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

@article {pmid40784117,
year = {2025},
author = {Zhang, J and Hu, H and Zhu, Y and Xin, X and Jin, Y and Zhao, Q and Zhang, H and Heng, D and Ma, Z and Chai, X and Lin, R and Zhao, Y and Ye, Y and Li, D},
title = {Polystyrene/polylactic acid microplastics impair transzonal projections and oocyte maturation via gut microbiota-mediated lipoprotein lipase inhibition.},
journal = {Journal of hazardous materials},
volume = {496},
number = {},
pages = {139475},
doi = {10.1016/j.jhazmat.2025.139475},
pmid = {40784117},
issn = {1873-3336},
abstract = {This study focuses on the impacts of polystyrene/polylactic acid microplastics (PS/PLA-MPs) on ovarian reserve and oocyte maturation in female mice, along with the underlying mechanisms. 1 μm PS-MPs and PLA-MPs were prepared, with PLA-MPs having a rougher surface and broader size distribution. In vitro, PLA-MPs showed higher cytotoxicity to granulosa cells compared to PS-MPs. In vivo, MPs exposure disrupted the estrous cycle, and damaged ovarian reserve. Granulosa cell apoptosis and cytokine activation led to transzonal projection retraction, oocyte oxidative stress, meiotic abnormalities, and reduced oocyte retrieval and polar body extrusion rate, thus reducing litter size. PS-MPs induced more severe intestinal and ovarian impairment. Analysis of feces 16S rRNA, serum metabolomics, and ovarian RNA sequencing revealed that lipoprotein lipase (LPL) was suppressed by both MPs, linking gut microbiota, lipid metabolism, and ovarian injury. Fecal microbiota transplantation as a rescue strategy in MPs exposed mice upregulated LPL, alleviating ovarian reserve decline. In PLA-MPs exposed mice, ovarian reserve related indicators partially recovered after a two-week exposure cessation. These results clarify the similarities and differences in how PS-MPs and PLA-MPs impair ovarian function via gut-ovary axis and lipid metabolism dysregulation.},
}

@article {pmid40783567,
year = {2025},
author = {Yang, J and Zhou, Y and Du, A and Zhang, Z and Wang, B and Tian, Y and Liu, H and Cai, L and Pang, F and Li, Y and Du, C and Wu, X and Yan, C and Wu, W and Jiang, M and Shen, K and Zhang, C and Feng, Y and Kang, Y and Shen, B and Zong, Z},
title = {Microbiome-mediated colonization resistance to carbapenem-resistant Klebsiella pneumoniae in ICU patients.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {157},
pmid = {40783567},
issn = {2055-5008},
support = {2019HXBH088//post-doctoral fund by West China Hospital of Sichuan University/ ; 2023YFC2308800//National Key Research and Development Program of China/ ; ZYYC08006 and no. ZYGD22001//1.3.5 project for disciplines of excellence grants by the West China Hospital of Sichuan University/ ; },
mesh = {Humans ; *Klebsiella Infections/microbiology/therapy ; *Klebsiella pneumoniae/drug effects/growth & development ; Intensive Care Units ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Mice ; *Carbapenems/pharmacology ; Animals ; Male ; *Carbapenem-Resistant Enterobacteriaceae/drug effects ; Anti-Bacterial Agents/pharmacology ; Female ; Middle Aged ; Feces/microbiology ; Probiotics/administration & dosage ; Aged ; },
abstract = {Carbapenem-resistant Klebsiella pneumoniae (CRKP) causes serious intensive care unit (ICU)-acquired infections, yet the mechanisms of microbiota-mediated colonization resistance remain unclear. We analyzed the gut microbiome and metabolic profiles of healthy individuals and ICU patients, distinguishing those with and without CRKP colonization. ICU patients showed distinct microbial communities compared to healthy controls, and CRKP-positive patients exhibited unique microbial and metabolic signatures. We demonstrated that a healthy gut microbiome is essential for providing resistance against CRKP colonization in antibiotic-perturbed mouse with fecal microbiota transplantation (FMT). Both in vitro and in vivo experiments revealed that Lactiplantibacillus plantarum and Bifidobacterium longum as significant contributors to the decolonization of CRKP. Furthermore, we showed that probiotic supplementation or FMT significantly improved CRKP colonization resistance. The findings highlight that a specific gut microbiome is essential for resisting CRKP colonization, and that targeted microbiome restoration may serve as a viable strategy to prevent CRKP colonization in ICU patients.},
}

Humans
*Klebsiella Infections/microbiology/therapy
*Klebsiella pneumoniae/drug effects/growth & development
Intensive Care Units
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Mice
*Carbapenems/pharmacology
Animals
Male
*Carbapenem-Resistant Enterobacteriaceae/drug effects
Anti-Bacterial Agents/pharmacology
Female
Middle Aged
Feces/microbiology
Probiotics/administration & dosage
Aged

@article {pmid40783052,
year = {2025},
author = {Formelli, MG and Palloni, A and Tavolari, S and Deiana, C and Andrini, E and Marco, MD and Campana, D and Lamberti, G and Brandi, G},
title = {Classic versus innovative strategies for immuno-therapy in pancreatic cancer.},
journal = {Advanced drug delivery reviews},
volume = {},
number = {},
pages = {115671},
doi = {10.1016/j.addr.2025.115671},
pmid = {40783052},
issn = {1872-8294},
abstract = {Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy with a dismal prognosis. Immunotherapy with immune checkpoint inhibitors (ICIs), either as monotherapy, in combination with other ICIs, or alongside chemotherapy, has significantly improved outcomes in several solid tumors. However, its efficacy in PDAC remains limited due to multiple resistance mechanisms. Key determinants of immunotherapy resistance in PDAC include physical barriers that hinder immune cells infiltration, such as aberrant vasculature, cancer-associated fibroblasts (CAFs), and excessive hyaluronic acid deposition in the tumor microenvironment (TME). Additionally, PDAC is characterized by an immunosuppressive TME enriched with regulatory T cells (Tregs) and myeloid-derived suppressor cells (MDSCs), and by low immunogenicity of tumor cells due to KRAS mutations, MYC overexpression, and a low tumor mutational burden, further impairing antitumor immunity. This review discusses advanced drug delivery systems to overcome determinants of immunotherapy resistance and to improve outcomes, explores emerging immunotherapy strategies, including adoptive cell therapies, cancer vaccines, and the potential role of microbiota as modulator of TME through fecal microbiota transplantation or intratumoral bacterial inoculation. Given the ambivalent role of microbiota in PDAC, the need for a clear definition of favorable strains and their selection is highlighted. Emerging approaches involving engineered bacteria and artificial intelligence applications are also explored. Finally, we propose a hypothetical conceptual framework for an innovative multimodal immunotherapy approach to overcome resistance and improve clinical outcomes in PDAC.},
}

@article {pmid40782764,
year = {2025},
author = {Wang, FY and Yi, J and Zhou, LL and Tan, JL and Cao, XY and Zhang, C and Wan, JJ and Song, L and Dai, AG},
title = {Unlocking the gut-lung axis: Feixin decoction as a novel modulator in hypoxic pulmonary hypertension.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {146},
number = {},
pages = {157118},
doi = {10.1016/j.phymed.2025.157118},
pmid = {40782764},
issn = {1618-095X},
abstract = {BACKGROUND: Feixin decoction (FXD) is an effective traditional Chinese medicine prescription for treating chronic pulmonary heart disease and hypoxic pulmonary hypertension (HPH), However, the pharmacological mechanism of FXD in preventing HPH remains unclear.

PURPOSE: This study aimed to evaluate the preventive and therapeutic effect of FXD on HPH and confirm the association between HPH, gut microbiota, and FXD.

METHODS: Multiple in vivo animal models were used, including HPH rat models, microbiota depletion models, and fecal microbiota transplantation (FMT) models. The HPH phenotype was evaluated through: right heart catheterization for hemodynamic parameters, doppler echocardiography for cardiac function assessment, hematoxylin-eosin staining for histopathological examination, and immunofluorescence labeling for specific protein expression analysis. Concurrently, transmission electron microscopy was utilized to observe the ultrastructure of the intestinal barrier, combined with immunofluorescence to examine the distribution characteristics of tight junction proteins. To elucidate the mechanism by which HPH ameliorates gut microbiota dysbiosis and associated metabolites, the study integrated 16S rRNA sequencing for microbiota composition analysis, dual-platform untargeted metabolomics for differential metabolite screening, and targeted metabolomics for quantitative validation.

RESULTS: FXD exhibited significant therapeutic effects in HPH rats, ameliorating pulmonary vascular remodeling, attenuating right ventricular hypertrophy, reducing systemic inflammation, and restoring intestinal barrier function. Additionally, FXD partially restored intestinal ecological balance by enriching beneficial species (Lactobacillus and Lactobacillus johnsonii) while reducing pathogenic genera (Escherichia-Shigella and Helicobacter rodentium). Concurrently, FXD treatment induced favorable metabolic alterations, characterized by elevated levels of beneficial metabolites including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), along with reduced concentrations of pro-inflammatory 5-hydroxytryptamine (5-HT). Gut microbiota depletion and fecal microbiota transplantation (FMT) studies established that FXD's therapeutic effects on HPH are mediated through gut microbiota modulation. Mechanistic investigations revealed that this protection likely involves inhibition of the TLR4/MyD88/NF-κB signaling pathway. In vitro studies further corroborated these findings, showing that FXD-enriched metabolites potently suppressed abnormal proliferation, migration and apoptosis in human pulmonary arterial smooth muscle cells (HPASMCs). Notably, EPA, the most significantly increased metabolite, specifically attenuates hypoxia-induced HPASMCs proliferation by interfering with the TLR4/MyD88/NF-κB signaling axis.

