostridioides difficile infection (CDI) with fidaxomicin in a real-world, multicenter cohort.

STUDY DESIGN: We performed a multicenter, retrospective, observational study of fidaxomicin treatment for primary or recurrent CDI (rCDI) in children ages 12 months to 18 years old identified from 2013 to 2021 at 5 centers via electronic medical records. Outcomes included assessment of clinical response at day 14 after initiation of fidaxomicin treatment and clinical and microbiologic outcomes at day 60 after initiation of fidaxomicin treatment in the initial responders.

RESULTS: Of the 95 patients included in this study, 84 (88.4%) were treated with fidaxomicin for a rCDI, and 82 (86.3%) had at least one medical or surgical comorbidity. At the completion of fidaxomicin treatment (ie, by day 14 after initiation), 50 patients (52.6%) had a clinical cure and an additional 29 (30.5%) had improvement of symptoms. Among 79 patients who responded to fidaxomicin treatment, 17 (21.5%) had a clinical and microbiologically confirmed recurrence of CDI by day 60, likely representing relapse. Patients with inflammatory bowel disease (IBD) were less likely to achieve clinical cure at day 14 (OR 0.27 (95% CI 0.11, 0.70)), but 20 patients with IBD who had initial clinical cure or response did not have a demonstrable increased risk of recurrence at day 60. The most common adverse events reported during therapy were abdominal pain and nausea.

CONCLUSIONS: In this retrospective, real-world study, fidaxomicin for children with CDI appears to be well tolerated and is associated with low rates of treatment failure.},
}

@article {pmid40482640,
year = {2025},
author = {DeLeon, O and Mocanu, M and Tan, A and Sidebottom, AM and Koval, J and Ceccato, HD and Kralicek, S and Colgan, JJ and St George, MM and Lake, JM and Cooper, M and Xu, J and Moore, J and Su, Q and Xu, Z and Ng, SC and Chan, FKL and Tun, HM and Cham, CM and Liu, CY and Rubin, DT and Martinez-Guryn, K and Chang, EB},
title = {Microbiome mismatches from microbiota transplants lead to persistent off-target metabolic and immunomodulatory effects.},
journal = {Cell},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cell.2025.05.014},
pmid = {40482640},
issn = {1097-4172},
abstract = {Fecal microbiota transplant (FMT) is an increasingly used intervention, but its suitability to restore regional gut microbiota, particularly in the small bowel (SB), must be questioned because of its predominant anaerobic composition. In human subjects receiving FMT by upper endoscopy, duodenal engraftment of anaerobes was observed after 4 weeks. We hypothesized that peroral FMTs create host-microbe mismatches that impact SB homeostasis. To test this, antibiotic-treated specific-pathogen-free (SPF) mice were given jejunal, cecal, or fecal microbiota transplants (JMTs, CMTs, or FMTs, respectively) and studied 1 or 3 months later. JMT and FMT altered regional microbiota membership and function, energy balance, and intestinal and hepatic transcriptomes; JMT favored host metabolic pathways and FMT favored immune pathways. MTs drove regional intestinal identity (Gata4, Gata6, and Satb2) and downstream differentiation markers. RNA sequencing (RNA-seq) of metabolite-exposed human enteroids and duodenal biopsies post-FMT confirmed transcriptional changes in mice. Thus, regional microbial mismatches after FMTs can lead to unintended consequences and require rethinking of microbiome-based interventions.},
}

@article {pmid40481571,
year = {2025},
author = {Feng, Y and Zhao, Q and Zhao, Y and Ma, C and Tian, M and Hu, X and Chen, F and Li, D},
title = {Lactobacillus plantarum-derived extracellular vesicles from dietary barley leaf supplementation attenuate Citrobacter rodentium infection and intestinal inflammation.},
journal = {Journal of nanobiotechnology},
volume = {23},
number = {1},
pages = {426},
pmid = {40481571},
issn = {1477-3155},
support = {32371511 and 32001677//the National Natural Science Foundation of China/ ; 2020M680256//the China Postdoctoral Science Foundation/ ; },
mesh = {Animals ; *Citrobacter rodentium ; Mice ; *Enterobacteriaceae Infections/microbiology ; *Extracellular Vesicles/metabolism/chemistry ; *Lactobacillus plantarum/metabolism/chemistry ; *Hordeum/chemistry ; Gastrointestinal Microbiome/drug effects ; Colitis/microbiology ; *Plant Leaves/chemistry ; Mice, Inbred C3H ; *Dietary Supplements ; Male ; Inflammation ; },
abstract = {BACKGROUND: Inflammatory bowel disease (IBD) is a gastrointestinal inflammatory disorder characterized by disturbed interactions between gut microbiota and host immune response. Barley leaf (BL) is a traditional Chinese herb recorded to have health-promoting effects. However, little is known about the beneficial role of BL against enteric infection-induced intestinal inflammation. Here, we uncover that BL protects against Citrobacter rodentium (C. rodentium)-induced infectious colitis by improving host-microbiota interactions.

METHODS: C3H/HeN mice were fed a diet with/without BL and infected with C. rodentium. Transcriptome sequencing, anti-CD4 antibody treatment, and flow cytometry were conducted to investigate the mechanisms of T cell immune modulation. The intervention involved administering anti-CD4 antibody at 500 µg each time for three times before and during C. rodentium infection. Analysis of gut microbiota composition was performed by 16S rRNA gene sequencing on fecal samples. Fecal microbiota transplantation was conducted by administering microbiota from donor group to recipient group via oral gavage to investigate the role of intestinal microbiota in immune modulation.

RESULTS: BL ameliorated the severity of C. rodentium-induced colitis, and this effect was linked to improved gut homeostasis and enhanced mucosal barrier function. BL enriched the pathways of T helper 1 (Th1)/Th2 and Th17 cell differentiation in the colon, suggesting the involvement of CD4[+] T cells. Consistent with this, anti-CD4 antibody treatment abrogated the effect of BL and flow cytometry analysis revealed that BL mitigated C. rodentium-induced pro-inflammatory Th1 immune response. Moreover, the protective effect of BL was associated with alleviation of gut microbiota dysbiosis and increased abundance of Lactobacillus. Our in vivo studies further revealed that live Lactobacillus plantarum (L. plantarum) administration attenuated the pathogenic effects induced by C. rodentium infection, whereas heat-inactivated L. plantarum did not show the same results. Mechanistically, BL supplementation enriched L. plantarum, which subsequently released nanosized extracellular vesicles (EVs) that serve as a key mediator in alleviating C. rodentium-associated pathology and Th1 cell dysregulation.

CONCLUSIONS: Our work thus provides evidence for utilizing BL and L. plantarum-derived EVs to manage enteric infection-associated IBD.},
}

Animals
*Citrobacter rodentium
Mice
*Enterobacteriaceae Infections/microbiology
*Extracellular Vesicles/metabolism/chemistry
*Lactobacillus plantarum/metabolism/chemistry
*Hordeum/chemistry
Gastrointestinal Microbiome/drug effects
Colitis/microbiology
*Plant Leaves/chemistry
Mice, Inbred C3H
*Dietary Supplements
Male
Inflammation

@article {pmid40478639,
year = {2025},
author = {Bathobakae, L and Bashir, R and Koodirile, A and Villegas, K and Rajab, I and Perez, EW and Cavanagh, Y and El-Sedfy, A and Suh, JS},
title = {Clostridioides difficile enteritis: a targeted review of current literature.},
journal = {Scandinavian journal of gastroenterology},
volume = {},
number = {},
pages = {1-11},
doi = {10.1080/00365521.2025.2515423},
pmid = {40478639},
issn = {1502-7708},
abstract = {Clostridioides difficile enteritis (CDE) is a rare but clinically significant form of Clostridioides difficile infection (CDI) affecting the small intestine. CDE poses a diagnostic challenge owing to its rarity, complexity, and nonspecific presentation. The current data is retrospective in the form of case reports and conference proceedings. The lack of widespread awareness and limited literature on CDE often result in diagnostic delays, contributing to increased morbidity. This targeted narrative review sought to consolidate the current knowledge on the epidemiology, pathophysiology, clinical presentation, and management of CDE, addressing a critical gap in the existing literature. Electronic databases, including PubMed, Embase, and Web of Science, were searched for published cases from inception to April 2024. The initial search yielded 2,120 articles, which were filtered using study design, English language, and human subjects. After screening for duplicates and excluding irrelevant articles, 44 articles comprising 49 patients were included in the final review. Of the 49 individual cases reviewed, 25 (51%) were male and 24 (49%) were female. The patients' ages ranged from 16 to 91 years, with a mean age of 53.4 years. Abdominal pain and diarrhea were the chief complaints reported in 37/49 (76%) and 35/49 (71%) cases, respectively. About 42/49 (86%) cases were effectively treated with antibiotics, while some cases required fecal microbiota transplantation or surgical exploration. Given its grave course, CDE warrants prompt and appropriate treatment to prevent complications such as fulminant enteritis, compartment syndrome, and bowel perforation.},
}

@article {pmid40478172,
year = {2025},
author = {Lasagna, A},
title = {Mitigation strategies for gastrointestinal (GI) immune-related adverse events for patients with solid tumors receiving immunotherapy.},
journal = {Immunotherapy},
volume = {},
number = {},
pages = {1-9},
doi = {10.1080/1750743X.2025.2516995},
pmid = {40478172},
issn = {1750-7448},
abstract = {Over the past decade, immunotherapy has revolutionized the treatment algorithm for solid tumors. Immune checkpoint inhibitors (ICIs) demonstrated efficacy against several tumor types, but they can favor the development of immune-related adverse events (irAEs). IrAEs can sometimes be life-threatening. In this review, we will briefly analyze the main gastro-intestinal toxicities and focus on potential strategies for mitigating irAEs, particularly through the modification of gut microbiota (GM) composition. Finally, we will briefly dwell on the potential role of artificial intelligence (AI) in the prediction of irAEs.},
}

@article {pmid40475999,
year = {2025},
author = {Hwang, D and Chong, E and Li, Y and Li, Y and Roh, K},
title = {Deciphering the gut microbiome's metabolic code: pathways to bone health and novel therapeutic avenues.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1553655},
pmid = {40475999},
issn = {1664-2392},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Bone and Bones/metabolism ; Animals ; Probiotics/therapeutic use ; *Bone Remodeling/physiology ; *Osteoporosis/metabolism/microbiology/therapy ; Prebiotics ; Fecal Microbiota Transplantation ; Bone Diseases/metabolism/microbiology/therapy ; },
abstract = {The gut microbiome plays an important role in the protection against various systemic diseases. Its metabolic products profoundly influence a wide range of pathophysiological events, including the regulation of bone health. This review discusses the recently established connections between the gut microbiome and bone metabolism, focusing on the impact of microbiome-derived metabolites such as SCFAs, Bile Acids, and tryptophan to the control of bone remodeling and immunoreactions. Recent advances in metagenomics and microbiome profiling have unveiled new exciting therapeutic opportunities, ranging from the use of probiotics, prebiotics, engineered microbes, and to fecal microbiota transplantation. Understanding of the interplay among diet, microbiota, and bone health provides new avenues for tailored interventions aimed at reducing disease risk in osteoporosis and other related disorders. By drawing knowledge from microbiology, metabolism, and bone biology, this review highlights the potential of microbiome-targeted therapies to transform skeletal health and the management of bone diseases.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Bone and Bones/metabolism
Animals
Probiotics/therapeutic use
*Bone Remodeling/physiology
*Osteoporosis/metabolism/microbiology/therapy
Prebiotics
Fecal Microbiota Transplantation
Bone Diseases/metabolism/microbiology/therapy

@article {pmid40472289,
year = {2025},
author = {Lim, LWZ and Toh, KY and Cook, AR and Lee, JWJ and Lim, JFY},
title = {Public knowledge, awareness and perception of gut microbiome and faecal microbiota transplantation in Singapore: a survey study.},
journal = {Singapore medical journal},
volume = {},
number = {},
pages = {},
pmid = {40472289},
issn = {2737-5935},
abstract = {INTRODUCTION: Despite the exponential increase in microbiome research, knowledge and beliefs about the gut microbiome and faecal microbiota transplantation (FMT) remain unclear. The aim of this study was to identify the extent of knowledge, awareness and perception among the general public regarding the gut microbiome and FMT.

METHODS: An online questionnaire on knowledge and beliefs about the gut microbiome and FMT was administered to 1831 participants. Data analysis software was used to generate descriptive statistics and explore associations between knowledge and sociodemographic variables.

RESULTS: Even though only 33% of participants had heard of the gut microbiome, more than 92% had consumed probiotic drinks or supplements. While 85% had not heard of the FMT procedure, 72% of respondents would consider having FMT to treat Clostridioides difficile infection (CDI). Willingness to receive FMT depended mainly on recommendation from healthcare providers (77%). Knowledge and awareness regarding the gut microbiome and FMT were relatively low, despite most participants having prior gut health-related behaviours.

CONCLUSION: This study identified the public's perceptions of FMT and the potential barriers to its uptake. Insights from the study highlight the need for health education to enhance acceptance of FMT and the importance of using information supported by medical professionals to immunise the public against poorly validated science.},
}

@article {pmid40471587,
year = {2025},
author = {Wei, M and Huang, Q and Yu, F and Luo, YF and Feng, X and Liao, D and Li, J and Zhang, B and Liu, ZY and Xia, J},
title = {Elevated phenylacetylglutamine caused by gut dysbiosis associated with type 2 diabetes increases neutrophil extracellular traps formation and exacerbates brain infarction.},
journal = {Clinical science (London, England : 1979)},
volume = {},
number = {},
pages = {},
doi = {10.1042/CS20242943},
pmid = {40471587},
issn = {1470-8736},
support = {2022YFC3602400, 2022YFC3602401//National Key Research and Development Projects/ ; 82271369; 82301514; 82471365//National Natural Science Foundation of China/ ; 2021JJ31109; 2023JJ41018//Natural Science Foundation of Hunan Province/ ; },
abstract = {Type 2 diabetes (T2D) aggravates ischemic stroke. The association between gut microbiota-derived metabolite phenylacetylglutamine (PAGln) and ischemic stroke patients with T2D remains unclear. Therefore, we aimed to explore the change of gut microbiota and its metabolite, PAGln in ischemic stroke patients with T2D, as well as investigate the role of PAGln in this disease. We performed two clinical cohort studies to investigate the changes of gut microbiota and PAGln in ischemic stroke patients with T2D. Then, we transplanted fecal microbiota from patients into rats and established a middle cerebral artery occlusion model. Finally, an intraperitoneal injection of PAGln was administered to rats to test whether it exacerbates brain infarction. Plasma PAGln levels were significantly higher in stroke patients with T2D compared to those without T2D. There was a positive correlation of Plasma PAGln with NETs. Enterobacteriaceae, Verrucomicrobiota, and Klebsiella were enriched in stroke patients with T2D and showed a significant positive correlation with PAGln levels. The rats transplanted with fecal microbes from stroke patients with T2D developed a more severe brain injury and had higher levels of plasma PAGln and NETs compared to the rats transplanted with fecal microbes from stroke patients without T2D. Additionally, rats treated with PAGln exhibited more severe brain injury accompanied by increased systemic inflammation, oxidative stress and NET formation. Our results suggest elevated circulating PAGln levels, resulting from gut dysbiosis in stroke patients with T2D, may exacerbate brain infarction through NETs formation, systemic inflammation, and oxidative stress.},
}

@article {pmid40470286,
year = {2025},
author = {Hetterich, J and Pees, M},
title = {Case Report: Oral fecal microbiota transplantation in a Mediterranean spur-thighed tortoise (Testudo graeca) suffering from chronic gastrointestinal disease-procedure, clinical outcome and follow-up.},
journal = {Frontiers in veterinary science},
volume = {12},
number = {},
pages = {1560689},
pmid = {40470286},
issn = {2297-1769},
abstract = {INTRODUCTION: Fecal microbiota transplantation (FMT) is the process of transferring fecal microbiota from a healthy donor into the gastrointestinal tract of a recipient. Although many mechanisms of FMT are still not completely understood at present, it has been described that the treatment of various gastrointestinal diseases in different species, including humans, is significantly improved by FMT therapy. Since the first report on FMT therapy in veterinary medicine in small mammals numerous cases have been reported, but little information has been published on the therapeutic effects of FMT treatment in reptiles. The present case report describes the effects of orally administered fecal microbiota transplantation in a Mediterranean spur-thighed tortoise (Testudo graeca) suffering from chronic gastrointestinal disorders.