CONCLUSIONS: Our study confirms that FXD alleviates HPH by regulating gut microbiota and its associated metabolites and validates the potential of FXD as a gut microbiota modulator and an HPH treatment, thereby providing a new therapeutic strategy to improve treatment efficacy.},
}

@article {pmid40781053,
year = {2025},
author = {Kociolek, LK and Sandora, TJ and Mehrotra, P},
title = {Clostridioides difficile in Children.},
journal = {Infectious disease clinics of North America},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.idc.2025.07.011},
pmid = {40781053},
issn = {1557-9824},
abstract = {After a significant increase in pediatric Clostridioides difficile infection (CDI) in the United States over the past 2 decades, incidence has declined over the past 5 y. Community-associated CDI incidence is 3 times higher than healthcare facility-associated CDI in children, but sources of community acquisition are poorly defined. Diagnosis of CDI is challenging because of high frequency of colonization in infants and some groups of older children. Recent data suggest that vancomycin should be considered a first-line treatment for CDI in children and that fidaxomicin and fecal microbiota transplantation are safe and effective therapies for recurrent CDI.},
}

@article {pmid40781016,
year = {2025},
author = {Rubin, J and Roman, M},
title = {Veterinary Medical Ozone Therapy: An Integrative Approach.},
journal = {The Veterinary clinics of North America. Small animal practice},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cvsm.2025.06.009},
pmid = {40781016},
issn = {1878-1306},
abstract = {Veterinary medical ozone therapy, a key component of integrative veterinary medicine, leverages advanced oxygenation techniques and natural immune-modulating effects to treat a broad range of clinical conditions in small, large and exotic animals. This article explores the mechanisms of action, clinical applications, safety considerations, and integration of medical ozone therapy with conventional and complementary treatments, providing veterinary professionals with a practical and comprehensive resource. With the growing challenge of antimicrobial resistance posing significant public health concerns, the role of medical ozone therapy has become increasingly vital.},
}

@article {pmid40780339,
year = {2025},
author = {Gao, Y and Lin, J and Liu, D and Zhao, W and Pei, J and El-Aty, AMA},
title = {A selenium-enriched glycosaminoglycan from sturgeon cartilage: characterization and anti-metabolic syndrome potential.},
journal = {International journal of biological macromolecules},
volume = {},
number = {},
pages = {146637},
doi = {10.1016/j.ijbiomac.2025.146637},
pmid = {40780339},
issn = {1879-0003},
abstract = {This study develops a novel selenium-enriched chondroitin sulfate (CSSE) from selenium-rich sturgeon cartilage that has potent multitarget activity against high-carbohydrate/high-fat diet-induced metabolic syndrome. Structural analyses (NMR/MALDI-TOF MS) confirmed Se-O-SO3 covalent bonds (δ 78.5 ppm in [13]C NMR) and a molecular weight of 16.8 kDa, indicating hepatic targeting with lower renal toxicity. Compared with sodium selenite, CSSE showed superior antioxidant capacity (65-80 % vs. 30-45 % DPPH scavenging) and biocompatibility (89.5 % vs. 66.4 % cell viability) (p = 0.009). In high-carbohydrate/high-fat diet (HCHF)-fed mice, CSSE markedly decreased body weight gain (-35 %), fasting glucose (-55 %), and triglyceride levels (-44 %), outperforming inorganic selenium by 2.1-3.5-fold. Mechanistically, CSSE inhibited mammalian target of rapamycin complex 1 (mTORC1) activation (32.7 % phosphorylated mammalian target of rapamycin (p-mTOR)/mammalian target of rapamycin (mTOR)), restored insulin signaling via the phosphoinositide 3-kinase-protein kinase B (PI3K-Akt)/insulin receptor substrate 1 (IRS-1) (↑103 % phosphorylated Akt (p-Akt)/protein kinase B (Akt), and upregulated the fibroblast growth factor 21 (FGF21)/fibroblast growth factor 19 (FGF19) gut-liver axis (p = 0.028). CSSE enriched beneficial gut bacteria (e.g., Ligilactobacillus) while suppressing Allobaculum, increasing short-chain fatty acid (SCFA) production by 58.1 % and enhancing gut barrier function (↓49 % fluorescein isothiocyanate (FITC)-dextran leakage, p = 0.007). Fecal microbiota transplantation (FMT) has validated microbiota-mediated benefits. The dual antioxidant and lipid-lowering actions of CSSE, combined with its targeted delivery and safety, position it as a pioneering marine organoselenium therapy. This study also establishes a sustainable approach to transform aquaculture byproducts into precision nutraceuticals, advancing metabolic health through circular bioeconomic solutions.},
}

@article {pmid40780229,
year = {2025},
author = {Rhode, P and Mehdorn, M and Lange, UG and Rabe, SM and Quart, J and Nowotny, R and Plum, PS and Niebisch, S and Stelzner, S},
title = {[Functional Outcome of Radiotherapy, Chemotherapy and Surgery in the Treatment of Rectal Cancer].},
journal = {Zentralblatt fur Chirurgie},
volume = {150},
number = {4},
pages = {353-361},
doi = {10.1055/a-2646-2695},
pmid = {40780229},
issn = {1438-9592},
mesh = {Humans ; *Rectal Neoplasms/therapy/pathology/surgery/drug therapy/radiotherapy ; Combined Modality Therapy ; Neoadjuvant Therapy ; Treatment Outcome ; Fecal Incontinence/etiology ; Neoplasm Staging ; Postoperative Complications/etiology ; },
abstract = {Treatment of rectal cancer is multimodal and based on tumour stage and location, as well as morphological and biological risk factors - using surgery, radiotherapy, and chemotherapy. In a large number of cases, there are several treatment options, some of which can cause similar and some of which can cause different functional limitations. Comparisons of functional outcomes between different treatment modalities are currently limited.This narrative review presents the functional outcomes of different treatment strategies for middle and lower third rectal cancer, as based on a literature search.This paper analyses the evidence on the functional outcomes of different treatment strategies, especially regarding fecal continence, urinary and sexual function. The functional outcome after organ-preserving strategies appears to be slightly better in terms of stool frequency compared to surgical therapy alone, but this has to be weighed up against chemotherapy-induced polyneuropathy and radiogenic toxicities such as cystitis, radionecrosis or fistula formation. In addition, the functional side effects of perioperative and surgical therapy accumulate in the event of incomplete remission. A few days of treatment during surgical therapy contrast with the significantly more protracted treatment of total neoadjuvant therapy. A conclusive evaluation based on the current evidence is only possible to a limited extent.This study emphasises the importance of providing patients with detailed information about the functional consequences, duration of treatment and possible complications and offers a decision-making aid for planning individual treatment, taking quality of life into account.},
}

Humans
*Rectal Neoplasms/therapy/pathology/surgery/drug therapy/radiotherapy
Combined Modality Therapy
Neoadjuvant Therapy
Treatment Outcome
Fecal Incontinence/etiology
Neoplasm Staging
Postoperative Complications/etiology

@article {pmid40778357,
year = {2025},
author = {Ren, J and Lian, XY and Ye, WQ and Wen, YL and Lu, CL and Cao, X},
title = {Gut microbiota regulates innate anxiety through neural activity of medial prefrontal cortex in male mice.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1599818},
pmid = {40778357},
issn = {1662-4548},
abstract = {INTRODUCTION: Innate anxiety, a stable personality trait conceptualized as trait anxiety, represents a fundamental dimension of individual differences in emotional regulation. Clinical evidence and animal studies indicate that elevated innate anxiety significantly increases susceptibility to psychiatric disorders. While the gut microbiota has been increasingly recognized as a critical modulator of neuropsychiatric health, its specific contribution to innate anxiety has yet to be fully elucidated.

METHODS: We investigated gut microbiota contributions to innate anxiety in mice using stratified behavioral phenotyping in the elevated plus maze (EPM), antibiotic (ABX)-mediated microbiota depletion, fecal microbiota transplantation (FMT), c-FOS staining, transcriptomic profiling, and vivo fiber photometry.

RESULTS: We found that innate high-anxiety (HA) and low-anxiety (LA) mice exhibited distinct gut microbial compositions. Microbiota depletion induced significant anxiolytic effects, while FMT from HA donors recapitulated anxiety-like behaviors. Neural activation mapping revealed elevated c-FOS expression in the medial prefrontal cortex (mPFC), basolateral amygdala (BLA), and central amygdala (CeA) of HA-FMT recipients. Transcriptomic analysis of mPFC tissue in HA- and LA-FMT recipients demonstrated microbiota driven regulation of transcriptional reprogramming, protein modification, and synapse modulation, indicating mechanistic connections along the microbiota gut-brain axis. Fiber photometry confirmed heightened mPFC neuronal activity during innate anxiety states in HA-FMT mice.

DISCUSSION: Our findings establish that gut microbiota modulates innate anxiety through mPFC neural activity, providing novel insights into microbiome-based interventions for anxiety.},
}

@article {pmid40776644,
year = {2025},
author = {Lin, Y and Wang, P and Hu, X and Wang, Q and Shi, Q and Zhou, Y and Liu, R and Cai, X},
title = {Recent Advancement of Fecal Microbiota Transplantation in the Treatment of Ulcerative Colitis- A Review.},
journal = {Current medicinal chemistry},
volume = {},
number = {},
pages = {},
doi = {10.2174/0109298673404225250730100935},
pmid = {40776644},
issn = {1875-533X},
abstract = {Fecal Microbiota Transplantation (FMT) involves the transfer of gut microbiota from healthy donors to recipients, aiming to reestablish microbial equilibrium within the gastrointestinal tract. The human gut harbors a complex and diverse microbial ecosystem, comprising bacteria, viruses, and fungi, that is essential for maintaining intestinal homeostasis. Emerging evidence indicates a strong association between gut microbial dysbiosis and the pathogenesis of Ulcerative Colitis (UC). FMT has been shown to modulate microbial composition, alter immune signaling pathways, enhance intestinal barrier function, and influence the production of proinflammatory mediators, thereby affecting disease progression. This review critically examines the efficacy, safety, modulatory factors, combination therapies, and predictive strategies associated with FMT in the context of UC. The findings suggest that FMT represents a highly promising therapeutic modality for UC. Overall, this review aims to provide a comprehensive and impartial synthesis of current knowledge regarding FMT, offering deeper insights into its therapeutic potential and clinical applicability in UC management.},
}

@article {pmid40776414,
year = {2025},
author = {Kong, X and Wu, SY and Jiang, JZ and Luo, S and Zhang, J and Yang, GF and Lu, GM and Zhang, LJ},
title = {Efficacies of Bifidobacterium and Fecal Microbiota Transplantation in Rats With Chronic Hepatic Encephalopathy Assessed by [[18]F]PBR146 Imaging of Neuroinflammation.},
journal = {The European journal of neuroscience},
volume = {62},
number = {3},
pages = {e70227},
doi = {10.1111/ejn.70227},
pmid = {40776414},
issn = {1460-9568},
support = {81401468//National Natural Science Foundation of China/ ; 81601486//National Natural Science Foundation of China/ ; 82127806//National Natural Science Foundation of China/ ; 82230068//National Natural Science Foundation of China/ ; 81830057//National Natural Science Foundation of China/ ; 81322020//National Natural Science Foundation of China/ ; 81230032//National Natural Science Foundation of China/ ; 81171313//National Natural Science Foundation of China/ ; 2020AAA0109500//Science and Technology Innovation 2030-Major Projects/ ; 021414380531//Fundamental Research Funds for the Central Universities of China/ ; 201801B055//Program B for Outstanding PhD Candidate of Nanjing University/ ; },
mesh = {Animals ; *Fecal Microbiota Transplantation/methods ; *Hepatic Encephalopathy/therapy/diagnostic imaging ; Rats ; Male ; Positron Emission Tomography Computed Tomography ; *Bifidobacterium ; Rats, Sprague-Dawley ; Brain/diagnostic imaging ; *Neuroinflammatory Diseases/diagnostic imaging/therapy ; Pyrimidines ; },
abstract = {Neuroinflammation significantly contributes to hepatic encephalopathy (HE). The radiotracer [[18]F]PBR146 is used for in vivo imaging of neuroinflammation. Promising treatments like Bifidobacterium (BIF) and fecal microbiota transplantation (FMT) are being explored for HE. This study evaluated and compared the efficacies of BIF and FMT in reducing neuroinflammation in chronic HE rats induced by bile duct ligation (BDL) using [[18]F]PBR146 micro-PET/CT imaging. Thirty rats were divided into four groups: (1) Sham-operated rats received normal saline (Sham + NS group), (2) BDL rats treated with NS (BDL + NS group), (3) BDL rats administered with BIF (BDL + BIF group), and (4) BDL rats administered with FMT (BDL + FMT group). Following the establishment of the chronic HE model, we conducted sequential behavioral assessments, collected fecal samples, and performed micro-PET/CT scans. Data analysis included average %ID/g values across the whole brain and specific regions, alongside biochemical and pathological evaluations. No significant differences in behavioral results or levels of IL-1β, IL-6, IL-10, and TNF-α were found among the groups. While there was no significant difference in global brain uptake values of [[18]F]PBR146 among the four groups (p = 0.053), regional analyses showed significant discrepancies in areas such as the bilateral accumbens and retrosplenial cortex. The Sham + NS group was enriched with Parasutterella, Streptococcus, and Anaeroplasma, the BDL + FMT group had Enterococcus, Aestuariispira, Lactobacillus, Pseudomonas, and Globicatella, while the BDL + BIF group contained Enterorhabdus. Results indicated that BIF inhibited neuroinflammation in BDL rats, whereas FMT showed no positive effects, possibly due to dysbiosis. Notably, [[18]F]PBR146 could effectively and noninvasively monitor the efficacies of gut-targeted treatments in chronic HE models.},
}

Animals
*Fecal Microbiota Transplantation/methods
*Hepatic Encephalopathy/therapy/diagnostic imaging
Rats
Male
Positron Emission Tomography Computed Tomography
*Bifidobacterium
Rats, Sprague-Dawley
Brain/diagnostic imaging
*Neuroinflammatory Diseases/diagnostic imaging/therapy
Pyrimidines

@article {pmid40774824,
year = {2025},
author = {Lee, I and Kim, BS and Suk, KT and Lee, SS},
title = {Gut Microbiome-Based Strategies for the Control of Carbapenem-Resistant Enterobacteriaceae.},
journal = {Journal of microbiology and biotechnology},
volume = {35},
number = {},
pages = {e2406017},
doi = {10.4014/jmb.2406.06017},
pmid = {40774824},
issn = {1738-8872},
mesh = {*Gastrointestinal Microbiome/drug effects ; *Carbapenem-Resistant Enterobacteriaceae/drug effects/physiology ; Humans ; Fecal Microbiota Transplantation ; *Enterobacteriaceae Infections/prevention & control/microbiology/therapy ; Anti-Bacterial Agents/pharmacology/therapeutic use ; Animals ; Carbapenems/pharmacology ; Antimicrobial Stewardship ; },
abstract = {Carbapenem-resistant Enterobacteriaceae (CRE) represent a critical antimicrobial resistance threat due to their resistance to last-resort antibiotics and high transmission potential. While conventional strategies-such as infection control, antimicrobial stewardship, and novel antibiotic development-remain essential, growing attention has shifted toward the gut microbiome, which plays a central role in mediating colonization resistance against CRE. Disruption of the intestinal microbiota-primarily driven by antibiotic exposure and further exacerbated by non-antibiotic drugs such as proton pump inhibitors-reduces microbial diversity and impairs functional integrity, facilitating CRE acquisition, prolonged carriage, and horizontal transmission. In response, microbiome-based strategies-including microbiome disruption indices (MDIs), fecal microbiota transplantation (FMT), and rationally designed symbiotic microbial consortia-are being explored as novel approaches for CRE prevention and decolonization. Mechanistic studies have shown that colonization resistance is mediated by both direct mechanisms (e.g., nutrient competition, short-chain fatty acid production) and indirect mechanisms (e.g., immune modulation via IL-36 signaling). Advances in metagenomics, metabolomics, and culturomics have enabled high-resolution profiling of gut microbial communities and their functional roles. Emerging preclinical and clinical evidence supports the potential of microbiome-informed interventions to predict infection risk, enhance antimicrobial stewardship, and guide the development of next-generation probiotics targeting CRE. Longitudinal studies continue to evaluate the efficacy of FMT and synthetic microbial consortia in eradicating intestinal CRE colonization. Collectively, these insights underscore the promise of gut microbiome science as a complementary and innovative strategy for CRE control in the post-antibiotic era.},
}

*Gastrointestinal Microbiome/drug effects
*Carbapenem-Resistant Enterobacteriaceae/drug effects/physiology
Humans
Fecal Microbiota Transplantation
*Enterobacteriaceae Infections/prevention & control/microbiology/therapy
Anti-Bacterial Agents/pharmacology/therapeutic use
Animals
Carbapenems/pharmacology
Antimicrobial Stewardship

@article {pmid40774378,
year = {2025},
author = {Chatonidi, G and Rosseel, R and Dalile, B and Satriawan, D and Vandermeulen, G and Van Holm, B and Comer, L and Maes, P and Everaert, N and Courtin, CM and Verbeke, K},
title = {Effect of whole meal yeast-leavened, sourdough-leavened and yeast-sourdough-leavened bread consumption on appetite, energy intake, and postprandial metabolic responses: A randomized, blinded, cross-over study.},
journal = {Appetite},
volume = {},
number = {},
pages = {108256},
doi = {10.1016/j.appet.2025.108256},
pmid = {40774378},
issn = {1095-8304},
abstract = {Bread is a major source of carbohydrates in Europe, and whole meal varieties may offer better metabolic responses and increased satiety than white bread. We compared the effects of three types of whole meal bread: whole meal yeast bread (WYB), whole meal sourdough bread (WSB), and whole meal sourdough and yeast bread (WSYB), on appetite regulation and metabolic outcomes in healthy subjects. The sourdough contained Fructilactobacillus sanfranciscensis and Maudiozyma humilis, and the process time depended on the leavening agent. In this double-blind, randomized crossover trial, 44 participants (25 ± 4 years, BMI: 22 ± 2 kg/m[2]) consumed 180g/day of each bread type for two weeks, separated by a 2-week washout period. Habitual food intake was reported and a fecal sample was collected for microbiota analysis. During a study visit on the final day of each intervention period, participants consumed 100g of the test bread for breakfast. Oral processing, gastric emptying, and postprandial glucose, C-peptide, appetite and hormonal responses were measured. The primary outcome was ad-libitum energy intake at the subsequent lunch. Ad-libitum energy intake at lunch did not differ after consumption of the test breads. WYB and WSYB were consumed more slowly than WSB and led to slightly higher satiety (p < 0.05). Compared to the other breads, WSYB led to higher C-peptide levels, WYB resulted in greater PYY responses, and both WSB and WYB stimulated higher GLP-1 release (p < 0.05). In contrast, gastric emptying, glucose responses, ad-libitum energy intake, habitual energy intake, cholesterol, or gut microbiota composition did not differ between breads (p > 0.05). Despite the small metabolic differences, our findings suggest that whole meal bread with baker's yeast and/or sourdough had similar effects on appetite regulation.},
}

@article {pmid40774255,
year = {2025},
author = {Carr, AV and Baliga, NS and Diener, C and Gibbons, SM},
title = {Personalized Clostridioides difficile colonization risk prediction and probiotic therapy assessment in the human gut.},
journal = {Cell systems},
volume = {},
number = {},
pages = {101367},
doi = {10.1016/j.cels.2025.101367},
pmid = {40774255},
issn = {2405-4720},
abstract = {Clostridioides difficile (C. difficile) colonizes up to 40% of community-dwelling adults without causing disease but can eventually lead to infection (C. difficile infection [CDI]). There has been a lack of focus on how to prevent colonization and facilitate the successful clearance of C. difficile prior to the emergence of CDI. We show that microbial community-scale metabolic models (MCMMs) accurately predict C. difficile colonization susceptibility in vitro and in vivo, offering mechanistic insights into microbiota-specific interactions involving metabolites like succinate, trehalose, and ornithine. MCMMs reveal distinct C. difficile metabolic niches-two growth-associated and one non-growth-associated-observed across 15,204 individuals from five cohorts. We further demonstrate that MCMMs can predict personalized C. difficile growth suppression by a probiotic cocktail designed to replace fecal microbiota transplants (FMTs) for the treatment of recurrent CDI, and we identify new probiotic targets for future validation. MCMMs represent a powerful framework for predicting pathogen colonization and assessing probiotic efficacy across diverse microbiota contexts. A record of this paper's transparent peer review process is included in the supplemental information.},
}

@article {pmid40772940,
year = {2025},
author = {Ryan, K and Cunningham, A and Runde, J},
title = {Reaching for Remission: Integrating Complementary and Alternative Strategies into Inflammatory Bowel Disease Management.},
journal = {Pediatric annals},
volume = {54},
number = {8},
pages = {e274-e279},
doi = {10.3928/19382359-20250612-07},
pmid = {40772940},
issn = {1938-2359},
mesh = {Humans ; *Complementary Therapies/methods ; *Inflammatory Bowel Diseases/therapy ; Child ; Gastrointestinal Microbiome ; Probiotics/therapeutic use ; Remission Induction ; Fecal Microbiota Transplantation ; Mind-Body Therapies ; },
abstract = {Pediatric inflammatory bowel disease (IBD) is increasing in prevalence in the United States. While medical therapy options continue to expand, patients and their families often inquire about applications of complementary and alternative medicine (CAM). In this article, we review the existing literature for a wide variety of CAMs, including mind-body practices, modulation of the gut microbiome, and herbal supplements, which can be integrated into traditional medical treatments. Mind-body practices, particularly cognitive behavioral therapy, yoga, and acupuncture, have promising data for improved quality of life and potential for disease modification. Methods for gut microbiome modulation, such as probiotics and fecal microbiota transplant, have potential for modifying disease in IBD but need more studies evaluating safety and efficacy. Plant-based traditional remedies with anti-inflammatory properties, including curcumin and Indigo naturalis (Qing dai), have shown promising results in clinical trials demonstrating improvements in ulcerative colitis disease activity, although more pediatric trials are needed.},
}

Humans
*Complementary Therapies/methods
*Inflammatory Bowel Diseases/therapy
Child
Gastrointestinal Microbiome
Probiotics/therapeutic use
Remission Induction
Fecal Microbiota Transplantation
Mind-Body Therapies

@article {pmid40772261,
year = {2025},
author = {Pan, Z and Gao, Z and Chen, J and Quan, Y and Xu, J and Liang, X and Xie, W and He, X and Wu, L},
title = {Does constipation affect the effectiveness of washed microbiota transplantation in treating autism spectrum disorders?.},
journal = {Frontiers in neuroscience},
volume = {19},
number = {},
pages = {1602681},
pmid = {40772261},
issn = {1662-4548},
abstract = {PURPOSE: Washed microbiota transplantation (WMT) has been shown to improve the symptoms of Autism Spectrum Disorder (ASD). It's currently unclear whether the presence of constipation affects the efficacy of WMT in children with ASD. This study aims to investigate whether constipation affects the efficacy of WMT in children with ASD.

PATIENTS AND METHODS: To investigate the efficacy of WMT for ASD, we conducted a retrospective analysis of changes in ASD-related symptoms, sleep disturbances, gastrointestinal manifestations, intestinal barrier integrity, and gut microbiota composition in 103 ASD patients undergoing WMT. They were divided into two groups according to whether constipation was present or not before treatment.