CASE PRESENTATION: A nine-year-old, 330 g, intact female Mediterranean spur-thighed tortoise (Testudo graeca) from the animal owner's own offspring was presented for consultation due to decreased general condition, anorexia and sialorrhea following oral intake of a lettuce species (Lactuca virosa) known for its poisonous plant ingredients (sesquiterpene lactones) 3 weeks prior to presentation. Pre-existing conditions were not reported. Clinical examination revealed sialorrhea and a reduced general condition. Diagnostic procedures included blood chemistry, radiography and ultrasonography. Despite repeated treatment attempts with various medical regimes over 158 days, the tortoise continued showing variable recurring gastrointestinal symptoms. An orally administered FMT was initiated and continued for a total of 3 weeks. Gastrointestinal signs improved rapidly within 1 week and resolved completely after 3 weeks. Over a follow up period of 9 months, no symptom recurrence or adverse effects were monitored.

CONCLUSION: This case report describes the first successful trial of fecal microbiota transplantation in chelonians. The outcome indicates that this therapeutic approach may be beneficial not only to small animals but also for the therapy of gastrointestinal disorders in reptiles, especially those cases with insufficient conventional therapy results.},
}

@article {pmid40469520,
year = {2025},
author = {Yu, L and Chen, Z and Yin, S and Guo, Q and Chen, Y and Li, J and Wang, Y and Liu, X and Xu, Z and Zhang, Y and Zhang, Y and Zheng, Z and Chen, K and Ding, Y and Fan, H and Liu, Z and Ding, Y},
title = {Gut-derived Lactobacillus from exceptional responders mitigates chemoradiotherapy-induced intestinal injury through methionine-driven epigenetic modulation.},
journal = {iMeta},
volume = {4},
number = {3},
pages = {e70043},
pmid = {40469520},
issn = {2770-596X},
abstract = {Acute chemoradiotherapy-induced intestinal injury (ACRIII) is a common and debilitating complication in patients with colorectal cancer, significantly impairing both quality of life and treatment outcomes. This study aimed to investigate the role of the gut microbiome in mitigating ACRIII. Through bioinformatics analysis of clinical fecal samples and fecal microbiota transplantation (FMT) experiments in mice, we identified a strong association between a high abundance of Lactobacillus species and the absence of ACRIII. From the fecal samples of rectal cancer patients who achieved complete remission without experiencing ACRIII during chemoradiotherapy, 10 novel Lactobacillus strains were isolated and characterized. Among these, Lacticaseibacillus rhamnosus DY801 exhibited a robust capacity to synthesize methionine through metB. This microbial methionine production modulated methionine metabolism in host gut lymphoid tissue inducer (Lti) cells, without diminishing the therapeutic efficacy of chemoradiotherapy. Supplementation with methionine increased intracellular levels of S-adenosylmethionine and enhanced histone H3 lysine 4 trimethylation (H3K4me3) in Lti cells. These epigenetic modifications led to the suppression of pro-inflammatory cytokines interleukin-17A (IL-17A) and interleukin-22 (IL-22), ultimately reducing ACRIII severity. Our findings suggest that specific Lactobacillus strains derived from patients with exceptional treatment responses may offer a novel therapeutic avenue for preventing or alleviating ACRIII. This microbiome-based approach holds significant potential for improving patient outcomes and enhancing the tolerability of chemoradiotherapy in colorectal cancer.},
}

@article {pmid40469517,
year = {2025},
author = {Zhang, F and Li, R and Liu, Y and Liang, J and Gong, Y and Xiao, C and Cai, J and Wang, T and You, Q and Zhang, J and Chen, H and Xiao, J and Zhang, Y and Yang, Y and Li, H and Yao, J and Zhang, Q and Zheng, J},
title = {Integrative cross-tissue analysis unveils complement-immunoglobulin augmentation and dysbiosis-related fatty acid metabolic remodeling during mammalian aging.},
journal = {iMeta},
volume = {4},
number = {3},
pages = {e70027},
pmid = {40469517},
issn = {2770-596X},
abstract = {Aging-related decline and adaptation are complex, multifaceted processes that affect various tissues and increase risk of chronic diseases. To characterize key changes in cross-tissue aging, we performed comprehensive proteomic and metabolomic analyses across 21 solid tissues and plasma samples, alongside shotgun metagenomic profiling of fecal microbial communities in young and aged mice. Our findings revealed widespread aging-rewired chronic inflammation, characterized by complement system activation in plasma and universal immunoglobulins accumulation across multiple solid tissues. This inflammatory remodeling significantly enhanced vulnerability to aging-related tissue injury. Moreover, we identified organ-specific and organ-enriched proteins with high functional specificity. Among these, aging-related proteins were closely linked to disorders arising from lipid metabolism dysfunction. Analysis of multi-tissue metabolomic and fecal metagenomic profiles revealed that aging significantly disrupted inter-tissue metabolic coupling, activities of polyunsaturated fatty acids metabolism, and gut microbiota homeostasis. Aged mice exhibited a marked decrease in Escherichia and an increase in Helicobacter, strongly correlating with alterations in omega-3 and omega-6 fatty acid abundances. Through multi-omics integration, we identified key molecular hubs driving organismal responses to aging. Collectively, our study uncovers extensive aging-associated alterations across tissues, emphasizing the interplay between systemic inflammation and dysbiosis-driven fatty acid remodeling. These findings provide deeper insights into the development of healthy aging from a cross-tissue perspective.},
}

@article {pmid40469413,
year = {2025},
author = {Shimizu, K and Ogura, H and Oda, J},
title = {Gut dysbiosis and its treatment in patients with critical illness.},
journal = {Acute medicine & surgery},
volume = {12},
number = {1},
pages = {e70068},
pmid = {40469413},
issn = {2052-8817},
abstract = {The gut is a target organ that functions as the "motor" of critical illness. In patients with critical illness, the disrupted gut microbiota following infection and injury could cause diarrhea, pneumonia, and systemic inflammation. For maintaining the gut microbiota, therapeutic approaches are required to modulate host responses and prevent systemic inflammation. Probiotics and synbiotics could maintain the gut microbiota and decrease not only the incidence of diarrhea but also that of ventilator-associated pneumonia. The effects of probiotics/synbiotics differ with the type of bacteria and disease severity. Adverse effects of probiotics have been reported; therefore, the selection of safe and effective probiotics/synbiotics is warranted. Refractory diarrhea with prolonged dysbiosis may require a novel intestinal therapy, such as fecal microbiota transplantation, to alleviate gut dysbiosis.},
}

@article {pmid40468650,
year = {2025},
author = {Cha, RR and Sonu, I},
title = {Fecal microbiota transplantation: present and future.},
journal = {Clinical endoscopy},
volume = {58},
number = {3},
pages = {352-359},
doi = {10.5946/ce.2024.270},
pmid = {40468650},
issn = {2234-2400},
support = {//Gyeongsang National University Fund/ ; },
abstract = {Fecal microbiota transplantation (FMT) involves transplanting fecal matter from healthy donors into patients with gut dysbiosis to restore microbial balance. It has been proven to be highly effective in treating recurrent Clostridioides difficile infection (CDI), and United States Food and Drug Administration-approved microbiome-based therapies, such as REBYOTA (fecal microbiota live-jslm) and VOWST (fecal microbiota spores live-brpk), offer promising treatment options. Although FMT is widely used to treat recurrent CDI, its use in gastrointestinal and metabolic diseases remains limited. Future research directions include optimizing donor selection, understanding microbial mechanisms, and exploring the potential of FMT for treating other diseases. Ongoing research not only aims to broaden its indications but also improves its safety and efficacy. Emerging therapies such as VE303 (Vedanta) are being studied to refine treatment approaches and expand the use of microbiota-based therapies. Further studies are needed to standardize guidelines, improve patient outcomes, and better define the role of FMT in the treatment of diseases beyond recurrent CDI.},
}

@article {pmid40466419,
year = {2025},
author = {Zhang, K and Dong, Y and Ding, Y and Wang, X and Liu, T and Zhong, W and Cao, H},
title = {Illuminating prospects of probiotic Akkermansia muciniphila in intestinal inflammation and carcinogenesis.},
journal = {Microbiological research},
volume = {299},
number = {},
pages = {128240},
doi = {10.1016/j.micres.2025.128240},
pmid = {40466419},
issn = {1618-0623},
abstract = {Akkermansia muciniphila (A. muciniphila) is portrayed as an advantageous enteric bacterium with a particular property of mucin utilization. Emerging data suggest A. muciniphila can reshape gut chronic inflammation, enhance intestinal epithelial tight junctions, and sensitize toll-like receptors 2 (TLR2) and TLR4 to restrain the infiltrating cytotoxic T lymphocytes and macrophages. As well, analogous role is detected in surface A. muciniphila-coated pili, outer-membrane protein Amuc_1100, β-galactosidase enzyme Amuc_2172, and extracellular vesicles. We rendered insights into empirical evidence on molecular mechanisms mediated by A. muciniphila in inflammatory bowel disease and intestinal cancers which include colitis-associated colorectal cancer and colorectal cancer. We discussed its potential preventive and therapeutic benefits on immune checkpoint inhibitors therapy. A. muciniphila supplementation through diet, probiotics-prebiotics, fecal microbiota transplantation, and certain drugs, would be a promising therapeutic strategy. Nevertheless, data profiles decipher A. muciniphila is linked to multiple sclerosis and Parkinson's disease occurrence and evolvement. Thus, how to avoid the deleterious effects triggered by A. muciniphila warrants further exploration. It ought to be considered to conduct a critical and cautious analysis of the next-generation beneficial microbe manipulation ahead of clinical application.},
}

@article {pmid40069438,
year = {2025},
author = {Park, M and Jung, J and Lee, JA and Lee, E and Lee, H and Eom, HS and Park, HJ},
title = {Understanding gut Microbiome changes in Korean children, adolescents, and young adults with hematologic malignancies.},
journal = {Annals of hematology},
volume = {104},
number = {5},
pages = {2947-2961},
pmid = {40069438},
issn = {1432-0584},
support = {2011500-1//National Cancer Center, Korea/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; Adolescent ; Child ; Male ; Female ; *Hematologic Neoplasms/therapy/microbiology/epidemiology ; Young Adult ; Republic of Korea/epidemiology ; Hematopoietic Stem Cell Transplantation ; Feces/microbiology ; Adult ; },
abstract = {We investigated whether changes in the gut microbiome composition are associated with infections and immunologic complications during the treatment of Korean children, adolescents, and young adults (AYAs) with hematologic malignancies. We analyzed stool samples from 26 patients and 10 healthy siblings using 16 S rRNA gene sequencing. At diagnosis, patients exhibited a lower abundance of Lachnospiraceae and a higher abundance of Enterococcaceae than their healthy siblings. Both the Chao1 and Shannon diversity indices declined from diagnosis to the end of induction chemotherapy. Patients with fever during induction had a lower baseline microbial diversity and higher Ruminococcus g4 abundance than those without fever. The use of either meropenem or piperacillin/tazobactam during induction was correlated with reduced richness and altered composition of the gut microbiome after induction. The Chao index and beta diversity of stool samples significantly differed before conditioning when compared with those of healthy siblings. During allogeneic hematopoietic stem cell transplantation, both the Chao1 and Shannon diversity indices significantly decreased on day 14 but recovered by day 60. Our study highlights the role of gut microbiome diversity and compositional structure in influencing treatment outcomes in children and AYA with hematologic malignancies, providing the information required to improve the gut microbiome configuration and treatment outcomes.},
}

Humans
*Gastrointestinal Microbiome/drug effects
Adolescent
Child
Male
Female
*Hematologic Neoplasms/therapy/microbiology/epidemiology
Young Adult
Republic of Korea/epidemiology
Hematopoietic Stem Cell Transplantation
Feces/microbiology
Adult

@article {pmid40464639,
year = {2025},
author = {Zhang, Q and Liu, Y and Li, Y and Bai, G and Pang, J and Wu, M and Li, J and Zhao, X and Xia, Y},
title = {Implications of gut microbiota-mediated epigenetic modifications in intestinal diseases.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508426},
doi = {10.1080/19490976.2025.2508426},
pmid = {40464639},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Epigenesis, Genetic ; Animals ; Dysbiosis/microbiology/therapy ; DNA Methylation ; Fecal Microbiota Transplantation ; Prebiotics/administration & dosage ; *Intestinal Diseases/microbiology/genetics/therapy ; Probiotics ; Inflammatory Bowel Diseases/microbiology/genetics/therapy ; Colorectal Neoplasms/microbiology/genetics ; },
abstract = {Intestinal diseases are highly prevalent, affecting millions worldwide and significantly contributing to global morbidity. The treatment of complex disorders, such as inflammatory bowel disease (IBD) and colorectal cancer (CRC), remains challenging due to multifactorial etiologies, diverse patient responses, and the limitations of current therapeutic strategies. Although the gut microbiota clearly plays a role in regulating the onset of intestinal diseases, few studies have explored the epigenetic factors by which the microbiota contributes to disease development. Here, the latest insights into the molecular mechanisms underlying the bidirectional influence between gut microbiota and epigenetic modifications are discussed, including DNA methylation, histone modifications, non-coding RNAs, and N6-methyladenosine (m[6]A). Importantly, mechanistic studies based on animal models or human cells have demonstrated that the gut microbiota, and other environmental factors, influence targeted gene expression and activate immune pathways through host epigenetic dysregulation, which are closely associated with the development of IBD and CRC. Furthermore, potential microbiome interventions, including probiotics, prebiotics and postbiotics, fecal microbiota transplantation (FMT), dietary modifications, and phage therapy, have been proposed as innovative therapeutic strategies to correct these abnormal epigenetic patterns associated with the diseases. Overall, addressing microbiome dysbiosis and its epigenetic consequences presents a promising frontier in the treatment of intestinal diseases, offering the potential to not only restore microbial balance but also provide more targeted and personalized therapeutic strategies for better patient outcomes.},
}

Humans
*Gastrointestinal Microbiome
*Epigenesis, Genetic
Animals
Dysbiosis/microbiology/therapy
DNA Methylation
Fecal Microbiota Transplantation
Prebiotics/administration & dosage
*Intestinal Diseases/microbiology/genetics/therapy
Probiotics
Inflammatory Bowel Diseases/microbiology/genetics/therapy
Colorectal Neoplasms/microbiology/genetics

@article {pmid40464558,
year = {2025},
author = {Ruan, Y and Zhu, T and Yang, R and Su, F and An, C and Hu, Z and Li, X and Li, Y and Chen, P and Shao, X and Qin, J and Chen, H and Chen, R},
title = {Donor-derived microbial engraftment and gut microbiota shifts associated with weight loss following fecal microbiota transplantation.},
journal = {Applied and environmental microbiology},
volume = {},
number = {},
pages = {e0012025},
doi = {10.1128/aem.00120-25},
pmid = {40464558},
issn = {1098-5336},
abstract = {Fecal microbiota transplantation (FMT) is a promising treatment for microbiota dysbiosis and may provide metabolic benefits for obesity. However, its mechanisms and variability in clinical outcomes remain poorly understood. This 12-week multicenter, single-arm study evaluated the efficacy of FMT for weight loss and explored the role of donor-derived microbial engraftment and functional shifts in mediating weight loss among overweight and obese individuals. Twenty-three participants (body mass index ≥24 kg/m[2]) without diabetes received three biweekly FMT sessions via a nasojejunal tube. Fecal samples from participants and donors were analyzed using metagenomic sequencing. By week 12, 52% of participants were classified as responders, achieving significant weight loss of ≥5% from baseline, with an average weight loss of 7.98 ± 2.69 kg (P < 0.001). In contrast, non-responders lost 2.90 ± 1.89 kg (P < 0.001). Responders exhibited a significantly higher proportion of donor-derived microbial strains post-FMT compared to non-responders (37.8% vs 15.2%, P = 0.020). Notably, key taxa, including Phascolarctobacterium (P = 0.034) and Acidaminococcaceae (P = 0.012), increased significantly in abundance in responders post-FMT, indicating successful microbial engraftment as a critical determinant of therapeutic success. These findings suggest that FMT is a viable intervention for weight loss in obese individuals. Successful donor-derived microbial engraftment strongly correlates with weight loss efficacy, highlighting the potential of microbiota-targeted therapies in obesity management and providing insights into the mechanisms underlying FMT outcomes.IMPORTANCEPrior research indicates that fecal microbiota transplantation (FMT) is a promising treatment for diseases related to microbiota imbalance, potentially providing metabolic benefits for obesity. However, the specific role of donor-derived microbial engraftment in driving clinical efficacy has remained unclear. In this study, we evaluated the efficacy of FMT in promoting weight loss and explored the role of donor-derived bacterial strains in this process. Our findings demonstrate that the successful engraftment of specific donor-derived taxa, such as Phascolarctobacterium and Acidaminococcaceae, is strongly associated with significant weight loss. This highlights the critical interplay between donor microbiota and recipient gut environment. These findings underscore the potential of microbiota-targeted therapies as a novel strategy for obesity management.CLINICAL TRIALSThis study is registered with the Chinese Clinical Trial Registry as ChiCTR1900024760.},
}

@article {pmid40463945,
year = {2025},
author = {Wu, C and Mi, Y and Song, J and Zhang, M and Wang, C},
title = {The Regulatory Effect of Human Umbilical Cord Mesenchymal Stem Cells on the Gut Microbiota in Diabetic Nephropathy Rats.},
journal = {Iranian journal of biotechnology},
volume = {23},
number = {1},
pages = {},
pmid = {40463945},
issn = {1728-3043},
abstract = {BACKGROUND: Chronic inflammation is increasingly recognized as a key factor in the progression of diabetic kidney disease (DKD). By discovering that the regulation of gut microbiota plays an important role in diabetic kidney disease, human umbilical cord mesenchymal stem cells (HU-MSCs) explore the mechanism of fibrosis in diabetic kidney disease through the regulation of chronic inflammation, providing new clinical insights for the prediction, diagnosis, and treatment of diabetic kidney disease.

OBJECTIVES: This study explores the regulatory effects of HU-MSCs on gut microbiota and their protective role on the intestinal barrier in diabetic nephropathy rats.

MATERIAL AND METHOD: Diabetic kidney disease (DKD) was induced in SD rats via intraperitoneal injection of streptozotocin. Three groups were established: control group, diabetic kidney disease (DKD) group, and treatment group (DKD+HU-MSCs) (10 rats each). After diabetic kidney disease (DKD) modeling, rats in the treatment group (DKD+HU-MSCs) received 2×10[6] HU-MSCs via tail vein injection weekly for four weeks. Blood, urine, kidney, and colon tissues were collected post-treatment. Pathological changes were observed microscopically; immunohistochemistry detected tight junction proteins ZO-1 and Occludin in colon tissues. DiR-labeled HU-MSCs distribution was assessed with in vivo imaging, and immunohistochemistry evaluated human mesenchymal stem cell markers CD44 and CD90. Fecal samples underwent metagenomic sequencing for gut microbiota analysis.

RESULTS: HU-MSCs transplantation significantly reduced Blood Urea Nitrogen (BUN), Serum Creatinine (SCr), and 24-hour urinary protein levels (all P < 0.05) and improved renal pathology. Markers CD44 and CD90 were present in DKD rat colon tissues. Tight junction proteins Occludin and ZO-1 were decreased in DKD rats but increased following HU-MSCs treatment. Metagenomic analysis showed enhanced abundance of beneficial bacteria (Bifidobacterium and Lactobacillus) with HU-MSCs. Urinary protein was positively correlated with Prevotella and negatively with Ligilactobacillus (p < 0.05).

CONCLUSIONS: HU-MSCs may improve intestinal barrier function in diabetic kidney disease (DKD) rats by restoring gut microbiota structure and increasing intestinal tight junction proteins, offering a potential pathway for enhancing renal function.},
}

@article {pmid40462220,
year = {2025},
author = {Chen, M and Pan, J and Song, Y and Liu, S and Sun, P and Zheng, X},
title = {Correction: Effect of inulin supplementation in maternal fecal microbiota transplantation on the early growth of chicks.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {138},
pmid = {40462220},
issn = {2049-2618},
}

@article {pmid40272189,
year = {2025},
author = {Zhang, L and Wang, H and Zhao, L and Zhang, J and Sun, W and Chu, J and Zhao, H and Yang, C and Yan, S and Chen, X and Xu, D},
title = {Unraveling the interplay between mesenchymal stem cells, gut microbiota, and systemic sclerosis: therapeutic implications.},
journal = {Microbiology spectrum},
volume = {13},
number = {6},
pages = {e0157624},
pmid = {40272189},
issn = {2165-0497},
support = {82171790//National Natural Science Foundation of China/ ; 82201925//National Natural Science Foundation of China/ ; 32000075//National Natural Science Foundation of China/ ; ZR2024QC071//Natural Science Foundation of Shandong Province/ ; ZR2024MH079//Natural Science Foundation of Shandong Province/ ; ZR2022QH203//Natural Science Foundation of Shandong Province/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; *Scleroderma, Systemic/therapy/chemically induced/microbiology/pathology ; Animals ; *Mesenchymal Stem Cells/physiology/metabolism ; Mice ; Humans ; *Mesenchymal Stem Cell Transplantation ; Disease Models, Animal ; Bacteria/classification/genetics/isolation & purification/metabolism ; Bleomycin ; Mice, Inbred C57BL ; Feces/microbiology ; Female ; },
abstract = {UNLABELLED: Systemic sclerosis (SSc) is an autoimmune disease with progressive fibrotic disorders in multiple organs. Mesenchymal stem cells (MSCs) have shown great potential in treating SSc, but the exact regulatory mechanism is not fully understood. In this study, we used human umbilical cord-derived MSCs (hUC-MSCs) to treat SSc mice induced by bleomycin. The gut microbiota composition and predicted functions were analyzed using 2bRAD sequencing of fecal samples from control, SSc, and MSCs-treated mice. Treatment with MSCs improved the bleomycin-induced SSc mice, characterized by significantly reduced collagen deposition and dermal thickness. The gut microbiota of SSc mice exhibited lower species evenness and was clearly separated from the control mice based on beta diversity. MSC treatment led to a significant reduction of conditionally pathogenic bacteria enriched in SSc, including Akkermansia muciniphila and Parasutterella excrementihominis. Conversely, the relative abundance of butyrate-producing bacteria, such as Roseburia, Butyricicoccus porcorum, and Gemmiger formicilis, was notably increased in MSCs-treated SSc mice. Additionally, the functional analysis revealed that MSCs intervention effectively enhanced sulfur metabolism, tryptophan metabolism, citrate cycle, RNA polymerase, and beta-lactam resistance. In summary, the findings in the present study have suggested the close association between gut microbiota and metabolic dysbiosis in mice with SSc. The administration of MSCs has been shown to regulate the disrupted metabolic pathways in SSc mice, thus restoring the normal function of the gut microbiota. This study provides valuable insights into the specific gut microbiota and metabolic pathways involved in the efficacy of MSC treatment, thereby proposing a novel therapeutic strategy for SSc.

IMPORTANCE: Human umbilical cord-derived mesenchymal stem cells (HUC‑MSCs) demonstrate efficacy in alleviating skin thickening and collagen deposition in systemic sclerosis (SSc) mice, which also regulate the gut microbiota composition and function. Specifically, MSC intervention leads to a notable increase in butyrate-producing bacteria, a decrease in Akkermansia muciniphila and Parasutterella excrementihominis, and a reversal of the dysregulated microbial function in SSc mice. These findings underscore the potential significance of gut microbiota in the therapeutic effects of MSCs in SSc.},
}

*Gastrointestinal Microbiome/physiology
*Scleroderma, Systemic/therapy/chemically induced/microbiology/pathology
Animals
*Mesenchymal Stem Cells/physiology/metabolism
Mice
Humans
*Mesenchymal Stem Cell Transplantation
Disease Models, Animal
Bacteria/classification/genetics/isolation & purification/metabolism
Bleomycin
Mice, Inbred C57BL
Feces/microbiology
Female

@article {pmid40462165,
year = {2025},
author = {Gao, H and Bai, H and Su, Y and Gao, Y and Fang, H and Li, D and Yu, Y and Lu, X and Xia, D and Mao, D and Luo, Y},
title = {Fecal microbiota transplantation from Helicobacter pylori carriers following bismuth quadruple therapy exacerbates alcohol-related liver disease in mice via LPS-induced activation of hepatic TLR4/NF-κB/NLRP3 signaling.},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {627},
pmid = {40462165},
issn = {1479-5876},
support = {42377426//National Natural Science Foundation of China/ ; 42077382//National Natural Science Foundation of China/ ; 21JCYBJC01200//Tianjin Municipal Natural Science Foundation/ ; 2023220//Research Project on Integrated Traditional Chinese and Western Medicine of Tianjin Municipal Health Commission/ ; },
abstract = {BACKGROUND: Helicobacter pylori infection is common in patients with alcohol-related liver disease (ALD), and bismuth quadruple therapy (BQT) is widely used for eradication. However, its impact on ALD remains unclear. This study aims to characterize BQT-induced gut microbiota alterations in asymptomatic H. pylori carriers and evaluate their effect on an ALD mouse model.

METHODS: Metagenomic sequencing was conducted to assess the gut microbiota composition of individuals before and after BQT. Fecal microbiota transplantation (FMT) from these donors was performed in an ALD mouse model. Gut microbiota in mice was analyzed by 16S rRNA sequencing. Liver and intestinal parameters were assessed using western blot, RT-qPCR, histopathology, ELISA, and flow cytometry.

RESULTS: BQT treatment significantly altered the gut microbiota in H. pylori carriers, increasing the abundance of opportunistic pathogens, including Klebsiella pneumoniae, Escherichia coli, Klebsiella quasipneumoniae, and Klebsiella variicola, while decreasing beneficial bacteria such as Bifidobacterium, Eubacterium, Bacteroides, Faecalibacterium, and Blautia. In ALD mice receiving FMT from post-BQT donors, exacerbated gut dysbiosis was observed, marked by an enrichment of Enterobacteriaceae and Escherichia-Shigella. These microbiota changes were associated with impairment of intestinal barrier integrity, as evidenced by reduced levels of mucins, tight junction proteins, and antimicrobial peptides, along with a decrease in Treg cells and an increase in Th17 and Th1 cells. Additionally, this dysbiosis led to elevated serum lipopolysaccharide (LPS) levels, which activated the hepatic NLRP3 inflammasome pathway and subsequently increased IL-18 and IL-1β levels. Furthermore, liver function and oxidative stress markers, including ALT, AST, MDA, GSSG/GSH ratio, and SOD, were significantly elevated, indicating severe liver dysfunction and increased oxidative stress. Finally, probiotic supplementation effectively mitigated the negative effects of BQT-induced gut microbiota remodeling on ALD in mice.

CONCLUSIONS: BQT markedly alters the gut microbiota in H. pylori carriers, promoting dysbiosis that exacerbates ALD in mice via LPS-mediated activation of hepatic inflammatory pathways. These findings highlight the need for careful consideration of BQT use in ALD patients.},
}

@article {pmid40461622,
year = {2025},
author = {Ferreira, J},
title = {Fecal microbiota transplantation therapy.},
journal = {Lab animal},
volume = {54},
number = {6},
pages = {133},
doi = {10.1038/s41684-025-01564-x},
pmid = {40461622},
issn = {1548-4475},
}

@article {pmid40461059,
year = {2025},
author = {Laiola, M and Koppe, L and Larabi, A and Thirion, F and Lange, C and Quinquis, B and David, A and Le Chatelier, E and Benoit, B and Sequino, G and Chanon, S and Vieille-Marchiset, A and Herpe, YE and Alvarez, JC and Glorieux, G and Krukowski, H and Geert, HRB and Raes, J and Fouque, D and Massy, ZA and Ehrlich, SD and Stengel, B and Wagner, S and , },
title = {Toxic microbiome and progression of chronic kidney disease: insights from a longitudinal CKD-Microbiome Study.},
journal = {Gut},
volume = {},
number = {},
pages = {},
doi = {10.1136/gutjnl-2024-334634},
pmid = {40461059},
issn = {1468-3288},
abstract = {BACKGROUND: The gut microbiota has been linked to non-communicable diseases, including chronic kidney disease (CKD). However, the relationships between gut microbiome composition changes, uraemic toxins (UTs) accumulation, and diet on CKD severity and progression remain underexplored.

OBJECTIVE: To characterise relationships between gut microbiome composition and functionality, UTs diet, and CKD severity and progression, as well as assess microbial contributions to UTs accumulation through mice faecal microbiota transplantation (FMT).

DESIGN: This study profiled the gut microbiome of 240 non-dialysis patients with CKD (CKD-REIN cohort) using shotgun metagenomics, with follow-up in 103 patients after 3 years, with comparisons with healthy volunteers from the Milieu Intérieur cohort. A multiomics approach identifies features associated with CKD severity (and progression), with validation in an independent Belgian cohort. Experimental models used FMT to test CKD gut microbiome effects on UTs and kidney fibrosis. Changes in gut microbiome over time were evaluated, and the impact of diet on these changes was assessed.

RESULTS: Compared with matched healthy controls, patients with CKD exhibited gut microbiota alteration, with enrichment of UT precursor-producing species. Patients with severe CKD exhibited higher UT levels and greater enrichment of UT (precursor)-producing species in the microbiota than patients with moderate CKD. Over time, UT (precursor)-producing species increased, and a plant-based low protein diet appeared to mitigate these changes. FMT from patients with CKD to antibiotic-treated CKD model mice increased serum UT levels and exacerbated kidney fibrosis.

CONCLUSIONS: This study highlights the role of the microbiome and UTs in CKD, suggesting a potential therapeutic target to slow disease progression.},
}

@article {pmid40460824,
year = {2025},
author = {Gogokhia, L and Tran, N and Grier, A and Nagayama, M and Xiang, G and Funez-dePagnier, G and Lavergne, A and Ericsson, C and Ben Maamar, S and Zhang, M and Battat, R and Scherl, E and Lukin, DJ and Longman, RS},
title = {Donor composition and fiber promote strain engraftment in a randomized controlled trial of fecal microbiota transplant for ulcerative colitis.},
journal = {Med (New York, N.Y.)},
volume = {},
number = {},
pages = {100707},
doi = {10.1016/j.medj.2025.100707},
pmid = {40460824},
issn = {2666-6340},
abstract = {BACKGROUND: Fecal microbiota transplantation (FMT) is an emerging treatment for ulcerative colitis (UC), but the impact of prebiotic fiber on FMT efficacy for UC is unclear. We performed a randomized, double-blind, placebo-controlled clinical trial to examine the efficacy of FMT with and without dietary fiber supplementation in patients with UC.