RESULTS: 1. Aberrant Behavior Checklist (ABC), Childhood Autism Rating Scale (CARS), and Sleep Disturbance Scale for Children (SDSC) scores in the non-constipation and constipation groups decreased with an increase in the number of WMT treatments. 2. Comparison of two groups: ABC scores in the non-constipation group decreased more after the first WMT course, whereas ABC scores in the constipation group decreased more after two WMT courses. 3. Intestinal Barrier Function: D-lactate levels decreased more in the constipation group after the first two courses. In general, WMT treatment had no significant effect on intestinal barrier function in patients with ASD. 4. Effect of WMT on constipation: As the number of WMT courses increased, Bristol Stool Form Scale (BSFS) scores in constipation group gradually approached 4. 5. Constipation group had lower microbial diversity than non-constipation group at baseline. After one course of WMT, constipation group showed an obvious increase in microbial diversity and a significant increase in the relative abundance of Bifidobacteria compared to non-constipation group.

CONCLUSION: Post WMT, core symptoms and sleep disorders were significantly improved in both groups. Feces returned to normal shape in the constipation group. A difference in efficacy between the two groups was observed in early stages, but after multiple courses of WMT no difference in efficacy was noted. Although in the short-term, children with ASD and comorbid constipation showed a significant increase in microbial diversity after receiving WMT, mid-term outcomes indicate that constipation does not affect the efficacy of WMT in treating ASD.},
}

@article {pmid40771816,
year = {2025},
author = {Ma, J and Fang, Y and Hu, J and Li, S and Zeng, L and Chen, S and Li, Z and Meng, R and Yang, X and Zhang, F and Ji, G and Liao, P and Chen, L and Wu, W},
title = {Innovative microbial strategies in atopic dermatitis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1605434},
pmid = {40771816},
issn = {1664-3224},
mesh = {Humans ; *Dermatitis, Atopic/therapy/microbiology/immunology ; Fecal Microbiota Transplantation/methods ; Probiotics/therapeutic use ; Animals ; *Gastrointestinal Microbiome/immunology ; Prebiotics/administration & dosage ; Dysbiosis/therapy ; *Microbiota ; },
abstract = {Atopic dermatitis (AD) is characterized by chronic and recurrent itching with a high burden of disability-adjusted life years (DALYs, a measure of overall disease burden). Traditional treatments mainly include corticosteroids, which have a good effect on controlling inflammation but adverse side effects. Recently, advancements in understanding the pathogenesis of AD have led to the emergence of a variety of novel therapeutic approaches, such as microbiome manipulation, offering renewed hope for more effective management of this condition. These strategies are particularly promising for mild-to-moderate AD, where dysbiosis and immune imbalance (e.g., Th2 skewing) are key drivers, though some approaches (e.g., fecal microbiota transplantation) are being explored for refractory cases. It has been shown that microbiome manipulation has the potential to improve disease states and regulates the balance of the inflammatory system in a variety of ways. Various approaches have been preclinically and clinically tested, including probiotics (and multiple co-applications), prebiotics, postbiotics, unmethylated CpG motifs, fecal microbiota transplantation, herbal fermentation technology with microorganisms and phage. In this review, we discuss these microbiome manipulation methods and emphasizes the potential of microbiome-based interventions to modulate Th1/Th2 balance with fewer side effects, ultimately leading to control of inflammation in AD. Further translational research in this field is needed to integrate when we apply this therapy and the capability for disease treatment and prevention.},
}

Humans
*Dermatitis, Atopic/therapy/microbiology/immunology
Fecal Microbiota Transplantation/methods
Probiotics/therapeutic use
Animals
*Gastrointestinal Microbiome/immunology
Prebiotics/administration & dosage
Dysbiosis/therapy
*Microbiota

@article {pmid40771692,
year = {2025},
author = {Cao, Q and Yang, M and Chen, M},
title = {Metabolic interactions: how gut microbial metabolites influence colorectal cancer.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1611698},
pmid = {40771692},
issn = {1664-302X},
abstract = {Colorectal cancer (CRC) is a growing public health concern due to its rising incidence and high rate of cancer-associated deaths. Emerging evidence suggests that gut microbiota and their metabolites are critically involved in the initiation and advancement of CRC. These metabolites, which originate from the breakdown of nutrients from food and host-related substances through microbial activity in the gut, can profoundly influence tumor formation. In addition to well-studied compounds such as short-chain fatty acids (SCFAs), bile acids (BAs), tryptophan metabolites, and polyamines, this review highlights emerging metabolites-including hydrogen sulfide (H2S) and formate-that have recently drawn attention for their roles in colorectal carcinogenesis. We also incorporate recent mechanistic insights, such as butyrate-induced ferroptosis and H2S-mediated protein persulfidation, to illustrate how microbial metabolites influence cancer cell metabolism. Moreover, the potential of microbial metabolites as biomarkers for early diagnosis and prognosis of CRC is discussed. Therapeutic strategies targeting microbial metabolites-such as dietary modulation, combination therapies, fecal microbiota transplantation (FMT), and phage therapy-are also reviewed. By providing a comprehensive and up-to-date overview of microbial metabolic networks associated with CRC, this review underscores the critical functions of gut microbial metabolites in tumorigenesis, offering novel insights into their utility as diagnostic and prognostic biomarkers, as well as promising therapeutic targets.},
}

@article {pmid40771615,
year = {2025},
author = {Safdar, N},
title = {PREVENTION OF HEALTH CARE-ASSOCIATED INFECTIONS IN U.S. HEALTH SYSTEMS: HARNESSING THE GUT MICROBIOME TO COMBAT INFECTION.},
journal = {Transactions of the American Clinical and Climatological Association},
volume = {135},
number = {},
pages = {260-268},
pmid = {40771615},
issn = {0065-7778},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *Fecal Microbiota Transplantation ; United States/epidemiology ; *Clostridium Infections/prevention & control/microbiology/therapy ; *Clostridioides difficile/pathogenicity ; *Cross Infection/prevention & control/microbiology/epidemiology ; Anti-Bacterial Agents/adverse effects/therapeutic use ; },
abstract = {Health care-associated infections (HAIs) remain a major challenge in the U.S. health care system, with Clostridioides difficile (C. difficile or C. diff) being the most prevalent. The use of antibiotics disrupts the gut microbiota, predisposing individuals to infection. Recent research has highlighted the role of the gut microbiome in preventing and treating C. difficile infections (CDI). Strategies such as fecal microbiota transplantation (FMT) and live biotherapeutic products (LBPs) offer promising alternatives to conventional antibiotic treatments. This paper explores the mechanisms underlying CDI, the role of the gut microbiome in infection prevention, and innovative therapeutic approaches.},
}

Humans
*Gastrointestinal Microbiome/drug effects
*Fecal Microbiota Transplantation
United States/epidemiology
*Clostridium Infections/prevention & control/microbiology/therapy
*Clostridioides difficile/pathogenicity
*Cross Infection/prevention & control/microbiology/epidemiology
Anti-Bacterial Agents/adverse effects/therapeutic use

@article {pmid40770861,
year = {2025},
author = {Drobnik, J and Pobrotyn, P and Grata-Borkowska, U and Madziarska, K and Baran, M},
title = {Trends and Efficacy in Clostridioides difficile Infection Management at a Polish Clinical Hospital.},
journal = {Medical science monitor : international medical journal of experimental and clinical research},
volume = {31},
number = {},
pages = {e948254},
doi = {10.12659/MSM.948254},
pmid = {40770861},
issn = {1643-3750},
mesh = {Humans ; *Clostridium Infections/drug therapy/epidemiology ; Poland/epidemiology ; Male ; Female ; Vancomycin/therapeutic use ; *Clostridioides difficile/drug effects/pathogenicity ; Middle Aged ; Fidaxomicin/therapeutic use ; Aged ; Anti-Bacterial Agents/therapeutic use ; Metronidazole/therapeutic use ; Treatment Outcome ; Adult ; Hospitalization ; Aged, 80 and over ; Retrospective Studies ; Drug Therapy, Combination ; },
abstract = {BACKGROUND Clostridioides difficile infection (CDI) is a significant clinical problem. Treatment includes fidaxomicin and vancomycin, with second and subsequent recurrences treated with decreasing doses or sequential therapy with rifaximin, as well as considering treatment with a fecal transplant. This study aimed to analyze the method of treatment of CDI among patients hospitalized at the University Clinical Hospital in Wrocław (Poland). MATERIAL AND METHODS The study was conducted by analyzing medical records from 316 patients treated between 2016 and 2018. Due to the limited number of patients treated with fidaxomicin and rifaximin per year, these cases were combined for analysis when exploring the relationship between the year of hospitalization and CDI treatment. Patients spanning the turn of the year were assigned to the year with a longer hospitalization duration for a more robust analysis. RESULTS The predominant treatments for CDI were metronidazole and vancomycin in combination (40.5%), metronidazole alone (26.9%), and vancomycin alone (20.6%). Fidaxomicin was rarely used (1.6%) despite its 100% effectiveness. Although administered to only 5 patients, fidaxomicin achieved a 100% cure rate, highlighting its therapeutic promise. Treatment patterns shifted over the study period, but no significant difference in mortality was observed between years (P=0.904). Overall mortality among CDI patients was 24.7%, compared to 1.52% in the general inpatient population. Patients who died were more likely to have received metronidazole + vancomycin (P=0.009). CONCLUSIONS The mortality rate among CDI patients was notably high. Use of metronidazole alone decreased while alternative therapies (rifaximin, fidaxomicin) increased, but without impacting year-to-year mortality differences. Given its 100% cure rate in our cohort, broader use of fidaxomicin could meaningfully improve patient outcomes.},
}

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

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

@article {pmid40768832,
year = {2025},
author = {Cintado, E and Muela, P and Martín-Rodríguez, L and Alcaide, I and Tezanos, P and Vlckova, K and Valderrama, B and Bastiaanssen, TFS and Rodríguez-Muñoz, M and de Ceballos, ML and Aburto, MR and Cryan, JF and Trejo, JL},
title = {Gut microbiota regulates exercise-induced hormetic modulation of cognitive function.},
journal = {EBioMedicine},
volume = {119},
number = {},
pages = {105876},
doi = {10.1016/j.ebiom.2025.105876},
pmid = {40768832},
issn = {2352-3964},
abstract = {BACKGROUND: Lifestyle factors, particularly physical exercise, significantly influence brain structure and cognitive function through a hormetic effect -a phenomenon where low to moderate doses of a stimulus (in this case, exercise) induce beneficial adaptations, while excessive doses could lead to detrimental effects. This effect depends on exercise intensity and duration, though the underlying mechanisms remain largely unexplored. Recently, the gut microbiota has emerged as potent modulator of lifestyle-induced changes in brain and behaviour.

METHODS: We used a 40-min, 1200 cm/min exercise protocol. We measured cognition through several tests and analysed microbiota composition comparing adult exercised animals to sedentary controls. Finally, we performed fecal microbiota transplantation from exercised to sedentary mice.