METHODS: 27 patients with mild to moderate UC were randomized to receive a single FMT or placebo with or without psyllium fiber supplementation for 8 weeks. The primary outcome was clinical response at week 8, and secondary outcomes included endoscopic improvement and clinical remission. Metagenomic sequencing of fecal DNA was analyzed to determine taxonomic profiles and donor strain engraftment.

FINDINGS: The trial was terminated early due to manufacturer discontinuation of FMT product. FMT induced clinical response, remission, and endoscopic improvement in UC patients compared to placebo (p < 0.05), but fiber did not improve clinical outcomes of FMT. Recipient microbiome composition post-FMT shifted toward donor composition in responders and non-responders, but the durability of this change was stronger in responders. Clinical response and durable change in microbiome composition following FMT was donor dependent. Strain tracking analysis also demonstrated a donor-dependent variability in the rate of successful engraftment and identified a consortium of engrafted bacteria associated with treatment response or fiber supplementation.

CONCLUSIONS: Single-dose FMT demonstrated clinical efficacy for mild to moderate UC compared to placebo but revealed no benefit of fiber supplementation. These results highlight proof of concept that donor selection and prebiotic fiber can shape strain-level engraftment. This study was registered at ClinicalTrials.gov: NCT03998488.

FUNDING: National Institutes of Health/National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK128257, to R.S.L.).},
}

@article {pmid40458824,
year = {2025},
author = {Huang, Y and Huang, J and Li, Y and Xu, T and Quan, G and Xu, P and Yang, X and Liu, Z and Xie, W},
title = {Therapeutic efficacy of fecal microbiota transplantation in severe food intolerance: a case report.},
journal = {Frontiers in nutrition},
volume = {12},
number = {},
pages = {1594022},
pmid = {40458824},
issn = {2296-861X},
abstract = {This report presents the first documented application of fecal microbiota transplantation (FMT) for the management of extensive multi-food intolerance involving 52 specific foods in a pediatric patient with autism spectrum disorder (ASD). A 7 years-old autistic child was diagnosed with food intolerance to 52 items, presenting with generalized rashes, diarrhea, and malnutrition (BMI of 12.9) upon exposure or ingestion of the implicated foods. The child received oral fecal microbiota capsule treatment, with a daily dose of nine capsules (a total of 120 capsules per course) for two consecutive treatment courses. The rashes resolved, the child regained tolerance to previously intolerable foods, nutritional status improved, and stool consistency normalized. This case suggests that FMT may hold therapeutic potential for managing food intolerance in autistic patients.},
}

@article {pmid40457025,
year = {2025},
author = {Elkrief, A and Pidgeon, R and Maleki Vareki, S and Messaoudene, M and Castagner, B and Routy, B},
title = {The gut microbiome as a target in cancer immunotherapy: opportunities and challenges for drug development.},
journal = {Nature reviews. Drug discovery},
volume = {},
number = {},
pages = {},
pmid = {40457025},
issn = {1474-1784},
abstract = {The gut microbiome has a critical role in shaping the patient's immune response and influencing the efficacy of anticancer immunotherapy. Emerging evidence suggests that modulating the gut microbiome through interventions such as faecal microbiota transplantation, probiotics, prebiotics and lifestyle modifications may enhance therapeutic outcomes. Consequently, drug development efforts in immuno-oncology have expanded to explore microbiome-based therapeutic strategies. In this Review, we examine the rationale for targeting the microbiome in cancer treatment, highlighting key advances in clinical microbiome characterization and their implications for immunotherapy. We discuss findings from recent clinical trials evaluating microbiome-based interventions and address the challenges associated with translating these approaches into clinical practice. Finally, we outline future directions for the development and integration of microbiome-targeted therapies in oncology, with a focus on optimizing efficacy, safety and patient stratification strategies.},
}

@article {pmid40456559,
year = {2025},
author = {Hu, Y and Wang, Y and Gao, H and Yang, G and Xie, J and He, Z and Lv, S and Gu, F and Huang, C and Hu, W},
title = {Piperine Improves DSS-Induced Colitis in Mice via Inhibition of Inflammation and Modulation of Gut Microbiota.},
journal = {Phytotherapy research : PTR},
volume = {},
number = {},
pages = {},
doi = {10.1002/ptr.8491},
pmid = {40456559},
issn = {1099-1573},
support = {ZDYF2024XDNY177//Hainan Province Science and Technology Special Fund/ ; 2023YFD1600200//National Key Research and Development Program of China/ ; 1630012025119//China Central Public-Interest Scientific Institution Basal Research Fund/ ; },
abstract = {Inflammatory bowel disease (IBD) is a global health concern with limited therapeutic options. Previous studies have demonstrated that piperine exhibited anti-inflammatory effects both in vitro and in vivo. However, its potential to ameliorate colitis in mice through modulation of gut microbiota has not been explored. This study aimed to investigate the role of gut microbiota in the protective effects of piperine against colitis using a dextran sulfate sodium (DSS)-induced mouse model. Mice were administered piperine (12.5 and 25 mg/kg) prior to DSS exposure. Fecal microbiota transplantation (FMT) was then performed, after which we evaluated colitis symptoms, inflammation levels, and intestinal barrier function. Subsequently, 16S rDNA-based high-throughput sequencing was employed to analyze the microbial composition of the mouse cecal contents. Piperine administration increased the colon length, decreased the spleen index, and improved colon histopathology. Furthermore, piperine modulated inflammatory responses by inhibiting NF-κB signaling, thereby reducing the release of pro-inflammatory cytokines and mediators. It also enhanced intestinal barrier integrity by increasing the expression of claudin-1, claudin-3, ZO-1, occludin, and mucin 2. Notably, the 16S rDNA sequencing results revealed that piperine increased the abundance of Dubosiella in the gut. Piperine effectively protected mice from DSS-induced colitis, suppressed inflammation, and improved poor intestinal barrier function. It reshaped the intestinal microbiota, ultimately alleviating DSS-induced colitis in mice. Our research highlighted the significant role of gut microbiota in the piperine-mediated alleviation of intestinal damage and suggested its therapeutic potential for promoting gut health and reducing the risk of colitis.},
}

@article {pmid40455241,
year = {2025},
author = {Yi, LT and Wang, XY and Zhou, L and Cheng, J and Xu, GH and Zhu, JX},
title = {Polysaccharides from Black Mulberry Attenuate Colitis through Gut Microbiota Mediated TNF-α/pNF-κB/ICAM-1 Signaling Pathway.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c01870},
pmid = {40455241},
issn = {1520-5118},
abstract = {Colitis is characterized by immune dysregulation and gut microbiota imbalance. This study investigates the therapeutic effects of polysaccharides from black mulberry (PBM) on dextran sulfate sodium-induced colitis in mice. PBM administration significantly alleviated colitis symptoms, including body weight loss, histological damage, and inflammation, while enhancing antioxidant capacity and strengthening tight junction protein expression. PBM modulated gut microbiota composition, notably increasing Weissella spp., which correlated with elevated short-chain fatty acids (SCFAs) and decreased pro-inflammatory markers. Colonic RNA sequencing revealed the role of PBM in attenuating colitis via the TNF-α/NF-κB/ICAM-1 signaling pathway. Fecal microbiota transplantation (FMT) from PBM-treated mice confirmed that microbiota modulation from PBM contributed to these therapeutic effects. These findings suggest PBM as a natural therapeutic agent for colitis, offering a multifaceted approach to restoring gut homeostasis through microbiota modulation and inflammatory pathway regulation. This study provides new insights into dietary polysaccharides as potential adjunctive therapies for colitis.},
}

@article {pmid40454811,
year = {2025},
author = {Millard, SA and Vendrov, KC and Young, VB and Seekatz, AM},
title = {Host origin of microbiota drives functional recovery and Clostridioides difficile clearance in mice.},
journal = {mBio},
volume = {},
number = {},
pages = {e0110825},
doi = {10.1128/mbio.01108-25},
pmid = {40454811},
issn = {2150-7511},
abstract = {UNLABELLED: Colonization resistance provided by the gut microbiota is essential for resisting both initial Clostridioides difficile infection (CDI) and potential recurrent infection (rCDI). Although fecal microbiota transplantation (FMT) has been successful in treating rCDI by restoring microbial composition and function, mechanisms underlying the efficacy of standardized stool-derived products remain poorly understood. Using a combination of 16S rRNA gene-based and metagenomic sequencing alongside metabolomics, we investigated microbiome recovery following FMT from human and murine donor sources in a mouse model of rCDI. We found that a human-derived microbiota was less effective in clearing C. difficile compared to a mouse-derived microbiota, despite recovery of taxonomic diversity, compositional changes, and bacterial functions typically associated with clearance. Metabolomic analysis revealed deficits in secondary metabolites compared to those that received murine FMT, suggesting a functional remodeling between human microbes in their new host environment. Collectively, our data revealed additional environmental, ecological, or host factors to consider in FMT-based recovery from rCDI.

IMPORTANCE: Clostridioides difficile is a significant healthcare-associated pathogen, with recurrent infections presenting a major treatment challenge due to further disruption of the microbiota after antibiotic administration. Despite the success of fecal microbiota transplantation (FMT) for the treatment of recurrent infection, the mechanisms mediating its efficacy remain underexplored. This study reveals that the effectiveness of FMT may be compromised by a mismatch between donor microbes and the recipient environment, leading to deficits in key microbial metabolites. These findings highlight additional factors to consider when assessing the efficacy of microbial-based therapeutics for C. difficile infection (CDI) and other conditions.},
}

@article {pmid40454495,
year = {2025},
author = {Bjørklund, G and Butnariu, M and Dadar, M and Semenova, Y},
title = {The Gut Microbiota-anxiety Connection: Evidence, Mechanisms, and Therapeutic Strategies.},
journal = {Current medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0109298673356125250409182218},
pmid = {40454495},
issn = {1875-533X},
abstract = {The gut-brain axis (GBA), a bidirectional communication system between the gut and the brain, has emerged as a critical player in mental health. The interest in the connection between anxiety disorders (AD) and the gut microbiota is growing. This paper provides an overview of gut microbiota's role in dysregulation in anxiety, including alterations in gut microbiota (dysbiosis), leaky gut, metabolic endotoxemia, and the effect of antipsychotic medications. The mechanisms underlying the gut microbiota-anxiety (GMA) connection, such as neurotransmitter production, immune dysregulation, and GBA communication, are discussed. Furthermore, the paper explores gut microbiota- based therapeutic strategies, including probiotics, prebiotics, symbiotics, fecal microbiota transplantation, and dietary interventions, as potential approaches for anxiety management. This research field's clinical implications and future directions are also examined, underscoring that more studies are needed on gut microbiota's role in anxiety disorders. The conclusion highlights the importance of this ongoing research and the potential for personalized therapeutic interventions, instilling hope and optimism for the future of anxiety management and providing reassurance about the potential for personalized therapeutic interventions in this field.},
}

@article {pmid40454186,
year = {2025},
author = {Sharma, VK},
title = {Diabetes-induced depression: unravelling the role of gut dysbiosis.},
journal = {Journal of diabetes and metabolic disorders},
volume = {24},
number = {1},
pages = {129},
pmid = {40454186},
issn = {2251-6581},
abstract = {Depression is a prevalent yet often underdiagnosed neuropsychiatric comorbidity of type 2 diabetes mellitus (T2DM), significantly complicating disease management, treatment adherence, and overall well-being. Emerging evidence suggests that gut microbiota dysbiosis plays a pivotal role in linking T2DM and depression through mechanisms such as epithelial barrier dysfunction, systemic inflammation, neurotransmitter imbalances, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and impaired neurogenesis. This review aims to explore the mechanistic pathways through which diabetes-induced dysbiosis contributes to depression and to appraise the therapeutic potential of microbiota-targeted interventions, including probiotics, prebiotics, and fecal microbiota transplantation, in mitigating depressive symptoms and improving metabolic outcomes. Understanding this gut-brain interplay may provide novel insights into therapeutic strategies for managing the dual burden of diabetes and depression.},
}

@article {pmid40448308,
year = {2025},
author = {Gu, BH and Jung, HY and Rim, CY and Kim, TY and Lee, SJ and Choi, DY and Park, HK and Kim, M},
title = {Comparative Colonisation Ability of Human Faecal Microbiome Transplantation Strategies in Murine Models.},
journal = {Microbial biotechnology},
volume = {18},
number = {6},
pages = {e70173},
pmid = {40448308},
issn = {1751-7915},
support = {2024-ER2113-00//the Korea National Institute of Health (KNIH) research project/ ; 20019505//the Ministry of Trade, Industry & Energy (MOTIE, Korea)/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; Humans ; Mice ; *Gastrointestinal Microbiome ; *Feces/microbiology ; Disease Models, Animal ; *Bacteria/classification/growth & development/isolation & purification/genetics ; Dysbiosis/therapy/microbiology ; Male ; Models, Animal ; },
abstract = {The gut microbiome plays a crucial role in maintaining intestinal homeostasis and influencing immune-mediated diseases. Human faecal microbiota transplantation (FMT) is often employed in murine models to investigate the role of human microbes in disease regulation, but methods for effective colonisation require refinement. This study aimed to assess the colonisation efficiency of human microbiota in a murine model using FMT with human faeces, focusing particularly on the impact of gut microbiota depletion via polyethylene glycol (PEG) and comparing oral-gastric gavage with enema administration routes. Our findings revealed that PEG-induced depletion enhanced human microbiome colonisation in mice. Oral-gastric gavage prolonged colonisation, while enema administration facilitated quicker resolution of dysbiosis, both inducing selective human microbial colonisation in a time-dependent manner. Notably, genera such as Bacteroides, Blautia, Medicaternibacter and Bifidobacteria were successfully colonised, whereas Roseburia, Anaerostipes, Anaerobutyricum and Faecalibacterium failed to establish in the murine gut post-FMT. These findings highlight the challenges of replicating human gut microbiota in murine models and underscore the importance of selecting appropriate FMT methods based on desired outcomes. This study provides valuable insights into the colonisation dynamics of human microbiota in mice, contributing to the development of more effective FMT strategies for disease treatment.},
}

Animals
*Fecal Microbiota Transplantation/methods
Humans
Mice
*Gastrointestinal Microbiome
*Feces/microbiology
Disease Models, Animal
*Bacteria/classification/growth & development/isolation & purification/genetics
Dysbiosis/therapy/microbiology
Male
Models, Animal

@article {pmid40448218,
year = {2025},
author = {Gao, ZK and Fan, CY and Zhang, BW and Geng, JX and Han, X and Xu, DQ and Arshad, M and Sun, HX and Li, JY and Jin, X and Mu, XQ},
title = {Cardiac function of colorectal cancer mice is remotely controlled by gut microbiota: regulating serum metabolites and myocardial cytokines.},
journal = {Animal microbiome},
volume = {7},
number = {1},
pages = {53},
pmid = {40448218},
issn = {2524-4671},
support = {NSFC81903631//The National Natural Science Foundation of China/ ; },
abstract = {Several studies have indicated that the dysregulation of microbial metabolites and the inflammatory environment resulting from microbial dysbiosis may contribute to the occurrence and progression of cardiovascular diseases. Therefore, restoring the disordered gut microbiota in patients with colorectal cancer by fecal microbiota transplantation (FMT) has the potential to reduce the incidence of cardiac disease. In this study, we identified cardiac dysfunction in azomethane and dextran sodium sulfate-induced colorectal cancer mice. Intestinal microbes from healthy mice were transferred to colorectal cancer mice, which vastly reversed the disorder of the gut microbiota and effectively alleviated cardiac dysfunction. Moreover, FMT regulated the expression of serum metabolites such as uridine triphosphate (UTP), tiamulin, andrographolide, and N-Acetyl-D-glucosamine, as well as cytokines like TGF-β, IRF5, and β-MHC in the heart. These findings uncover that the disturbed gut microbiota causes cardiac dysfunction in colorectal cancer mice by modulating the expression of serum metabolites and cytokines, which could be alleviated by treatment with FMT.},
}

@article {pmid39752608,
year = {2025},
author = {Holtan, SG and Bolaños-Meade, J and Al Malki, MM and Wu, J and Kitko, CL and Reshef, R and Rezvani, AR and Shaffer, BC and Solh, MM and Yao, JM and Runaas, L and Elmariah, H and Larkin, KT and El Jurdi, N and Gooptu, M and Loren, AW and Hall, AC and Alousi, AM and Jamy, O and Clark, W and Kean, L and Bhatt, AS and Perales, MA and Applegate, K and Efebera, YA and Leifer, E and Jones, RJ and Horowitz, MM and Mattila, D and Saber, W and Hamadani, M and Martens, MJ},
title = {Improved Patient-Reported Outcomes With Post-Transplant Cyclophosphamide: A Quality-of-Life Evaluation and 2-Year Outcomes of BMT CTN 1703.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {43},
number = {8},
pages = {912-918},
pmid = {39752608},
issn = {1527-7755},
support = {U10 HL069294/HL/NHLBI NIH HHS/United States ; U24 CA076518/CA/NCI NIH HHS/United States ; U24 HL138660/HL/NHLBI NIH HHS/United States ; UG1 HL138645/HL/NHLBI NIH HHS/United States ; },
mesh = {Humans ; *Cyclophosphamide/therapeutic use/administration & dosage/adverse effects ; *Patient Reported Outcome Measures ; *Graft vs Host Disease/prevention & control ; *Quality of Life ; *Bone Marrow Transplantation/adverse effects ; Female ; Male ; Middle Aged ; Adult ; *Immunosuppressive Agents/therapeutic use ; Methotrexate/administration & dosage/therapeutic use ; Tacrolimus/administration & dosage/therapeutic use ; Mycophenolic Acid/administration & dosage/therapeutic use/analogs & derivatives ; Aged ; Treatment Outcome ; },
abstract = {The BMT CTN 1703 phase III trial confirmed that graft-versus-host disease (GVHD) prophylaxis with post-transplantation cyclophosphamide (PTCy), tacrolimus (Tac), and mycophenolate mofetil (MMF) results in superior GVHD-free, relapse-free survival (GRFS) compared with Tac/methotrexate (MTX) prophylaxis. This companion study assesses the effect of these regimens on patient-reported outcomes (PROs). Using the Lee Chronic GVHD Symptom Score and PROMIS subscales (physical function, GI symptoms, social role satisfaction) as primary end points and hemorrhagic cystitis symptoms and Lee subscales as secondary end points, responses from English and Spanish speakers were analyzed at baseline and days 100, 180, and 365 after transplant. PRO scores were compared between the arms using inverse probability weighted-independent estimating equation models. The PTCy arm had significantly lower scores on the Lee Chronic GVHD Symptom Scale (P = .01), indicating lower GVHD symptom burden. Lee Scale nutrition and mouth subscores were also better in the PTCy arm compared with the Tac/MTX arm (P < .01 for both). Older participants (age >65 years) reported better Lee Scale psychological subscores than younger participants (P = .003). No significant differences were identified in hemorrhagic cystitis or in the PROMIS subscales between treatment arms. The updated clinical end points at 2 years for the parent trial confirmed that PTCy/Tac/MMF maintained a significant advantage over Tac/MTX in GRFS (42.4% v 28.8%, P = .001). In addition to improved GRFS, patients randomly assigned to the PTCy arm reported lower symptom burden during the first year after transplant.},
}

Humans
*Cyclophosphamide/therapeutic use/administration & dosage/adverse effects
*Patient Reported Outcome Measures
*Graft vs Host Disease/prevention & control
*Quality of Life
*Bone Marrow Transplantation/adverse effects
Female
Male
Middle Aged
Adult
*Immunosuppressive Agents/therapeutic use
Methotrexate/administration & dosage/therapeutic use
Tacrolimus/administration & dosage/therapeutic use
Mycophenolic Acid/administration & dosage/therapeutic use/analogs & derivatives
Aged
Treatment Outcome

@article {pmid40447159,
year = {2025},
author = {Jeong, SH and Vasavada, SP and Lashner, B and Werneburg, GT},
title = {Fecal microbiota transplant is associated with resolution of recurrent urinary tract infection.},
journal = {Urology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.urology.2025.05.052},
pmid = {40447159},
issn = {1527-9995},
abstract = {OBJECTIVE: To investigate the association of fecal microbiota transplant (FMT) therapy, an effective treatment for recurrent C. difficile colitis, with resolution of recurrent UTI (rUTI).

METHODS: A prospectively accrued database of patients who underwent FMT for recurrent Clostridoides difficile colitis was retrospectively reviewed for individuals with rUTI in the two years prior to FMT. Recurrent UTI status (defined as two UTI episodes in six months or three UTI episodes in one year) and UTI frequency in the two years prior to the FMT were compared to those in the two year follow up period after FMT using the two-tailed Wilcoxin matched pairs signed rank test. A p-value <0.05 was considered statistically significant.

RESULTS: Of 11 patients who had rUTI in the two years preceding FMT, no patient had rUTI over the follow up period following FMT (p=0.001). The average number of UTIs in the two years prior to FMT was 3.7 (range 2-6), and the average number of UTIs in the follow up period was 0.27 (range 0-1) (p=0.001). The Kaplan-Meier estimate, the median time to UTI recurrence, was 19.6 months (95% CI: 15.2 - 23.9). There was no marked difference in antibiotic susceptibility profiles before and after FMT.

CONCLUSIONS: FMT was associated with resolution of rUTI and reduction in UTI frequency in this cohort. The results of this study support the hypothesis that modulation of the gut microbiome may reduce rUTI risk, and support a clinical trial to further assess the safety and efficacy of FMT for rUTI.},
}

@article {pmid40446472,
year = {2025},
author = {Chen, L and Ahmad, M and Li, J and Li, J and Yang, Z and Hu, C},
title = {Gut microbiota manipulation to mitigate the toxicities of environmental pollutants.},
journal = {Aquatic toxicology (Amsterdam, Netherlands)},
volume = {285},
number = {},
pages = {107425},
doi = {10.1016/j.aquatox.2025.107425},
pmid = {40446472},
issn = {1879-1514},
abstract = {The gut microbiome, commonly termed as a "super organ", plays a crucial role in the modulation of various biological functions associated with metabolism, endocrinology, immunology, and neurology. However, gut microbiome is extremely susceptible to the risks of environmental pollutants, which will drive gut microbial community to dysbiosis. Simultaneously, restoring healthy gut microbiome can protect the hosts from the health hazards of pollutants. It is increasingly verified that probiotics, prebiotics, and fecal microbiota transplantation (FMT) are efficacious measures to manipulate and remediate gut microecosystem. Among various probiotic strains, lactic acid bacteria are the most extensively applied in toxicity mitigation, which is characterized by shaping gut microbiota structure and metabolism, increasing gut epithelial barrier integrity, promoting fecal elimination of pollutants, suppressing inflammation symptoms, and then improving host systemic physiology. Prebiotics are dietary fibers that cannot be digested by the host, but can be fermented by specific gut bacteria to produce short chain fatty acids, which are identified as the key effect molecules in the manifestation of prebiotic toxicity mitigation actions. In addition, by transplanting the entire community of healthy gut microbiota, FMT also shows effective performances in counteracting the adverse effects of environmental pollutants and recovering host animal health. Intriguingly, FMT from young donors is even found to inhibit the toxic disturbances in healthy aging progression. Based on current evidence, this review summarized the findings about using probiotics, prebiotics, and FMT to manipulate gut microbiota and alleviate the health impairment of environmental pollutants. Key mechanistic insights into the interactive behaviors were underlined. Furthermore, the challenges and future directions in harnessing gut microbiota manipulation as a novel therapeutic approach to mitigate pollutant-induced toxicities were postulated. This review is expected to advocate comprehensive scientific research and literally favor the application of health intervention strategies.},
}

@article {pmid40446358,
year = {2025},
author = {Porcari, S and Ng, SC and Zitvogel, L and Sokol, H and Weersma, RK and Elinav, E and Gasbarrini, A and Cammarota, G and Tilg, H and Ianiro, G},
title = {The microbiome for clinicians.},
journal = {Cell},
volume = {188},
number = {11},
pages = {2836-2844},
doi = {10.1016/j.cell.2025.04.016},
pmid = {40446358},
issn = {1097-4172},
mesh = {Humans ; *Microbiota ; Clinical Trials as Topic ; },
abstract = {Despite promising evidence in diagnostics and therapeutics, microbiome research is not yet implemented into clinical medicine. Several initiatives, including the standardization of microbiome research, the refinement of microbiome clinical trial design, and the development of communication between microbiome researchers and clinicians, are crucial to move microbiome science toward clinical practice.},
}

Humans
*Microbiota
Clinical Trials as Topic

@article {pmid40444969,
year = {2025},
author = {Xie, J and Kim, T and Liu, Z and Panier, H and Bokoliya, S and Xu, M and Zhou, Y},
title = {Young gut microbiota transplantation improves the metabolic health of old mice.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0160124},
doi = {10.1128/msystems.01601-24},
pmid = {40444969},
issn = {2379-5077},
abstract = {UNLABELLED: The gut microbiota evolves over a lifetime and significantly impacts the aging process. Targeting the gut microbiota represents a novel avenue to delay aging and aging-related physical and mental decline. However, the underlying mechanism by which the microbiota modulates the aging process, particularly age-related physical and behavioral changes is not completely understood. We conducted fecal microbiota transplantation (FMT) from young or old male donor mice to the old male recipients. Old recipients with young microbiota had a higher alpha diversity than the old recipients with old microbiota. Compared to FMT with old microbiota, FMT with young microbiota reduced body weight and prevented fat accumulation in the old recipients. FMT with young microbiota also lowered frailty, increased grip strength, and alleviated depression and anxiety-like behavior in the old recipients. Consistent with observed physical changes, untargeted metabolomic analysis of serum and stools revealed that FMT with young microbiota lowered age-related long-chain fatty acid levels and increased amino acid levels in the old recipients. Bulk RNAseq analysis of the amygdala of the brain showed that FMT with young microbiota downregulated inflammatory pathways and upregulated oxidative phosphorylation in the old recipients. Our results demonstrate that FMT with young microbiota has substantial positive influences on age-related body composition, frailty, and psychological behaviors. These effects are associated with changes in host lipid and amino acid metabolism in the periphery and transcriptional regulation of neuroinflammation and energy utilization in the brain.

IMPORTANCE: The gut microbiome is a key hallmark of aging. Fecal microbiota transplantation (FMT) using young microbiota represents a novel rejuvenation strategy to delay aging. Our study provides compelling evidence that transplanting microbiota from young mice significantly improved grip strength, frailty, and body composition in aged recipient mice. At the molecular level, FMT improved aging-related metabolic markers in the gut and circulation. Additionally, FMT from young microbiota rejuvenated the amygdala of the aged brain by downregulating inflammatory pathways. This study highlights the importance of metabolic reprogramming via young microbiota FMT in improving physical and metabolic health in elderly recipients.},
}

@article {pmid40443229,
year = {2025},
author = {Lee, MA and Slead, T and Suchodolski, J and Tolbert, MK and Marsilio, S},
title = {Adverse events after fecal microbiota transplantation in nine cats: a case series.},
journal = {Journal of feline medicine and surgery},
volume = {27},
number = {5},
pages = {1098612X251337274},
doi = {10.1177/1098612X251337274},
pmid = {40443229},
issn = {1532-2750},
mesh = {Animals ; Cats ; *Cat Diseases/therapy ; *Fecal Microbiota Transplantation/veterinary/adverse effects ; Female ; Male ; Diarrhea/veterinary/therapy ; },
abstract = {This case series describes nine cases of fecal microbiota transplantation in cats and associated adverse events (AEs) from two tertiary referral hospitals. AEs were graded according to criteria established by the Veterinary Cooperative Oncology Group's Common Terminology Criteria for Adverse Events (VCOG-CTCAE v2) for clinical trials. Cats received 5-6 g/kg donor feces 2-6 times for chronic enteropathy (n = 4) or therapy-resistant diarrhea (n = 5). AEs included lethargy (n = 7), vomiting (n = 5), diarrhea (n = 5), weight loss (n = 5), inappetence (n = 5), dehydration (n = 5), abdominal pain (n = 2), gastroenterocolitis based on ultrasound (n = 2) and anorexia (n = 1). Temperatures of up to 103.4°F were noted but did not meet the criteria for AEs (>103.5°F). Cats responded to antimicrobials (metronidazole, marbofloxacin), anthelmintics (fenbendazole), supportive care with fluids, ondansetron and mirtazapine (n = 5), gabapentin (n = 2), pradofloxacin (n = 1) or self-resolved (n = 1). Positive response to fecal microbiota transplantation for the presenting complaint was seen in eight cats (seven complete, one partial and transient).Relevance and novel informationFecal microbiota transplantation is increasing in usage among companion animals. Fecal microbiota transplantations in cats have been rarely described in the literature as have AEs after administration. This case series represents the first description of AEs after fecal microbiota transplantation in cats.},
}

Animals
Cats
*Cat Diseases/therapy
*Fecal Microbiota Transplantation/veterinary/adverse effects
Female
Male
Diarrhea/veterinary/therapy

@article {pmid40443227,
year = {2025},
author = {Green, GBH and Cox-Holmes, AN and Marlow, GH and Potier, ACE and Wang, Y and Zhou, L and Chen, D and Morrow, CD and McFarland, BC},
title = {Human microbiota influence the immune cell composition and gene expression in the tumor environment of a murine model of glioma.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2508432},
doi = {10.1080/19490976.2025.2508432},
pmid = {40443227},
issn = {1949-0984},
mesh = {Animals ; *Glioma/immunology/microbiology/genetics ; Mice ; Humans ; *Gastrointestinal Microbiome/immunology ; Disease Models, Animal ; *Tumor Microenvironment/immunology/genetics ; *Brain Neoplasms/immunology/microbiology/genetics ; Cell Line, Tumor ; Feces/microbiology ; Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology ; RNA, Ribosomal, 16S/genetics ; Bacteria/classification/genetics/isolation & purification ; Mice, Inbred C57BL ; },
abstract = {BACKGROUND: Immunotherapy has shown success against other cancers but not glioblastoma. Previous data has revealed that microbiota influences anti-PD-1 efficacy. We have previously found that, when using gnotobiotic mice transplanted with human fecal microbiota, the gut microbial composition influenced the response to anti-PD-1 in a mouse model of glioma. However, the role of the human microbiota in influencing the mouse immune cells in the glioma microenvironment and anti-PD-1 response was largely unknown. Using two distinct humanized microbiome (HuM) lines, we used single-cell RNA sequencing (scRNA-seq) to determine how gut microbiota affect immune infiltration and gene expression in a murine glioma model.

METHODS: 16S rRNA sequencing was performed on fecal samples from HuM1 (H1) and HuM2 (H2) mice. Mice were intracranially injected with murine glioma cells (GL261), and on day 13 treated with one dose of isotype control or anti-PD1. Mice were euthanized on day 14 for analysis of all immune cells in the tumors by scRNA-seq.