FINDINGS: Exercise enhances cognitive abilities related to object recognition and object location memory, as well as increases hippocampal neurogenesis. However, these cognitive and neurogenic benefits vanish when the exercise intensity or duration is increased. Furthermore, we identified significant changes in alpha and beta diversity and distinct bacteria composition profiles in the gut microbiota associated with different exercise regimens. Specific bacterial families showed altered relative abundances depending on exercise intensity and duration, with certain families' quantities significantly correlating with cognitive performance (Angelakisella, Acetatifactor, Erysipelatoclostridium, and Coriobacteriaceae UCG-002.). To explore causal mechanisms, we performed fecal microbiota transplantation from exercised to sedentary mice, which replicated the cognitive and neurogenic changes observed in the donor animals.

INTERPRETATION: These findings suggest that the hormetic effects of physical exercise on cognitive function and neurogenesis are mediated by corresponding changes in the gut microbiota, highlighting a novel mechanistic link between exercise, brain function, and gut microbiota composition.

FUNDING: E.C. and P.M. were funded by predoctoral fellowship (FPI) grants from the Spanish Ministry of Economy and Competitiveness (BES-2017/080415 E.C.) and the Spanish Ministry of Science and Innovation (PRE2020/093032 P.M.), and P.T. by a predoctoral fellowship (FPU) from the Spanish Ministry of Universities (18/00069). Work was supported by project grants PID2019-110292RB-100 and PID2022-136891NB-I00 (from Spanish Ministry of Science and Innovation), (to J.L.T.).},
}

@article {pmid40768805,
year = {2025},
author = {Chen, J and Zhang, L and Chen, Y and Yan, Y and Lu, C},
title = {Alpha-tocopheryl quinone attenuates liver fibrosis through enriching Christensenella minuta and modulating bile acids metabolism via gut-liver axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {146},
number = {},
pages = {157108},
doi = {10.1016/j.phymed.2025.157108},
pmid = {40768805},
issn = {1618-095X},
abstract = {BACKGROUND: Liver fibrosis, characterized by the progressive accumulation of excessive extracellular matrix (ECM), remains a major global health issue with limited treatment options. The gut-liver axis, particularly the dynamics of gut microbiota and bile acids (BAs), plays a pivotal role in modulating hepatic fibrogenesis. Alpha-tocopheryl quinone (TQ), a vitamin E metabolite, exhibits antioxidative and anti-inflammatory properties; however, its impact on liver fibrosis remains unexplored.

METHODS: A murine fibrosis model was induced using carbon tetrachloride (CCl4), coupled with gut microbiota depletion via antibiotic cocktail (Abx) and fecal microbiota transplantation (FMT) from cirrhotic donors, to evaluate TQ's therapeutic effects. Biochemical and histological analyses assessed liver injury and fibrosis, while 16S rRNA sequencing determined gut microbiota composition. BAs profiles were quantified using LC-MS/MS. Glycine-β-muricholic acid (Gly-MCA), a gut-restricted farnesoid X receptor (FXR) antagonist, was employed for investigating mechanistic pathways.

RESULTS: TQ treatment significantly alleviated liver damage and fibrosis in CCl4-treated mice, with a notable reshaping of the gut microbiota, particularly an increased abundance of Christensenella minuta (C. minuta). Mechanistically, TQ activated the intestinal FXR/FGF15 pathway, resulted in reduced hepatic BAs synthesis and enhanced fecal excretion. Abx and FMT experiments confirmed the microbiota-dependent antifibrotic effects of TQ, with C. minuta identified as a key mediator. Co-treatment with Gly-MCA abrogated the protective effects of C. minuta, highlighting the critical role of intestinal FXR signaling.

CONCLUSIONS: TQ attenuates liver fibrosis via modulation of gut microbiota, particularly enriching C. minuta abundance, and regulating BAs metabolism via activation of the intestinal FXR/FGF15 axis. These results establish TQ as a promising therapeutic targeting the gut-liver axis, with C. minuta identified as a pivotal mediator in BAs metabolism and fibrotic resolution. This study lays the groundwork for microbiota-centered therapeutic strategies against hepatic fibrosis.},
}

@article {pmid40767874,
year = {2025},
author = {Sadhu, S and Paul, T and Yadav, N},
title = {Therapeutic engineering of the gut microbiome using synthetic biology and metabolic tools: a comprehensive review with E. coli Nissle 1917 as a model case study.},
journal = {Archives of microbiology},
volume = {207},
number = {9},
pages = {213},
pmid = {40767874},
issn = {1432-072X},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Escherichia coli/genetics/metabolism/enzymology ; *Metabolic Engineering/methods ; *Synthetic Biology/methods ; Probiotics/therapeutic use ; Phenylalanine Ammonia-Lyase/genetics/metabolism ; Phenylketonurias/therapy ; },
abstract = {The human gut microbiome significantly influences host physiology, metabolism, and immune function. The engineering of microbial communities represents a significant advancement in contemporary biotechnology. Conventional methods, including Fecal Microbiota Transplantation (FMT) and probiotic administration, exhibit limitations in efficacy and raise safety and reproducibility concerns; however, they have shown potential therapeutic benefits. Recent progress in biocatalysis and metabolic engineering has led to the development of genetically tractable gut bacteria for targeted therapeutic purposes, particularly in the last five years. This chapter offers an overview of the development of microbiota-based interventions, from early recombinant probiotics to advanced synthetic biology platforms that can detect and respond to host and environmental signals. This analysis examines the mechanistic aspects of enzyme engineering, including improvements in metabolic pathways for the production of short-chain fatty acids, the breakdown of harmful metabolites, and the biosynthesis of immunomodulatory compounds. This review also examines conditions including inflammatory bowel disease, metabolic dysfunction, and colorectal cancer, highlighting microbial production systems pertinent to gut health. The engineering of Escherichia coli Nissle 1917 to produce phenylalanine ammonia-lyase (PAL) and L-amino acid deaminase (LAAD) represents a significant advancement in gut-based metabolic intervention for patients with phenylketonuria (PKU) by degrading excess phenylalanine. Recent studies offer peer-reviewed evidence supporting the translational potential of these inventions, as demonstrated through figures and tables highlighting engineered metabolic circuits, therapeutic outputs, and strain performance metrics. This combination of developments demonstrates the potential of synthetic microbiome engineering to provide precision biotherapeutics for various gut-related conditions.},
}

*Gastrointestinal Microbiome
Humans
*Escherichia coli/genetics/metabolism/enzymology
*Metabolic Engineering/methods
*Synthetic Biology/methods
Probiotics/therapeutic use
Phenylalanine Ammonia-Lyase/genetics/metabolism
Phenylketonurias/therapy

@article {pmid40766454,
year = {2025},
author = {Liow, YJ and Eshima, S and Talay, M and Yeliseyev, V and Bry, L and Carmody, RN},
title = {Polyunsaturated fatty acids promote appetite via the microbiome-gut-brain axis.},
journal = {bioRxiv : the preprint server for biology},
volume = {},
number = {},
pages = {},
doi = {10.1101/2025.07.29.667447},
pmid = {40766454},
issn = {2692-8205},
abstract = {UNLABELLED: Appetite is regulated by nutrient-sensing systems that integrate long-term signals from energy stores and short-term cues from dietary intake, yet this regulation is increasingly disrupted by industrialized diets. Although the physiological effects of industrialized diets are well documented, the continued rise in metabolic and eating disorders underscores a critical gap in our understanding of how these diets shape neural regulation of eating behavior. Here, we tested how distinct properties of industrialized diets alter brain neurochemistry and change appetite. We probed the properties of an industrialized diet through contrasts targeting the overall diet pattern (Western vs. control), enriched macronutrients (fat vs. sugar), and isocaloric trade-offs of macronutrient variants (saturated fatty acids vs. polyunsaturated fatty acids [PUFA]). The most salient effects emerged from the finest-grained contrast: PUFA conditioning increased appetite through a mechanism involving elevated brain 5-hydroxyindoleacetic acid (5-HIAA), a primary serotonin catabolite associated with the gut microbiome. Fecal microbiota transplants into germ-free mice confirmed that the PUFA-conditioned gut microbiota carries an appetite-enhancing signature. Together, our findings delineate a diet-microbiome-gut-brain axis through which dietary components of industrialized diets can modulate appetite and contribute to altered eating behavior.

ONE SENTENCE SUMMARY: Dietary polyunsaturated fatty acids enhance appetite via a gut microbiome-serotonergic pathway.},
}

@article {pmid40762371,
year = {2025},
author = {Li, X and Chen, Y and Gao, Z and Liu, X and Song, Z and Gao, F and Wang, S and Yu, C and Sun, L and Huang, Y and Zheng, L and Wang, G and Sun, Y and Li, J and Yang, X and Bao, Y},
title = {TSP50 in Neural Stem Cells Regulates Aging-Related Cognitive Decline and Neuroinflammation by Altering the Gut Microbiota.},
journal = {Aging cell},
volume = {},
number = {},
pages = {e70188},
doi = {10.1111/acel.70188},
pmid = {40762371},
issn = {1474-9726},
support = {GZC20240236//Postdoctoral Fellowship Program of CPSF/ ; 20230204067YY//the Science and Technology Development Program of Jilin Province/ ; 135131002//Fundamental Research Funds for the Central Universities/ ; },
abstract = {Aging is a process of gradual decline in physical and cognitive function and is a major risk factor for mortality. Despite the increasing number of relevant studies, the mechanisms regulating the aging process have not been fully elucidated. Genetic factors have long been recognized as key factors in controlling the rate of aging. Testes-specific protease 50 (TSP50) has been shown to be involved in the regulation of embryonic development and intestinal homeostasis, but its role in the regulation of aging remains unclear. Here, we showed that TSP50 expression was reduced in the hippocampus of both aged humans and mice. TSP50 deficiency in neural stem cells (NSCs) drove accelerated aging in mice, characterized by exacerbated age-related cognitive impairments and significantly elevated neuroinflammation. Notably, aged mice with NSCs-specific knockout of TSP50 exhibited impaired intestinal mucosal barriers, dysbiosis of gut microbiota, and a marked reduction in the production of short-chain fatty acids (SCFAs). Restoring gut microbial ecology using fecal microbiota transplantation (FMT) and overexpressing TSP50 successfully alleviated aging-associated cognitive decline and neuroinflammation. Taken together, our study suggests that TSP50 plays a critical role in the aging process and identifies gut microbiota as a pivotal mediator of TSP50's influence on age-related cognitive decline and neuroinflammation. These findings highlight the potential therapeutic value of targeting TSP50 and gut microbiota for aging, offering insights into aging mechanisms and interventions for aging-related neurodegenerative diseases.},
}

@article {pmid40760849,
year = {2025},
author = {Gong, H and Zhang, L and Liu, Y and Yuan, X and Liu, Y and Tang, J and Zhou, M and Song, J and Zhang, T},
title = {Oxidative Stress and Gut Microbiota Interplay Exacerbates Periodontitis in Diabetic Mice.},
journal = {Journal of clinical periodontology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jcpe.70003},
pmid = {40760849},
issn = {1600-051X},
support = {82170968//National Natural Science Foundation of China/ ; U22A20314//National Natural Science Foundation of China/ ; 2022YFC2504200//National Key Research and Development Program of China/ ; YXQN202401//Chongqing Municipal Youth Science and Technology Talent Training Project/ ; },
abstract = {AIM: To investigate the interplay between oxidative stress and gut microbiota in the pathogenesis of increased periodontitis in diabetic mice and explore potential therapeutic strategies.

MATERIALS AND METHODS: Diabetic periodontitis (DP) mouse models were established and subjected to interventions including antioxidant treatment, co-housing experiments and faecal microbiota transplantation (FMT). Alveolar bone loss, periodontal inflammation, oxidative stress markers, gut microbiota composition and intestinal barrier function were evaluated.

RESULTS: Diabetes exacerbated alveolar bone loss and inflammation markers in mice with periodontitis. DP mice exhibited significantly elevated systemic oxidative stress and gut dysbiosis compared to controls. Curcumin treatment effectively improved these parameters. Co-housing experiments between curcumin-treated and untreated DP mice showed that beneficial gut microbiota could be transferred between cage mates, leading to improved periodontal outcomes in untreated mice. Additionally, FMT from healthy donors reduced alveolar bone loss and periodontal inflammatory markers while improving oxidative stress parameters and restoring gut microbiota balance and barrier function.

CONCLUSIONS: This study demonstrates that the interaction between oxidative stress and gut dysbiosis may form a pathogenic loop associated with the exacerbation of periodontitis in diabetic conditions. The successful outcomes of antioxidant treatment and FMT suggest multiple adjunctive therapeutic approaches for managing DP.},
}

@article {pmid40759593,
year = {2025},
author = {Kwon, WA and Kim, H and Song, YS},
title = {Prostate Cancer at the Microbial Crossroads: Illuminating a New Frontier in Precision Medicine.},
journal = {The world journal of men's health},
volume = {},
number = {},
pages = {},
doi = {10.5534/wjmh.250045},
pmid = {40759593},
issn = {2287-4208},
abstract = {The human body harbors a complex, dynamic community of trillions of microbes, collectively termed the microbiota, which profoundly affects homeostasis and disease processes, including cancer. Prostate cancer remains a major cause of morbidity and mortality among men worldwide; however, critical questions remain regarding its etiology, progression, and resistance to therapy. Multiple epidemiological studies have found associations between certain urinary and intestinal microorganisms and an increased prostate cancer risk, although the causal mechanisms remain incompletely understood. Recent studies suggest that dysregulated microbial communities, or dysbiosis, are hypothesized to drive chronic inflammation, induce genotoxic insults, and modulate steroid metabolism, thereby influencing tumor initiation and progression. Conflicting findings across different investigations often stem from heterogeneous sampling methods, population differences, and disparate bioinformat ics pipelines, underscoring the critical need for standardized protocols and reproducible data analytics. For example, diet induced alterations in the gut microbiota can shift systemic inflammatory and hormonal pathways in ways that predispose individuals to malignant transformation. Simultaneously, prostatic and urinary microbes are hypothesized to fuel local inflam mation and promote precursor lesions, although whether this microbial activity is causative or merely reflective of the exist ing tumor biology remains a key unresolved question. Microbiota-driven mechanisms also shape responses to radiotherapy, chemotherapy, and emerging immunotherapies, highlighting the potential of interventions such as probiotics, prebiotics, and fecal microbiota transplantation to enhance treatment efficacy and mitigate side effects. Innovative approaches, including ar tificial intelligence-assisted predictive modeling, CRISPR (Clustered Regularly Interspaced Short Palindromic Repeats)-based microbial gene editing, and immunomodulatory strategies (e.g., chimeric antigen receptor-T cells), offer new avenues for exploiting microbiota for therapeutic benefits. Nevertheless, unresolved questions regarding the long-term safety, ecological balance, and individual patient factors require caution. By integrating rigorous methodologies with these novel technologies, prostate cancer research may ultimately harness microbial insights to refine diagnostic tools, personalize therapies, and im prove patient outcomes.},
}

@article {pmid40522093,
year = {2025},
author = {Dolo, O and Coulibaly, F and Somboro, AM and Sun, S and Diarra, M and Maiga, A and Bore, S and Fofana, DB and Marcelin, A-G and Diakite, B and Kassogue, Y and Holl, JL and Calvez, V and Traoré, CB and Murphy, R and Fodor, AA and Maiga, M and Maiga, AI},
title = {The human gut microbiome and its metabolic pathway dynamics before and during HIV antiretroviral therapy.},
journal = {Microbiology spectrum},
volume = {13},
number = {8},
pages = {e0220524},
pmid = {40522093},
issn = {2165-0497},
mesh = {Humans ; *Gastrointestinal Microbiome/drug effects ; *HIV Infections/drug therapy/microbiology ; *Dysbiosis/microbiology ; *Metabolic Networks and Pathways ; Male ; Adult ; Female ; Middle Aged ; *Bacteria/classification/genetics/metabolism/isolation & purification ; *Anti-HIV Agents/therapeutic use ; Feces/microbiology ; *Anti-Retroviral Agents/therapeutic use ; Whole Genome Sequencing ; },
abstract = {The human gut microbiome consists of highly complex microbial populations that play important roles in disease pathogenesis. Changes in the gut microbiome are associated with HIV infection. However, it is unclear whether gut microbiome dysbiosis is causally linked to disease or whether it simply reflects disease-induced changes in the host immune and metabolic systems. This study aims to describe and compare intestinal microbial compositions and derived metabolic pathways in people living with HIV (PL-HIV) from prior to antiretroviral therapy (ART) to 6 and 12 months after ART initiation, compared to HIV-negative individuals. Whole-genome microbiome sequencing coupled with bioinformatics analysis was used to characterize participants' intestinal microbial structures and derived metabolic pathways. Pre- and post-ART gut microbiota characterization of PL-HIV revealed substantial dysbiosis compared to HIV-negative people. An enrichment of pro-inflammatory microorganisms was the hallmark of dysbiosis in the PL-HIV pre-ART, with a decline in Proteobacteria at 6 months of ART, continuing until 12 months of ART. Lower proportions of Bacteroidetes were noted pre-ART, but they increased slightly at 6 months of ART before decreasing again at 12 months of ART. Additionally, we reported metabolic changes that are particularly important for health and are associated with dysbiosis both before and post-ART. Alteration of the pyruvate fermentation to the isobutanol metabolic pathway persisted in PL-HIV after 12 months of ART, and this mechanism was correlated with a decrease in Ruminococcus bromii species. ART initiation appears to lead to changes in several crucial metabolic pathways and may not entirely restore the dysbiosis of the gut microbiota caused by HIV.IMPORTANCEResearchers are facing a major challenge in the treatment of HIV infection due to the continuous use of antiretroviral (ARV) molecules. However, regularly monitoring these molecules is necessary because they are not without consequences. They have toxicity and side effects and could also destabilize the intestinal microbiota, which could harm the metabolic pathways essential to good health. This study reveals that ARV treatment only partially restores gut microbiota dysbiosis and alters metabolic pathways due to pathogenic taxa. This provides additional insights into the relationship between antiretroviral therapy and the microbiome, potentially leading to new prevention and treatment strategies such as probiotic/prebiotic or microbiota transplants.},
}

Humans
*Gastrointestinal Microbiome/drug effects
*HIV Infections/drug therapy/microbiology
*Dysbiosis/microbiology
*Metabolic Networks and Pathways
Male
Adult
Female
Middle Aged
*Bacteria/classification/genetics/metabolism/isolation & purification
*Anti-HIV Agents/therapeutic use
Feces/microbiology
*Anti-Retroviral Agents/therapeutic use
Whole Genome Sequencing

@article {pmid40759441,
year = {2025},
author = {Hadi, DK and Baines, KJ and Jabbarizadeh, B and Miller, WH and Jamal, R and Ernst, S and Logan, D and Belanger, K and Esfahani, K and Elkrief, A and Parvathy, SN and Silverman, MS and Routy, B and Maleki Vareki, S and Lenehan, JG},
title = {Improved survival in advanced melanoma patients treated with fecal microbiota transplantation using healthy donor stool in combination with anti-PD1: final results of the MIMic phase 1 trial.},
journal = {Journal for immunotherapy of cancer},
volume = {13},
number = {8},
pages = {},
doi = {10.1136/jitc-2025-012659},
pmid = {40759441},
issn = {2051-1426},
mesh = {Humans ; *Melanoma/therapy/mortality/pathology ; *Fecal Microbiota Transplantation/methods ; Male ; Female ; Middle Aged ; Aged ; Adult ; *Immune Checkpoint Inhibitors/therapeutic use/pharmacology ; *Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Combined Modality Therapy ; },
abstract = {BackgroundMicrobiome manipulation research is focused on developing techniques to modify the gut microbiome and augment responses to immune checkpoint inhibitors (ICI). Fecal microbiota transplantation (FMT) represents a potential strategy to overcome primary or acquired resistance to ICI. 20 patients with advanced melanoma were enrolled in a phase I multicenter trial to evaluate the safety and response to anti-PD1 combined with FMT using healthy donor stool as first-line treatment (MIMic, NCT03772899). Combination therapy was safe, and the objective response rate (ORR) was 65%. We now report survival data based on over 3 years of follow-up. Patients with advanced melanoma and treatment-naïve for advanced disease received a single FMT with healthy donor stool followed by standard anti-PD1 therapy. Progression-free survival (PFS) and overall survival (OS) were measured from the date of FMT to event. Radiographic response was measured using RECIST 1.1 criteria. Both median PFS (mPFS) and median OS (mOS) were determined using the Kaplan-Meier method. Post hoc analyses assessed the impact of specific factors on survival outcomes. Minimum follow-up was 40 months from the date of FMT of the last patient, with the longest surviving patient in complete response at 62.2 months. At the time of data analysis, eight patients were alive and seven patients were without progression. No patients remain on anti-PD1 therapy. Only two patients received additional lines of therapy. The mPFS was 29.6 months and mOS 52.8 months. The 1, 2, and 3 years estimated survival rates were 95%, 74% and 53%, respectively. Post hoc analysis demonstrated significantly improved mPFS in responders and patients with FMT-specific toxicity. Combining first-line anti-PD1 therapy and oral FMT with healthy donor stool in this small cohort was safe and demonstrated an improvement in ORR, mPFS, and mOS, compared with randomized trials. Our sample size was small, and results were only hypothesis generating. The potential benefit of microbiome manipulation using oral FMT from healthy donors prior to ICI in patients with advanced melanoma will be evaluated in the ME.17 randomized phase 2 Canadian study (NCT06623461).},
}

Humans
*Melanoma/therapy/mortality/pathology
*Fecal Microbiota Transplantation/methods
Male
Female
Middle Aged
Aged
Adult
*Immune Checkpoint Inhibitors/therapeutic use/pharmacology
*Programmed Cell Death 1 Receptor/antagonists & inhibitors
Combined Modality Therapy

@article {pmid40759431,
year = {2025},
author = {Yao, Y and Cai, X and He, D and Zheng, Y and Liu, M and Zhang, M and Li, Z and Fei, W and Zheng, C},
title = {Short-chain fatty acids regulate T cell heterogeneity to alleviate recurrent spontaneous abortion.},
journal = {British journal of pharmacology},
volume = {},
number = {},
pages = {},
doi = {10.1111/bph.70155},
pmid = {40759431},
issn = {1476-5381},
support = {LHDMZ23H190002//Huadong Medicine Joint Funds of the Zhejiang Provincial Natural Science Foundation of China/ ; },
abstract = {BACKGROUND AND PURPOSE: The aetiology of recurrent spontaneous abortion (RSA) is multifactorial, with immune factors playing a critical role. Gut microbiota and its metabolites have been found to participate in host immune regulation. This study explores the role of gut microbiota-derived short-chain fatty acids (SCFAs) in immune tolerance in RSA.