RESULTS: HuM1 and HuM2 mice had different microbial populations, with HuM1 being primarily dominated via Alistipes, and HuM2 being primarily composed of Odoribacter. Sc-RNA-seq of the tumor immune cells revealed 21 clusters with significant differences between H1 and H2 samples with a larger population of M1 type macrophages in H1 samples. Gene expression analysis revealed higher expression of inflammatory markers in the M1 population in H2 mice treated with anti-PD-1.

CONCLUSIONS: Microbial gut communities influence the presence and gene activation patterns of immune cells in the brain tumors of mice both under control (isotype) and following anti-PD-1 treatment.},
}

Animals
*Glioma/immunology/microbiology/genetics
Mice
Humans
*Gastrointestinal Microbiome/immunology
Disease Models, Animal
*Tumor Microenvironment/immunology/genetics
*Brain Neoplasms/immunology/microbiology/genetics
Cell Line, Tumor
Feces/microbiology
Programmed Cell Death 1 Receptor/antagonists & inhibitors/immunology
RNA, Ribosomal, 16S/genetics
Bacteria/classification/genetics/isolation & purification
Mice, Inbred C57BL

@article {pmid40441587,
year = {2025},
author = {Luo, M and Du, Y and Liu, X and Zhang, S and Zhu, W and Liu, K and Ren, X and Zhang, N},
title = {Fecal Microbiota Transplantation Alleviates Cirrhotic Portal Hypertension in Rats via Butyrate-Mediated HDAC3 Inhibition and PI3K/Akt/eNOS Signaling Regulation.},
journal = {European journal of pharmacology},
volume = {},
number = {},
pages = {177781},
doi = {10.1016/j.ejphar.2025.177781},
pmid = {40441587},
issn = {1879-0712},
abstract = {BACKGROUND: Portal hypertension (PHT) is a severe complication of liver cirrhosis, with limited therapeutic options. Despite emerging evidence linking gut microbiota dysbiosis to PHT progression, the mechanisms by which microbial metabolites modulate liver sinusoidal endothelial cells (LSECs) dysfunction and the therapeutic efficacy of fecal microbiota transplantation (FMT) remain poorly understood. This study investigated the potential of FMT to alleviate PHT in cirrhotic rats, exploring the underlying mechanisms involving butyrate-mediated HDAC3 inhibition and PI3K/Akt/eNOS signaling regulation in LSECs.

METHODS: Cirrhosis with PHT was induced in Sprague-Dawley rats via intraperitoneal carbon tetrachloride injection, followed by FMT or butyrate supplementation via oral gavage. Analyses included portal hemodynamic measurements, gut microbiota sequencing, serum SCFA metabolomics profiling, HDAC3 activity assays, NO level quantification, and assessments of liver fibrosis, liver function, and LSEC ultrastructure. LSECs were isolated for PI3K/Akt/eNOS signaling analysis via qRT-PCR, Western blotting, and immunofluorescence staining.

RESULTS: A two-week FMT intervention in cirrhotic rats with PHT enriched butyrate-producing bacteria and increased serum butyrate levels, which were associated with reduced portal pressure and intrahepatic vascular resistance, without affecting liver fibrosis, function, or LSEC ultrastructure. FMT reduced HDAC3 activity by 2.17-fold and increased Akt and eNOS phosphorylation in primary LSECs by 1.69-fold and 1.25-fold, respectively, elevating plasma NO levels by 1.66-fold compared to untreated controls. In vitro experiments with primary LSECs confirmed these butyrate-mediated effects.

CONCLUSION: FMT alleviates cirrhotic PHT through butyrate-mediated HDAC3 inhibition and subsequent PI3K/Akt/eNOS signaling activation in LSECs, highlighting the therapeutic potential of targeting the gut-liver axis via microbial metabolites for PHT management.},
}

@article {pmid40441086,
year = {2025},
author = {Sharma, P and Das, S and Rituraj, R and Bhagyashree, B},
title = {Understanding oncobiosis in ovarian cancer: Emerging concepts in tumor progression.},
journal = {Pathology, research and practice},
volume = {271},
number = {},
pages = {156026},
doi = {10.1016/j.prp.2025.156026},
pmid = {40441086},
issn = {1618-0631},
abstract = {Ovarian cancer is a leading cause of gynecologic cancer mortality and has recently been linked to microbial dysbiosis or oncobiosis. Tumorigenesis is a highly complex process, and recent research has revealed numerous new mechanisms showing how tumors interact with their surrounding microenvironment. The inclusion of microbiome studies has significantly advanced this field revealing the important role microbes play, not only in maintaining normal physiological functions of the human body but also in influencing oncogenic pathways. This expanding knowledge is deepening our understanding of tumor pathophysiology and is helping to create new diagnostic, prognostic, therapeutic and preventive strategies for specific cancers. This review explores the role of the microbiome in ovarian carcinogenesis, focusing on its interaction with the tumor microenvironment (TME) and its influence on inflammation, immune regulation and metabolic signaling. This review studied dysbiosis in several anatomical compartments such as the gut, oral cavity, lower and upper genital tracts and ovarian tissues, in relation to ovarian oncobiosis. Emerging clinical implications of these studies include the use of microbial profiles as diagnostic or prognostic biomarkers. Therapeutic strategies such as fecal microbiota transplantation and probiotics are also discussed for their ability to restore microbial balance and enhance treatment efficacy. This review highlights the importance of continued research to explore causal relationships between the microbiome and tumorigenesis, positioning microbiome studies as promising tools in ovarian cancer management and improving patient care.},
}

@article {pmid40438840,
year = {2025},
author = {Saleem, MM and Masood, S and Rahmatullah, MM and Ayesha Imdad, I and Mohammed Aslam Sange, A and Nasr, D},
title = {Gut Microbiota Dysbiosis and Its Role in the Development of Irritable Bowel Syndrome.},
journal = {Cureus},
volume = {17},
number = {4},
pages = {e83084},
pmid = {40438840},
issn = {2168-8184},
abstract = {The gut microbiota refers to the diverse community of symbiotic and pathogenic microorganisms inhabiting the host digestive tract. This microbiome plays a vital role in maintaining the integrity of the digestive system. Irritable bowel syndrome (IBS) is a functional gastrointestinal disorder (FGID) characterized by chronic abdominal pain and altered bowel habits. Although the pathophysiology of IBS remains unclear, recent studies suggest that the disruption of the gut microbiota (dysbiosis) may play a significant role. This study aims to examine the role of the gut microbiota in the development of IBS, analyze factors influencing the gut microbiome, and explore the potential for microbiota-targeted therapies. Relevant literature published from 2014 until 2024 was sourced from Google Scholar, PubMed, and Scopus using the keywords "microbiome", "irritable bowel syndrome", "dysbiosis", "faecal transplantation", and "probiotics". This review revealed consistent evidence of gut microbiota dysbiosis in individuals with IBS, characterized by altered microbial diversity, composition, and metabolic function. Contributing factors included a reduced abundance of beneficial commensals, overgrowth of potentially pathogenic species, and disrupted host-microbiota interactions. This dysbiosis was also frequently associated with symptom severity and specific IBS subtypes. Emerging evidence further highlights the role of diet, stress, and genetic factors in modulating gut microbiota and influencing IBS development. The growing body of research supports a strong link between dysbiosis and the pathogenesis and symptomatology of IBS. Understanding the microbial underpinnings of IBS opens avenues for potential diagnostic biomarkers and innovative therapeutic interventions aimed at restoring a balanced gut microbiota. However, further research is needed to elucidate the underlying mechanisms and translate these insights into effective clinical strategies for the management of IBS. This review underscores the significance of gut microbiota in IBS and its potential as a target for future therapeutic interventions.},
}

@article {pmid40438215,
year = {2025},
author = {Hanna, A and Abbas, H and Yassine, F and AlBush, A and Bilen, M},
title = {Systematic review of gut microbiota composition, metabolic alterations, and the effects of treatments on PCOS and gut microbiota across human and animal studies.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1549499},
pmid = {40438215},
issn = {1664-302X},
abstract = {INTRODUCTION: Polycystic ovary syndrome (PCOS) is an endocrine disorder affecting around 12% of women globally, associated with infertility and various comorbidities. Emerging evidence suggests a crucial role of gut microbiota in PCOS pathophysiology, prompting research to investigate alterations in gut microbial composition in patients with PCOS.

METHODS: This systematic review aims to analyze human and animal studies that compare gut microbiota composition, gut-derived metabolites, and treatment interventions in PCOS patients versus healthy controls. A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science, yielding studies examining gut microbiota, metabolomic shifts, and treatment responses in PCOS models and human populations.

RESULTS: Our analysis revealed decreases in alpha diversity in PCOS patients, with more pronounced changes in beta diversity in animal models. Specific bacterial taxa, such as Bacteroides vulgatus, Escherichia-Shigella and Lactobacillus, showed implication in PCOS pathogenesis, suggesting potential microbial markers. Furthermore, discrepancies between human and animal studies show the need for humanized mouse models to bridge this gap. Interventions like probiotics and fecal microbiota transplantation (FMT) showed varying levels of efficacy, with FMT emerging as a more promising but invasive option, offering live bacteriotherapy as a potential therapeutic alternative. Alterations in gut-derived metabolites, including short-chain fatty acids and bile acids, highlighted the multifaceted nature of PCOS, with implications extending to metabolic, hormonal, and gut-brain axis disruptions.

DISCUSSION: In conclusion, PCOS exhibits complex interactions between gut microbiota and metabolic pathways, necessitating further research with standardized methods and larger sample sizes to elucidate the microbiome's role in PCOS.},
}

@article {pmid40437401,
year = {2025},
author = {Unrug-Bielawska, K and Sandowska-Markiewicz, Z and Pyśniak, K and Piątkowska, M and Czarnowski, P and Goryca, K and Mróz, A and Żeber-Lubecka, N and Wójcik-Trechcińska, U and Bałabas, A and Dąbrowska, M and Surynt, P and Radkiewicz, M and Mikula, M and Ostrowski, J},
title = {Western Diet and fecal microbiota transplantation alter phenotypic, liver fatty acids, and gut metagenomics and metabolomics in Mtarc2 knockout mice.},
journal = {Genes & nutrition},
volume = {20},
number = {1},
pages = {13},
pmid = {40437401},
issn = {1555-8932},
support = {2018/29/B/NZ7/00809//Narodowe Centrum Nauki/ ; },
}

@article {pmid40436727,
year = {2025},
author = {Qingsong, L},
title = {Comment on "Alteration of gut microbial composition associated with the therapeutic efficacy of fecal microbiota transplantation in Clostridium difficile infection".},
journal = {Journal of the Formosan Medical Association = Taiwan yi zhi},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jfma.2025.05.033},
pmid = {40436727},
issn = {0929-6646},
}

@article {pmid40433559,
year = {2025},
author = {Zhang, J and Chen, K and Chen, F},
title = {Exploring the impact of the liver-intestine-brain axis on brain function in non-alcoholic fatty liver disease.},
journal = {Journal of pharmaceutical analysis},
volume = {15},
number = {5},
pages = {101077},
pmid = {40433559},
issn = {2214-0883},
abstract = {This study investigates the molecular complexities of non-alcoholic fatty liver disease (NAFLD)-induced brain dysfunction, with a focus on the liver-intestine-brain axis and potential therapeutic interventions. The main objectives include understanding critical microbiota shifts in NAFLD, exploring altered metabolites, and identifying key regulatory molecules influencing brain function. The methods employed encompassed 16S ribosomal RNA (rRNA) sequencing to scrutinize stool microbiota in NAFLD patients and healthy individuals, non-targeted metabolomics using LC-MS to uncover elevated levels of deoxycholic acid (DCA) in NAFLD mice, and single-cell RNA sequencing (scRNA-seq) to pinpoint the pivotal gene Hpgd in microglial cells and its downstream Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway. Behavioral changes and brain function were assessed in NAFLD mice with and without Fecal microbiota transplantation (FMT) treatment, utilizing various assays and analyses. The results revealed significant differences in microbiota composition, with increased levels of Bacteroides in NAFLD patients. Additionally, elevated DCA levels were observed in NAFLD mice, and FMT treatment demonstrated efficacy in ameliorating liver function and brain dysfunction. Hpgd inhibition by DCA activated the JAK2/STAT3 pathway in microglial cells, leading to inflammatory activation, inhibition of mitochondrial autophagy, induction of neuronal apoptosis, and reduction in neuronal action potentials. This study elucidates the intricate molecular mechanisms underlying the liver-gut-brain axis in NAFLD, and the identification of increased DCA and the impact of JAK2/STAT3 signaling on microglial cells highlight potential therapeutic targets for addressing NAFLD-induced brain dysfunction.},
}

@article {pmid40431274,
year = {2025},
author = {Schiavone, N and Isoldi, G and Calcagno, S and Rovida, E and Antiga, E and De Almeida, CV and Lulli, M},
title = {Exploring the Gut Microbiota-Retina Axis: Implications for Health and Disease.},
journal = {Microorganisms},
volume = {13},
number = {5},
pages = {},
doi = {10.3390/microorganisms13051101},
pmid = {40431274},
issn = {2076-2607},
abstract = {The gut microbiota represents a rich and adaptive microbial network inhabiting the gastrointestinal tract, performing key functions in nutrient processing, immune response modulation, intestinal wall protection, and microbial defense. Its composition remains highly personalized and responsive to external influences, including lifestyle patterns, physical activity, body composition, and nutritional intake. The interactions of the gut microbiota with bodily systems are conventionally interpreted as broad systemic impacts on organ balance. Yet, emerging research-exemplified by the gut microbiota-brain axis-suggests the potential existence of more targeted and direct communication mechanisms. Dysbiosis, characterized by microbial ecosystem disturbance, generates multiple metabolic compounds capable of entering systemic circulation and reaching distant tissues, notably including ocular structures. This microbial imbalance has been associated with both systemic and localized conditions linked to eye disorders. Accumulating scientific evidence now supports the concept of a gut-retina axis, underscoring the significant role of microbiota disruption in generating various retinal pathologies. This review comprehensively investigates gut microbiota composition, functional dynamics, and dysbiosis-induced alterations, with specific focus on retinal interactions in age-related macular degeneration, diabetic retinopathy, glaucoma, and retinal artery occlusion. Moreover, the review explores microbiota-targeted therapeutic strategies, including precision nutritional interventions and microbial transplantation, as potential modulators of retinal disease progression.},
}

@article {pmid40431196,
year = {2025},
author = {Harder, JW and Ma, J and Collins, J and Alard, P and Jala, VR and Bodduluri, H and Kosiewicz, MM},
title = {Characterization of Sex-Based Differences in Gut Microbiota That Correlate with Suppression of Lupus in Female BWF1 Mice.},
journal = {Microorganisms},
volume = {13},
number = {5},
pages = {},
doi = {10.3390/microorganisms13051023},
pmid = {40431196},
issn = {2076-2607},
support = {Target Identification in Lupus Grant//Alliance for Lupus Research/ ; R01AR067188/NH/NIH HHS/United States ; },
abstract = {Systemic lupus erythematosus (SLE) is more prevalent in female mice and humans and is associated with microbiota dysbiosis. We analyzed the fecal microbiota composition in female and male NZBxNZWF1 (BWF1) mice, a model of SLE, using 16S RNA gene sequencing. Composition of gut microbiota differed between adult disease-prone female (pre-disease) and disease-resistant male mice. Transfer of male cecal contents by gavage into female mice suppressed kidney disease (decreased proteinuria) and improved survival. After our mouse colony was moved to a new barrier facility with similar housing, male cecal transplants failed to suppress disease in female recipients. After two years, the protective phenotype reemerged: male cecal transplants once again suppressed disease in female mice. We compared the gut microbiota composition in female and male BWF1 mice for the three different periods, during which the male microbiota either protected or failed to protect female recipients. In female vs. male mice and in female mice receiving male cecal transplants, we found Bacteroides was high, Clostridium was low (high Bacteroides/Clostridium ratio), and Alistipes was present during periods when male cecal transplants suppressed disease. These data suggest that specific bacterial populations may have opposing effects on disease suppression in a model of microbiota transplantation.},
}