EXPERIMENTAL APPROACH: Single-cell sequencing was used to analyse the cell profile of RSA patients. 16S rDNA sequencing was used to analyse the gut microbiota structure. Faecal microbiota transplantation (FMT) was used to explore the role of the gut microbiota in immune-related RSA in mice. SCFAs supplementation was used to explore the role of SCFAs in immune-related RSA mice. Conventional molecular biology methods were used to explore molecular mechanisms.

KEY RESULTS: The peripheral immune cell profile of RSA patients was altered. The gut microbiota structure of RSA patients was also altered, with a decrease in their SCFA levels. FMT significantly improved pregnancy outcomes in immune-related RSA in mice. SCFAs affected the differentiation of peripheral CD4[+] T cells and the expression of marker genes. SCFA supplementation altered the gut microbiota structure in immune-related RSA mice and improved colonic barrier function. SCFAs regulate CD4[+] T cell differentiation by targeting GPR43. Finally, the colon-targeted SCFA delivery nanoparticle system that we designed optimised the therapeutic effects of SCFAs.

CONCLUSION AND IMPLICATIONS: Gut microbiota-derived SCFAs regulate T cell heterogeneity to alleviate RSA. The findings of this study increase the understanding of maternal-fetal immune tolerance mechanisms and provide new insights for future therapeutic strategies for RSA.},
}

@article {pmid40759389,
year = {2025},
author = {Berry, P and Tariq, R and Pardi, D and Khanna, S},
title = {Effectiveness and Safety of Fecal Microbiota Transplantation for Recurrent Clostridioides difficile Infection in Immunocompromised Patients.},
journal = {Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cgh.2025.06.043},
pmid = {40759389},
issn = {1542-7714},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) poses a significant health risk to immunocompromised hosts due to the increased risk of severe infection and recurrence. Microbiota-based therapies have emerged as a promising strategy for CDI, but safety and efficacy in immunocompromised populations remain underexplored.

METHODS: A comprehensive literature search across Ovid MEDLINE(R), Ovid EMBASE, Clinicaltrials.gov, and Scopus from inception until December 16, 2024, identified studies meeting inclusion criteria, covering fecal microbiota transplantation (FMT) for recurrent CDI (rCDI) in immunocompromised individuals, including those on immunosuppressants, transplant recipients, undergoing chemotherapy, and with advanced HIV. Case reports and studies not separately reporting outcomes in immunocompromised patients were excluded. Statistical analysis was performed using random-effects models to account for heterogeneity among studies.

RESULTS: A total of 44 studies (31 full-text articles, 13 abstracts) were included, comprising 3,476 participants, of whom 1,208 were immunocompromised. The population included solid organ transplant recipients (n=219), cancer patients on chemotherapy (n=101), hematopoietic stem cell transplant recipients (n=29), and advanced HIV patients (n=11). The most common FMT route was colonoscopy (n=12 studies), followed by upper gastrointestinal routes, capsules, and rectal retention enemas. The clinical resolution rate after a single FMT was 75.3% (95% CI 71.7%-78.6%), increasing to 87.4% (95% CI 84.8%-89.6%) with consecutive treatments. The recurrence rate was 23.9% (95% CI 19.2%-29.4%), and the serious adverse event rate was 10.1% (95% CI 6.7%-14.8%).

CONCLUSIONS: The safety and effectiveness outcomes of FMT in mild to moderately immunocompromised populations for recurrent CDI are comparable to those in immunocompetent cohorts.},
}

@article {pmid40755720,
year = {2025},
author = {Bi, Y and Cheng, B and Zou, B and Liu, S and Cui, Z},
title = {The current landscape of fecal microbiota transplantation in treating inflammatory bowel disease.},
journal = {Translational gastroenterology and hepatology},
volume = {10},
number = {},
pages = {55},
pmid = {40755720},
issn = {2415-1289},
abstract = {Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn's disease (CD), is a chronic, immune-mediated disorder that impacts the intestinal tract. The gut microbiota, a diverse community of microorganisms, plays a pivotal role in the initiation, development, and progression of IBD by modulating inflammation, and immune responses, and maintaining gut homeostasis. Dysbiosis, or an imbalance in the gut microbiota, is frequently observed in IBD patients and is believed to contribute to the pathogenesis of the disease by disrupting the mucosal immune system. Fecal microbiota transplantation (FMT) involves transferring feces from a healthy donor (HD) into a recipient and has emerged as a promising therapeutic approach for IBD. The primary goal of FMT is to restore microbial balance in the recipient's gut, improving both microbiota composition and immune function. Numerous preclinical and clinical studies have demonstrated varying degrees of success in alleviating IBD symptoms through FMT. The benefits of FMT include modulation of gut bacteria abundance, restoration of microbial diversity, and enhancement of immune system regulation, all of which contribute to reducing IBD-related inflammation. This review presents a comprehensive analysis of animal studies and clinical trials exploring using FMT as a treatment for IBD. Understanding the underlying mechanisms of FMT in IBD is crucial for designing effective therapeutic strategies and optimizing its clinical impact.},
}

@article {pmid40755230,
year = {2025},
author = {Groenewegen, B and Ruissen, MM and Crossette, E and Menon, R and Prince, AL and Norman, JM and Ballieux, BEPB and Lamb, HJ and Terveer, EM and Keller, JJ and Tushuizen, ME},
title = {Consecutive fecal microbiota transplantation for metabolic dysfunction-associated steatotic liver disease: a randomized controlled trial.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2541035},
doi = {10.1080/19490976.2025.2541035},
pmid = {40755230},
issn = {1949-0984},
mesh = {Humans ; *Fecal Microbiota Transplantation ; Male ; Middle Aged ; Female ; Gastrointestinal Microbiome ; *Fatty Liver/therapy/microbiology ; Adult ; Double-Blind Method ; Aged ; Feces/microbiology ; Liver/metabolism ; Bacteria/classification/isolation & purification/genetics ; Treatment Outcome ; },
abstract = {The gut microbiota is increasingly considered a contributory factor in metabolic dysfunction-associated steatotic liver disease (MASLD). This double-blind RCT evaluated the effect of three consecutive fecal microbiota transplantations (FMT) on hepatic steatosis in MASLD. Twenty patients with MASLD were randomized (1:1) to receive allogeneic or autologous FMTs at weeks 0, 3, and 6, with follow-up through week 12. FMT material was derived from two donors. We assessed changes in hepatic steatosis (magnetic resonance imaging-derived proton density fat fraction (MRI-PDFF)), glucose tolerance (oral glucose tolerance test), liver biochemistry, and gut microbiota composition/engraftment. Change in MRI-PDFF from baseline to week 12 was notsignificantly different between groups (p = 0.50). Liver biochemistry and glucose tolerance also showed no significant overall changes. Patients' stool microbiota exhibited high baseline alpha diversity and similar composition across treatment groups, diverging by week 12 (p = 0.02). Two microbial taxa belonging to the families Gastranaerophilaceae and Rikenellaceae were associated with triglyceride levels after FMT. No further microbiota signatures were associated with FMT-treatment or response. Donor microbiota engraftment appeared donor-specific, but not treatment- or response-specific. In conclusion, FMT did not significantly affect hepatic steatosis, glucose tolerance, liver biochemistry, or gut microbiota signatures. Future studies should consider including patients with low microbiota diversity. Dutch Trial Register: NL-OMON48776; Central Committee on Research Involving Human Subjects: NL66705.058.18; Clinicaltrials.gov: NCT04465032.},
}

Humans
*Fecal Microbiota Transplantation
Male
Middle Aged
Female
Gastrointestinal Microbiome
*Fatty Liver/therapy/microbiology
Adult
Double-Blind Method
Aged
Feces/microbiology
Liver/metabolism
Bacteria/classification/isolation & purification/genetics
Treatment Outcome

@article {pmid40754032,
year = {2025},
author = {Liu, X and Zhao, J and Liu, J and Deng, W and Yan, L and Huang, Y and Zhang, L and Liu, Z and Cui, M and Xiao, H and Liu, X},
title = {Ganoderma lucidum sporoderm-broken spore powder alleviates kidney aging by modulating gut microbiota.},
journal = {Journal of ethnopharmacology},
volume = {},
number = {},
pages = {120344},
doi = {10.1016/j.jep.2025.120344},
pmid = {40754032},
issn = {1872-7573},
abstract = {Ganoderma lucidum (G. lucidum), a revered medicinal mushroom in traditional Chinese medicine (TCM), has been historically documented for its anti-aging properties and nephroprotective effects. Nevertheless, its mechanism of action through gut microbiota modulation to attenuate renal and systemic aging remains incompletely understood.

AIM OF THE STUDY: To elucidate the gut microbiota-dependent anti-aging mechanisms of G. lucidum on renal and systemic senescence using integrative multi-omics approaches.

MATERIALS AND METHODS: We systematically evaluated the anti-aging efficacy of G. lucidum sporoderm-broken spore powder (Gl-SBSP) via the gut-kidney axis in naturally aged and radiation-induced premature senescence mouse models. Renal aging phenotypes were assessed using histopathological analyses (hematoxylin-eosin and Masson staining), immunofluorescence (IF), complete blood counts, enzyme-linked immunosorbent assay (ELISA), and quantitative real-time PCR (RT-qPCR). Gut microbiota involvement was confirmed via antibiotic-treated mice and fecal microbiota transplantation (FMT). Multi-omics integration of 16S rRNA sequencing and metabolomic profiling identified microbiota-derived metabolites, functionally validated in HK-2 cells and aged mice. Mechanistic pathways were elucidated via transcriptomic analysis.

RESULTS: Gl-SBSP attenuated kidney aging phenotypes in both natural aging and irradiation models. It selectively enriched Lachnospiraceae, whose metabolite nicotinamide riboside (NR) elevated renal NAD[+] levels (in vitro and in vivo), rejuvenated senescent kidneys, and improved renal function through steroid metabolism regulation.