@article {pmid40431182,
year = {2025},
author = {Matsumoto, H and Gu, T and Yo, S and Sasahira, M and Monden, S and Ninomiya, T and Osawa, M and Handa, O and Umegaki, E and Shiotani, A},
title = {Fecal Microbiota Transplantation Using Donor Stool Obtained from Exercised Mice Suppresses Colonic Tumor Development Induced by Azoxymethane in High-Fat Diet-Induced Obese Mice.},
journal = {Microorganisms},
volume = {13},
number = {5},
pages = {},
doi = {10.3390/microorganisms13051009},
pmid = {40431182},
issn = {2076-2607},
support = {JP 19K11484//Japanese Grant-in-Aid Scientific Reserach/ ; },
abstract = {The gut microbiota plays an important role in the development of colorectal tumors. However, the underlying mechanisms remain unclear. In this study, we examined the effects of fecal microbiota transplantation (FMT) on azoxymethane (AOM)-induced colorectal tumors in obese mice. We divided the study subjects into the following five groups: high-fat diet (HFD), normal diet (ND), ND+exercise (Ex), HFD+FMT from ND-alone donor (HFD+FMT(ND alone)), and HFD+FMT from ND+Ex donor (HFD+FMT(ND+Ex)). The Ex group performed treadmill exercise for 15 weeks. Thereafter, fecal and colonic mucus samples were extracted for microbiome analysis. The deoxyribonucleic acid sample was collected from the feces and colonic mucosa, and V3-V4 amplicon sequencing analysis of the 16S rRNA gene was performed using MiSeq. The number of polyps was significantly lower in the ND (6.0 ± 1.6) and ND+Ex (1.8 ± 1.3) groups than in the HFD group (11.4 ± 1.5). The ND+Ex group had significantly fewer polyps than the ND group. The HFD+FMT(ND alone) (5.2 ± 0.8) and HFD+FMT(ND+Ex) (2.8 ± 2.6) groups also had significantly fewer polyps than the HFD group. The IL-15 mRNA levels in the colonic tissues were significantly higher in the HFD+FMT(ND alone) group than in the ND group. Fecal ω-muricholic acid concentrations were significantly higher in the HFD+FMT(ND alone) group than in the ND group and in the HFD+FMT(ND+Ex) group than in the ND+Ex group. The ND, ND+Ex, HFD+FMT(ND alone), and HFD+FMT(ND+Ex) groups had a significantly higher abundance of Lacyobacillaceae than the HFD group. In the FMT group, Erysipelotrichaceae and Tannerellaceae were significantly less abundant. Compared with the HFD group, the ND, ND+Ex, HFD+FMT(ND alone), and HFD+FMT(ND+Ex) groups had a significantly higher abundance of Muribaculaceae and a significantly higher abundance of Lactobacillaceae and Rikenellaceae in common among the ND and ND+Ex groups. The common and significantly less common species were Bacteroidaceae in the FMT group and Lactobacillaceae and Rikenellaceae in the ND alone and ND+Ex groups. Bacteroidaceae and Lachnospiraceae were significantly less common in the FMT group. We found that FMT inhibited AOM-induced colorectal tumorigenesis in obese mice. Furthermore, the fecal concentrations of short-chain fatty acids, bile acids, microbiota, and mucosa-associated microbiota differed between the FMT and diet/EX groups, suggesting that the inhibitory effect of FMT on colorectal tumorigenesis may be due to mechanisms different from those of ND alone and ND+Ex.},
}

@article {pmid40430481,
year = {2025},
author = {Zhou, Q and Yang, C and Jia, M and Qu, Q and Peng, X and Ren, W and Li, G and Xie, Y and Li, B and Shi, X},
title = {Gut Microbiota-Targeted Intervention of Hyperlipidemia Using Monascus-Fermented Ginseng.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {18},
number = {5},
pages = {},
doi = {10.3390/ph18050661},
pmid = {40430481},
issn = {1424-8247},
support = {82174093//National Natural Science Foundation of China/ ; },
abstract = {Background/Objectives: Hyperlipidemia (HLP) encompasses a spectrum of poorly understood lipid metabolism disorders that are frequently overlooked or misdiagnosed, potentially leading to multiple complications. While the gut microbiota has been implicated in HLP pathogenesis, the causal relationships and molecular mechanisms remain elusive. This study aimed to investigate the therapeutic mechanisms of Monascus-fermented ginseng (MFG) on HLP through gut microbiota modulation and explore treatment potential via fecal microbiota transplantation (FMT). Methods: The MFG-modulated gut microbiota was transplanted into HLP mice. Systemic evaluations, including serum biochemical parameter detection, histopathological section analysis, 16S rRNA sequencing, and fecal metabolomics, were conducted to assess therapeutic efficacy and identify associated metabolic pathways. Results: FMT significantly improved lipid profiles, reduced body weight, and attenuated hepatic lipid accumulation in HLP mice. Mechanistically, it enhanced cholesterol excretion and fatty acid β-oxidation while suppressing lipogenic regulators, concurrently promoting primary-to-secondary bile acid conversion. Gut microbiota analysis revealed that the MFG intervention effectively normalized the Firmicutes/Bacteroidetes ratio and enriched beneficial microbiota. Conclusions: These findings demonstrate FMT's therapeutic value in HLP management and provide new perspectives on utilizing fermented herbal medicines for metabolic disorders via gut microbiota reprogramming.},
}

@article {pmid40428769,
year = {2025},
author = {Datkhayeva, Z and Iskakova, A and Mireeva, A and Seitaliyeva, A and Skakova, R and Kulniyazova, G and Shayakhmetova, A and Koshkimbayeva, G and Sarmuldayeva, C and Nurseitova, L and Koshenova, L and Imanbekova, G and Maxutova, D and Yerkenova, S and Shukirbayeva, A and Pernebekova, U and Dushimova, Z and Amirkhanova, A},
title = {The Multifactorial Pathogenesis of Endometriosis: A Narrative Review Integrating Hormonal, Immune, and Microbiome Aspects.},
journal = {Medicina (Kaunas, Lithuania)},
volume = {61},
number = {5},
pages = {},
doi = {10.3390/medicina61050811},
pmid = {40428769},
issn = {1648-9144},
mesh = {Humans ; *Endometriosis/physiopathology/microbiology/immunology/etiology ; Female ; *Gastrointestinal Microbiome/physiology/immunology ; Estrogens/metabolism ; Dysbiosis/complications ; Inflammation ; },
abstract = {Endometriosis (EM) is a common estrogen-dependent chronic inflammatory disorder affecting reproductive-aged women, yet its pathogenesis remains incompletely understood. Recent evidence suggests that the gut microbiota significantly influence immune responses, estrogen metabolism, and systemic inflammation, potentially contributing to EM progression. This narrative review explores the relationship between the gut microbiota and EM, emphasizing microbial dysbiosis, inflammation, estrogen regulation, and potential microbiome-targeted therapies. Studies published within the last 30 years were included, focusing on the microbiota composition, immune modulation, estrogen metabolism, and therapeutic interventions in EM. The selection criteria prioritized peer-reviewed articles, clinical trials, meta-analyses, and narrative reviews investigating the gut microbiota's role in EM pathophysiology and treatment. Microbial dysbiosis in EM is characterized by a reduced abundance of beneficial bacteria (Lactobacillus, Bifidobacterium, and Ruminococcaceae) and an increased prevalence of pro-inflammatory taxa (Escherichia/Shigella, Streptococcus, and Bacteroides). The gut microbiota modulate estrogen metabolism via the estrobolome, contributing to increased systemic estrogen levels and lesion proliferation. Additionally, lipopolysaccharides (LPS) from Gram-negative bacteria activate the TLR4/NF-κB signaling pathway, exacerbating inflammation and EM symptoms. The interaction between the gut microbiota, immune dysregulation, and estrogen metabolism suggests a critical role in EM pathogenesis. While microbiota-targeted interventions offer potential therapeutic benefits, further large-scale, multi-center studies are needed to validate microbial biomarkers and optimize microbiome-based therapies for EM. Integrating microbiome research with precision medicine may enhance the diagnostic accuracy and improve the EM treatment efficacy.},
}

Humans
*Endometriosis/physiopathology/microbiology/immunology/etiology
Female
*Gastrointestinal Microbiome/physiology/immunology
Estrogens/metabolism
Dysbiosis/complications
Inflammation

@article {pmid40427529,
year = {2025},
author = {Daude, N and Machado, I and Arce, L and Yang, J and Westaway, D},
title = {Microbial Composition, Disease Trajectory and Genetic Background in a Slow Onset Model of Frontotemporal Lobar Degeneration.},
journal = {Biomolecules},
volume = {15},
number = {5},
pages = {},
doi = {10.3390/biom15050636},
pmid = {40427529},
issn = {2218-273X},
support = {N/A//Nanostring AD panel/ ; N/A//SynAD ADRD/ ; 16308/CAPMC/CIHR/Canada ; 173286/CAPMC/CIHR/Canada ; NIF 21633//Canada Foundation for Innovation/ ; NIF 39588//Canada Foundation for Innovation/ ; N/A//Campus Alberta Neuroscience/ ; APRIIEP201600033//Alberta Prion Research Institute/ ; N/A//Hope for Tomorrow/ ; },
mesh = {Animals ; Mice ; Mice, Transgenic ; Disease Models, Animal ; tau Proteins/metabolism/genetics ; *Frontotemporal Lobar Degeneration/genetics/microbiology/pathology/metabolism ; Mice, Inbred C57BL ; *Gastrointestinal Microbiome/genetics ; Genetic Background ; Humans ; Male ; },
abstract = {Slow-onset neurodegenerative disease in a low-expresser 2N4R P301L transgenic (Tg) mouse model is marked by neuroinflammation and by differing patterns of CNS deposition and accumulation of tau conformers, with such heterogeneities present even within inbred backgrounds. Gut microbial genotypes were notably divergent within C57BL6/Tac or 129SvEv/Tac congenic (Cg) sublines of TgTau[P301L] mice, and these sublines differed when challenged with antibiotic treatment and fecal microbial transplantation. Whereas aged, transplanted Cg 129SvEv/Tac TgTau[P301L] mice had neuroanatomical deposition of tau resembling controls, transplanted Cg C57BL6/Tac TgTau[P301L] mice had different proportions of rostral versus caudal tau accumulation (p = 0.0001). These data indicate the potential for environmental influences on tau neuropathology in this model. Furthermore, Cg C57BL6/Tac TgTau[P301L] cohorts differed from 129SvEv/Tac counterparts by showing 28% versus 9% net intercurrent loss (p = 0.0027). While the origin of this phenomenon is not established, it offers a parallel to differing patterns of frailty observed in C57BL6 versus 129 SvEv Tg mice expressing the 695 amino acid isoform of human amyloid precursor protein. We infer that generalized responses to protein aggregation might account for similar reductions in viability even when expressing different human proteins in the same inbred strain background.},
}

Animals
Mice
Mice, Transgenic
Disease Models, Animal
tau Proteins/metabolism/genetics
*Frontotemporal Lobar Degeneration/genetics/microbiology/pathology/metabolism
Mice, Inbred C57BL
*Gastrointestinal Microbiome/genetics
Genetic Background
Humans
Male

@article {pmid40427424,
year = {2025},
author = {Golenia, A and Olejnik, P},
title = {The Role of Oxidative Stress in Ischaemic Stroke and the Influence of Gut Microbiota.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {14},
number = {5},
pages = {},
doi = {10.3390/antiox14050542},
pmid = {40427424},
issn = {2076-3921},
abstract = {Ischaemic stroke is the most prevalent stroke subtype, accounting for 80-90% of all cases worldwide, and remains a leading cause of morbidity and mortality. Its pathophysiology involves complex molecular cascades, with oxidative stress playing a central role. During cerebral ischaemia, reduced blood flow deprives neurons of essential oxygen and nutrients, triggering excitotoxicity, mitochondrial dysfunction, and excessive production of reactive oxygen and nitrogen species (RONS). Not only do these species damage cellular components, but they also activate inflammatory pathways, particularly those mediated by the transcription factor nuclear factor kappa-B (NF-κB). The pro-inflammatory milieu intensifies neuronal damage, compromises blood-brain barrier integrity, and exacerbates reperfusion-induced damage. Recent findings highlight the importance of the gut microbiota in modulating stroke outcomes, primarily through metabolic and immunological interactions along the gut-brain axis. Dysbiosis, characterised by reduced microbial diversity and an imbalance between beneficial and harmful strains, has been linked to increased systemic inflammation, oxidative stress, and worse prognoses. Specific gut-derived metabolites, including short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO), appear to either mitigate or intensify neuronal injury. SCFAs may strengthen the blood-brain barrier and temper inflammatory responses, whereas elevated TMAO levels may increase thrombotic risk. This narrative review consolidates both experimental and clinical data demonstrating the central role of oxidative stress in ischaemic stroke pathophysiology and explores the gut microbiota's ability to modulate these damaging processes. Therapeutic strategies targeting oxidative pathways or rebalancing gut microbial composition, such as antioxidant supplementation, dietary modulation, probiotics, and faecal microbiota transplantation, present promising paradigms for stroke intervention. However, their widespread clinical implementation is hindered by a lack of large-scale, randomised trials. Future efforts should employ a multidisciplinary approach to elucidate the intricate mechanisms linking oxidative stress and gut dysbiosis to ischaemic stroke, thereby paving the way for novel, mechanism-based therapies for improved patient outcomes.},
}

@article {pmid40426604,
year = {2025},
author = {Xia, YM and Zhang, MX and Ma, XY and Tan, LL and Li, T and Wu, J and Li, MA and Zhao, WJ and Qiao, CM and Jia, XB and Shen, YQ and Cui, C},
title = {Intranasal Transplantation of Microbiota Derived from Parkinson's Disease Mice Induced Astrocyte Activation and Neurodegenerative Pathology from Nose to Brain.},
journal = {Brain sciences},
volume = {15},
number = {5},
pages = {},
doi = {10.3390/brainsci15050433},
pmid = {40426604},
issn = {2076-3425},
support = {82171429//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Parkinson's disease (PD) is characterized by early-onset olfactory dysfunction preceding motor symptoms, yet its mechanisms remain elusive. Based on the studies on microbiota-gut-brain axis, the microbiota-nose-brain axis might be involved in the pathogenesis of PD. However relative studies are rare.

METHODS: By consecutive 14-days intranasally transplanting bacteria, we established mice models exhibiting nasal microbiota dysbiosis (NMD), including animal group received intranasal drops of fecal bacterial suspension from normal mice (NB group) and animal group received intranasal drops of fecal bacterial suspension from PD mice (PB group), with animals that only received anesthesia used as the control group. Then we analyzed the nasal microbiota composition via 16S rRNA sequencing, evaluated the olfactory and motor functions through behavioral experiments, including buried food test, open field test, pole descent test, and traction test. The neuropathology in olfactory-related and PD-related brain regions, including olfactory bulb, pyriform cortex, hippocampus, substantia nigra and striatum, was also detected by western blotting, immunofluorescence and immunohistochemical experiments using the antibodies of NeuN, TH and GFAP.

RESULTS: 16S rRNA sequencing revealed that PB mice were primarily characterized by an increase in bacteria associated with inflammation and PD. Behavioral assessments revealed that mice with NMD demonstrated impairments in the buried food test and pole descent test, indicative of olfactory and motor dysfunction. By detecting NeuN and GFAP expression, we identified neuronal loss and astrocytes activation in olfactory-related brain regions and adjacent structures, including the olfactory bulb, pyriform cortex, hippocampus, substantia nigra and striatum of both NMD groups, which may contribute to the observed functional disorders. Notably, animals exposed to PD-derived bacteria exhibited more pronounced changes in nasal bacteria, with more severe neuropathology.

CONCLUSIONS: We present evidence supporting the microbiota-nose-brain axis, and the NMD-induced astrocyte activation and neurodegenerative pathology along the olfactory pathway may serve as a link between nose and brain.},
}

@article {pmid40424882,
year = {2025},
author = {Huang, YY and Qin, SM and Nguyen, MT and Chen, W and Si, XM and Huang, YQ and Zhang, HY},
title = {The protective effects of dietary resistant starch against post-antibiotic bone loss in meat ducks associated with the recovery of caecal microbiota dysbiosis.},
journal = {Poultry science},
volume = {104},
number = {8},
pages = {105238},
doi = {10.1016/j.psj.2025.105238},
pmid = {40424882},
issn = {1525-3171},
abstract = {Compromised bone quality increases the risk of fractures in domesticate birds, resulting in pain and altered behaviour. Although dietary resistant starch (RS) supplementation show promise for improving inferior bone mass, the diet-mediated gut microbiota alterations as a potential mechanism underlying RS positive roles in bone remains uncertain. With a post-antibiotic model and faecal microbiota transplantation (FMT), this study investigated the effects of a RS diet on antibiotic-induced bone loss and gut microbial composition in meat ducks. Ducklings were assigned to 4 treatments with 6 replicate pens until 21 d, including the control group (Ctrl, feeding a basal diet) and the RS-fed group, and post-antibiotic treatment following the gavage of phosphate-buffered saline (Post-anti-PBS) or faecal microbiota transplantation (Post-anti-FMT). The RS diet increased the proportion of Firmicutes, improved intestinal integrity, and reduced inflammation-induced bone resorption, all of which contributed to an increase in tibial bone volume (P < 0.05). Post-antibiotic treatment was found to reduce tibial quality by stimulating bone resorption and inhibiting bone formation, accompanied by gut microbiota dysbiosis, increased intestinal permeability (P = 0.059), and inflammatory flare compared to control birds. FMT from RS-fed ducks into the antibiotic-treated birds reversed bone loss by primarily blocking osteoclastic frequency and activity. Furthermore, FMT increased the ratio of Firmicutes to Bacteroidetes (P < 0.05) and suppressed the release of pro-osteoclastogenic cytokines such as tumour necrosis factor-α (P = 0.062) and interleukin-1β (P < 0.05) in the bone marrow. These results demonstrated the involvement of gut microbiota in improving bone quality of meat ducks by RS, and FMT of RS-fed birds corrected the imbalance of ceca microbiota and attenuated bone loss in meat ducks with enhanced bone resorption.},
}

@article {pmid40335381,
year = {2025},
author = {Vuyk, W and Bobholz, M and Emmen, I and Lail, A and Minor, N and Bhimalli, P and Eickhoff, JC and Ries, HJ and Machkovech, H and Wei, W and Weiler, A and Richardson, A and DePagter, C and VanSleet, G and Bhasin, M and Kamal, S and Wolf, S and Virdi, A and Bradley, T and Gifford, A and Benito, M and Shipe, A and Mohamed, R and Smith, J and Wilson, N and Friedrich, TC and O'Connor, DH and Garonzik-Wang, J},
title = {Longitudinal Assessment of Solid Organ Transplant Recipients With SARS-CoV-2 Infection.},
journal = {Transplantation proceedings},
volume = {57},
number = {5},
pages = {922-930},
doi = {10.1016/j.transproceed.2025.04.004},
pmid = {40335381},
issn = {1873-2623},
mesh = {Humans ; *COVID-19/diagnosis/virology/epidemiology/immunology ; Middle Aged ; *SARS-CoV-2/genetics/isolation & purification ; Male ; *Organ Transplantation/adverse effects ; *Immunocompromised Host ; Female ; Virus Shedding ; *Transplant Recipients ; Prospective Studies ; Adult ; RNA, Viral ; Longitudinal Studies ; Viral Load ; Aged ; Feces/virology ; },
abstract = {BACKGROUND: Compared with immunocompetent individuals, those who are immunocompromised, including solid organ transplant (SOT) recipients, have higher SARS-CoV-2-related morbidity and mortality. We determined the duration of SARS-CoV-2 RNA positivity to evaluate viral persistence in SOT recipients.

METHODS: This study prospectively followed SOT recipients who recently tested positive for SARS-CoV-2. The duration of viral RNA shedding in nasal swabs and stool samples was tracked, and viral genome sequencing was performed where possible. Persistent infection was defined as a positive nucleic acid amplification test (NAAT) for SARS-CoV-2 at 28 days or later after initial infection. This duration was chosen based on the U.S. Centers for Disease Control and Prevention (CDC) recommendation that immunocompromised individuals isolate for at least 20 days [1], compared with 10 days for non-immunocompromised individuals.

RESULTS: Of 30 SOT recipients, 12 (40%) had positive SARS-CoV-2 RNA in nasal swabs or stool (cycle threshold [Ct] < 40) at 28 or more days after the first positive SARS-CoV-2 test. Immunocompromised (IC) subject 015 had high viral loads (Ct < 30) at 28 days, with continued detection for 54 days.

CONCLUSIONS: In 12 of 30 SOT subjects, SARS-CoV-2 RNA was detected at or beyond 28 days post-detection (dpd), despite vaccination and antibody and/or antiviral treatment in most participants. Three subjects tested positive for SARS-CoV-2 RNA past 50 dpd. Viral persistence in the setting of host immune suppression, coupled with exposure to antiviral treatments, raises concern about the selection of unusual viral variants.},
}

Humans
*COVID-19/diagnosis/virology/epidemiology/immunology
Middle Aged
*SARS-CoV-2/genetics/isolation & purification
Male
*Organ Transplantation/adverse effects
*Immunocompromised Host
Female
Virus Shedding
*Transplant Recipients
Prospective Studies
Adult
RNA, Viral
Longitudinal Studies
Viral Load
Aged
Feces/virology

@article {pmid40422666,
year = {2025},
author = {Gaspar, BS and Roşu, OA and Enache, RM and Manciulea Profir, M and Pavelescu, LA and Creţoiu, SM},
title = {Gut Mycobiome: Latest Findings and Current Knowledge Regarding Its Significance in Human Health and Disease.},
journal = {Journal of fungi (Basel, Switzerland)},
volume = {11},
number = {5},
pages = {},
doi = {10.3390/jof11050333},
pmid = {40422666},
issn = {2309-608X},
abstract = {The gut mycobiome, the fungal component of the gut microbiota, plays a crucial role in health and disease. Although fungi represent a small fraction of the gut ecosystem, they influence immune responses, gut homeostasis, and disease progression. The mycobiome's composition varies with age, diet, and host factors, and its imbalance has been linked to conditions such as inflammatory bowel disease (IBD) and metabolic disorders. Advances in sequencing have expanded our understanding of gut fungi, but challenges remain due to methodological limitations and high variability between individuals. Emerging therapeutic strategies, including antifungals, probiotics, fecal microbiota transplantation, and dietary interventions, show promise but require further study. This review highlights recent discoveries on the gut mycobiome, its interactions with bacteria, its role in disease, and potential clinical applications. A deeper understanding of fungal contributions to gut health will help develop targeted microbiome-based therapies.},
}

@article {pmid40421334,
year = {2025},
author = {Ponce Alencastro, JA and Salinas Lucero, DA and Solis, RP and Herrera Giron, CG and Estrella López, AS and Anda Suárez, PX},
title = {Molecular Mechanisms and Emerging Precision Therapeutics in the Gut Microbiota-Cardiovascular Axis.},
journal = {Cureus},
volume = {17},
number = {4},
pages = {e83022},
pmid = {40421334},
issn = {2168-8184},
abstract = {A microbiome in the gut plays a significant role in cardiovascular health and disease. Dysbiosis is an imbalance in the gut microbiome, leading to multiple cardiovascular diseases (CVD) such as atherosclerosis, hypertension, and heart failure. Gut microbe-derived metabolites such as trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs) are important mediators of the gut-heart axis. Evaluation of the relationship between the gut microbiome and host biomarkers with CVD requires the integration of metagenomics and metabolomics with meta-omics approaches. The literature review found that microbes and metabolic signatures are associated with the risk and progression of CVD. The development of precision therapeutic approaches for targeting gut microbiota includes preventing adverse microbial effects using probiotics, prebiotics, and the drug-as-bug approach to inhibit harmful metabolites of microbiomes, and fecal microbiota transplantation (FMT). However, the implication and practice of these findings in clinical settings face challenges due to the heterogeneity of study designs, difficulty in the determination of causality, and the impact of confounding factors such as diet, medication, and potential inter-individual gut microbiome variability. Future researchers are recommended to conduct longitudinal studies to further establish both gut microbiome associations with CVD and develop successful precision therapeutics approaches based on the microbiome for the treatment of CVD.},
}

@article {pmid40420583,
year = {2025},
author = {He, X and Luthuli, S and Wen, Q and Wang, C and Ding, J and Cui, B and Zhang, F},
title = {Washed microbiota transplantation for ribotype 027 Clostridioides difficile infection in a pregnant woman with two-year follow-up: a case report.},
journal = {Journal of biomedical research},
volume = {},
number = {},
pages = {1-4},
doi = {10.7555/JBR.39.20250063},
pmid = {40420583},
issn = {1674-8301},
abstract = {Clostridioides difficile (C. difficile) is one of the major causes of nosocomial infections. The pregnant women, who were considered at low risk for C. difficile infection (CDI), have attracted attention with increasing reports. Oral vancomycin, the only first-line treatment for the pregnant women infected with C. difficile, came with the problem of increasing strains resistance that was associated with decreased efficacy. Fecal microbiota transplantation (FMT) is recommended for severe, fulminant and recurrent CDI, while it is avoided in the pregnant women due to safety concerns. We reported a pregnant woman case with primary ribotype 027 CDI, who got a successful outcome with washed microbiota transplantation (WMT), an improved FMT, via enema. The specific strain of ribotype 027 was related to severe outcomes but was not reported in the pregnant women. The follow-up lasted two years, the patient's diarrhea was fully alleviated without recurrence. The baby had normal growth and development and no adverse events were recorded in both of them. This case provides evidence for the efficacy and safety of WMT in the pregnant women infected with C. difficile, indicating that WMT via enema may be a strategy for this population in treating CDI.},
}

@article {pmid40419682,
year = {2025},
author = {Nishinarita, Y and Miyoshi, J and Kuronuma, S and Wada, H and Oguri, N and Hibi, N and Takeuchi, O and Akimoto, Y and Lee, STM and Matsuura, M and Kobayashi, T and Hibi, T and Hisamatsu, T},
title = {Characteristic gene expression profile of intestinal mucosa early in life promotes bacterial colonization leading to healthy development of the intestinal environment.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {18437},
pmid = {40419682},
issn = {2045-2322},
support = {19K23977//Japan Society for the Promotion of Science/ ; 21K07900//Japan Society for the Promotion of Science/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/genetics ; Mice ; *Intestinal Mucosa/microbiology/metabolism ; Fecal Microbiota Transplantation ; *Bacteria/genetics/growth & development/classification ; Germ-Free Life ; *Transcriptome ; Male ; Gene Expression Profiling ; Female ; Feces/microbiology ; Mice, Inbred C57BL ; },
abstract = {The gut microbiome early in life plays a crucial role in development of the host and affects health throughout life. The definition of a healthy microbiome early in life has not been established, and the underlying mechanism of how a young host selects appropriate microbes for colonization remains unclear. Understanding the mechanism may provide insights into novel preventive and therapeutic strategies by correcting dysbiosis early in life. We employed germ-free mice early in life (4 weeks of age) and later in life (10 weeks of age) for fecal microbiota transfer (FMT) from specific pathogen-free mice. We performed age-unmatched FMT between recipients early in life and donors early or later in life, in addition to common age-matched FMT. Age-matched FMT resulted in significantly different bacterial compositions between recipients early vs. later in life. When the gut microbiome from donors early or later in life was transferred to recipients early in life, bacterial compositions of recipients from donors later in life were similar to those of recipients from donors early in life. This finding suggests that the host early in life has mechanisms to select microbes appropriate for age from the exposed microbiome. We hypothesized that the age-specific intestinal environment promotes age-appropriate intestinal microbiome colonization and examined gene expression in the intestinal mucosa of germ-free mice. We observed that gene expression profiles were different between early vs. later in life. Correlation analysis demonstrated that genera Lachnospiraceae NK4A136 group and Roseburia were positively correlated to genes expressed predominantly early in life, but negatively with genes expressed predominantly later in life. We confirmed that the relative abundance of these genera was significantly higher in specific pathogen-free mice early in life compared with mice later in life. The characteristic gene expression of the intestinal mucosa early in life might play roles in selecting specific bacteria in the intestinal microbiome early in life.},
}

Animals
*Gastrointestinal Microbiome/genetics
Mice
*Intestinal Mucosa/microbiology/metabolism
Fecal Microbiota Transplantation
*Bacteria/genetics/growth & development/classification
Germ-Free Life
*Transcriptome
Male
Gene Expression Profiling
Female
Feces/microbiology
Mice, Inbred C57BL

@article {pmid40419041,
year = {2025},
author = {Chen, L and Zhao, S and Chen, Q and Luo, P and Li, X and Song, Y and Pan, S and Wu, Q and Zhang, Y and Shen, X and Chen, Y},
title = {Poria cocos polysaccharides ameliorate AOM/DSS-induced colorectal cancer in mice by remodeling intestinal microbiota composition and enhancing intestinal barrier function.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {144477},
doi = {10.1016/j.ijbiomac.2025.144477},
pmid = {40419041},
issn = {1879-0003},
abstract = {Colorectal cancer (CRC) remains a leading cause of cancer-related mortality, necessitating the development of novel therapeutic strategies. Poria cocos polysaccharides (PCP), bioactive components of the traditional medicinal fungus Poria cocos, exhibit significant anticancer potential. This study investigates the protective effects of PCP against azoxymethane/dextran sulfate sodium (AOM/DSS)-induced CRC in mice, with a focus on its impact on intestinal microbiota composition, intestinal barrier integrity, and inflammatory responses. PCP treatment significantly reduced tumor incidence, tumor size, and tumor burden while improving histopathological features and inhibiting Ki67-positive cell proliferation. Mechanistically, PCP enhanced intestinal barrier function by restoring tight junction proteins (E-cadherin, ZO-1, Claudin-3) and mucin secretion (MUC2), thereby reducing intestinal permeability and systemic lipopolysaccharide (LPS) levels. Furthermore, PCP exhibited potent anti-inflammatory effects by downregulating pro-inflammatory cytokines (TNF-α, IL-6, IL-1β) and upregulating the anti-inflammatory cytokine IL-10. 16S rRNA sequencing results revealed that PCP modulated the intestinal microbiota, decreasing pathogenic bacteria such as Helicobacter and Eisenbergiella while promoting beneficial taxa including Limosilactobacillus, Paraprevotella, and Muribaculum. Fecal microbiota transplantation (FMT) further confirmed the microbiota-mediated protective effects of PCP, as FMT from PCP-treated donors significantly suppressed tumorigenesis, restored intestinal barrier integrity, and alleviated inflammation in CRC mice. Additionally, PCP demonstrated a favorable safety profile, with no adverse effects on major organs. These findings highlight PCP as promising natural agents for CRC prevention and therapy, acting through modulation of the intestinal microbiota, enhancement of intestinal barrier function, and suppression of inflammation.},
}