CONCLUSION: Gl-SBSP counters renal aging through Lachnospiraceae-driven gut microbiota remodeling, where NR serves as the core rejuvenating metabolite. By activating NAD[+] biosynthesis and modulating steroid metabolism via the gut-kidney axis, this mechanism offers a novel therapeutic strategy against age-related renal decline and validates Ganoderma lucidum's ethnopharmacological relevance.},
}

@article {pmid40754005,
year = {2025},
author = {Hegazy, RA},
title = {Unraveling Liver Cirrhosis: Bridging Pathophysiology to Innovative Therapeutics.},
journal = {Journal of gastroenterology and hepatology},
volume = {},
number = {},
pages = {},
doi = {10.1111/jgh.70037},
pmid = {40754005},
issn = {1440-1746},
abstract = {Liver cirrhosis is a complex and progressive condition resulting from sustained liver injury and chronic inflammation. Characterized by extensive fibrosis, disrupted liver architecture, and impaired function, cirrhosis represents the end stage of many chronic liver diseases. While traditionally considered irreversible, emerging evidence suggests that targeted interventions may modify disease progression, offering new hope for patients. This review explores the evolving understanding of liver cirrhosis, integrating insights into pathophysiology, systemic implications and innovative therapeutic approaches. At the core of cirrhosis development lies the activation of hepatic stellate cells (HSCs), driven by a cascade of pro-fibrotic signals, including transforming growth factor-beta (TGF-β) and Wnt/β-catenin pathways. Recent studies highlight the pivotal role of epigenetic regulation, mechanotransduction and cellular crosstalk in perpetuating fibrogenesis. Advances in single-cell transcriptomics and spatial biology are revealing unprecedented details of the cellular and molecular heterogeneity within cirrhotic tissue. Beyond the liver, cirrhosis exerts systemic effects, involving the gut-liver axis, vascular remodeling, and multi-organ dysfunction. The gut microbiome has emerged as a critical modulator, with dysbiosis and microbial translocation contributing to inflammation and disease progression. Therapeutic strategies targeting microbiome restoration, such as probiotics and fecal microbiota transplantation (FMT), are showing promise. Diagnostics are undergoing a paradigm shift with the advent of noninvasive tools, including elastography and liquid biopsy technologies. Circulating biomarkers, such as extracellular vesicles and noncoding RNAs, offer real-time insights into disease dynamics. On the therapeutic front, anti-fibrotic agents, senolytics, and regenerative approaches, such as stem cell therapy and liver organoids, are being explored. As artificial intelligence and computational modeling enhance predictive capabilities, a precision medicine approach to cirrhosis management is becoming feasible. This review highlights the need for interdisciplinary research to translate these advances into effective clinical solutions, bridging the gap between pathophysiology and innovative therapeutics.},
}

@article {pmid40753182,
year = {2025},
author = {Lan, Q and Liufu, S and Chen, B and Wang, K and Chen, W and Xiao, L and Liu, X and Yi, L and Liu, J and Xu, X and Liu, C and Liu, M and Yin, Y and Ma, H},
title = {Gut-resident Phascolarctobacterium succinatutens decreases fat accumulation via MYC-driven epigenetic regulation of arginine biosynthesis.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {150},
doi = {10.1038/s41522-025-00792-w},
pmid = {40753182},
issn = {2055-5008},
support = {2023ZD04046//Biological Breeding-National Science and Technology Major Project/ ; U23A20229//National Natural Science Foundation of China/ ; U23A20229//National Natural Science Foundation of China/ ; 202305AF150211//Program of talent of science & technology and platforms of Yunnan Province/ ; 202305AF150211//Program of talent of science & technology and platforms of Yunnan Province/ ; 202202AE090032//Major Science and Technology Special Plan of Yunnan Province/ ; 202202AE090032//Major Science and Technology Special Plan of Yunnan Province/ ; 2021kjc-js072//Breeding of Lancang Black Pigs and its application/ ; 2021kjc-js072//Breeding of Lancang Black Pigs and its application/ ; SNQYKJXT-01//Key technologies for the exploration of excellent genetic resources and their efficient farming and its application in Tibetan pigs/ ; SNQYKJXT-01//Key technologies for the exploration of excellent genetic resources and their efficient farming and its application in Tibetan pigs/ ; },
mesh = {Animals ; *Arginine/biosynthesis/blood ; Swine ; *Epigenesis, Genetic ; Mice ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; *Proto-Oncogene Proteins c-myc/genetics/metabolism ; *Clostridiales ; },
abstract = {Uncovering the mechanisms of excessive fat accumulation in livestock can not only protect animal health but also maintain the revenue of the intensive feeding industry. In this study, a bacteria-wide association study was conducted in a cohort of 129 commercial Yorkshire pigs. We found that Phascolarctobacterium succinatutens (P. succinatutens) was a key bacterium with greater abundance in low backfat thickness (LBF) pigs and was positively correlated with serum arginine concentrations. Fecal microbiota transplantation (FMT) experiment verified the beneficial roles of P. succinatutens in intestinal and lipid homeostasis. Administration of P. succinatutens in mice curbed weight gain, reduced adipocyte size, attenuated gut inflammation aggravation, and elevated circulating arginine levels. Propionate, a main metabolite produced by P. succinatutens, played a significant role in the above effects. Mechanistically, we indicated that P. succinatutens-generated propionate alleviated colonic inflammation by inhibiting the TLR4 signaling cascade. Importantly, propionate was found to stimulate the de novo synthesis of arginine by inhibiting the chromatin accessibility of MYC near the intron region. Finally, we found that the increase of arginine induced by P. succinatutens reduced fat deposition by suppressing the PI3K/Akt/FOXO3a signaling pathway. Our work provides novel insights into the epigenetic regulation of probiotic-mediated anti-obesity effects and highlights the potential of P. succinatutens in combating excessive obesity in commercial pigs.},
}

Animals
*Arginine/biosynthesis/blood
Swine
*Epigenesis, Genetic
Mice
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
*Proto-Oncogene Proteins c-myc/genetics/metabolism
*Clostridiales

@article {pmid40752199,
year = {2025},
author = {Zhou, X and You, Y and Ren, L and Akhtar, M and Ji, H and Wang, T and Meng, N and Fan, X and Yang, S and Zhou, Z and Xiao, Y and Shi, D},
title = {Lactobacillus gallinarum improves broiler performance by enhancing antioxidant capacity and regulating intestinal microbiota.},
journal = {Poultry science},
volume = {104},
number = {10},
pages = {105537},
doi = {10.1016/j.psj.2025.105537},
pmid = {40752199},
issn = {1525-3171},
abstract = {The predominant objective in large-scale poultry farming has consistently been to enhance broiler. In this context, the supplementing of probiotics, specifically Lactobacilli, has emerged as a promising strategy to improve production efficiency. Numerous studies have demonstrated that Lactobacilli could modulate intestinal microbiota. To identify effective growth-promoting Lactobacilli, the present study replicated the "high body weight" phenotype of broiler chickens through fecal microbiota transplantation (FMT) and subsequently isolated target strains from FMT recipients exhibiting high body weight. The results demonstrated that Lactobacillus gallinarum CD-13 (CD-13) produced protease and exhibited inhibitory (P < 0.05) effects against pathogenic Gram-positive and Gram-negative bacteria. In vivo experimentation revealed that an average daily gain of broilers in the CD-13 group was increased by 17.72 %, along with enhanced (P < 0.05) duodenal villus height in the CD-13 group compared to the control group (Ctrl). Furthermore, the antioxidant capacity of broilers was improved, as evidenced by elevated levels of catalase (CAT) (P < 0.05) and glutathione peroxidase (GSH-Px) (P < 0.05) in the serum, while the level of malondialdehyde (MDA) was reduced (P < 0.05). 16S rRNA analysis revealed, the CD-13 group exhibited an increase (P < 0.05) in the diversity index of the intestinal microbiota, an elevated Bacteroidota/Firmicutes ratio, and the relative abundance of Bacteroides, whereas a decrease in the relative (P < 0.05) abundance of Alistipes compared with the Ctrl group. In conclusion, CD-13 demonstrated the capacity to enhance broiler growth performance through modulation of the intestinal microbiota and improvement of antioxidant capacity, thereby reducing of intestinal inflammation. The findings of this investigation substantiated the probiotic properties of CD-13 and provided a theoretical foundation for its potential application as a probiotic additive in the poultry industry.},
}

@article {pmid40751371,
year = {2025},
author = {El-Salhy, M and Valeur, J and Brønstad, I and Gilja, OH and Hatlebakk, JG},
title = {Possible Role of Butyric Acid in Long-Term Symptom Relief in Irritable Bowel Syndrome Patients Following Fecal Microbiota Transplantation.},
journal = {Neurogastroenterology and motility},
volume = {},
number = {},
pages = {e70115},
doi = {10.1111/nmo.70115},
pmid = {40751371},
issn = {1365-2982},
support = {//Helse Vest/ ; },
abstract = {BACKGROUND: We previously found that the fecal levels of short-chain fatty acids (SCFAs) changed in irritable bowel syndrome (IBS) patients at 1 month and 1 year after fecal microbiota transplantation (FMT). This study analyzed SCFAs at 2 and 3 years after FMT in the same IBS patients included in those previous studies.

METHODS: This study randomized 113 IBS patients into placebo, 30-g, and 60-g groups, who received FMT with 30 g of their own feces and with 30 g and 60 g of the donor's feces, respectively. The patients completed four questionnaires to assess IBS symptoms, fatigue, and quality of life, and supplied fecal samples at the baseline and at 2 and 3 years after FMT. The fecal SCFA levels were measured using gas chromatography.

RESULTS: The butyric acid level was significantly increased at 2 and 3 years after FMT in the 30-g and 60-g groups, and was significantly higher than that in the placebo group. The total SCFA and acetic acid levels decreased significantly in the 30-g and 60-g groups at 2 and 3 years after FMT, while the propionic acid level decreased in the 60-g group at both time points. The butyric acid level was inversely correlated with IBS symptoms and fatigue.

CONCLUSION AND INFERENCES: The increased butyric acid levels in IBS patients at 2 and 3 years after FMT and their inverse correlation with both IBS symptoms and fatigue suggest that butyric acid contributes to the long-term improvement seen after FMT (www.

CLINICALTRIALS: gov: NCT03822299).},
}

@article {pmid40750814,
year = {2025},
author = {Wan, M and Li, Q and Xiao, Y and Zhou, D and Lei, Q and Wang, S},
title = {Gut microbiota from Mori fructus (Morus alba L.) polyphenols and polysaccharides-dosed mice activates the PPARα/PGC-1α signaling pathway to mitigate HFD-induced metabolic syndrome in mice.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {28137},
pmid = {40750814},
issn = {2045-2322},
support = {2020YFS0031//the Sichuan Province Science and Technology Support Program/ ; 21JR11RM044//the Science and Technology Planning Project of Gansu Province/ ; 2024QB-120//the Gansu Provincial University Young Doctoral Support Project/ ; XYBYZK2310//the Ph.D. Foundation Program of Long Dong University/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Metabolic Syndrome/metabolism/etiology ; *Polyphenols/pharmacology ; *Morus/chemistry ; Mice ; Signal Transduction/drug effects ; *Polysaccharides/pharmacology/administration & dosage ; *Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism ; Diet, High-Fat/adverse effects ; *PPAR alpha/metabolism ; Male ; Fecal Microbiota Transplantation ; Plant Extracts/pharmacology ; Disease Models, Animal ; Mice, Inbred C57BL ; },
abstract = {Mori Fructus, rich in polysaccharides and polyphenols, has long been used in East Asia as a functional food and medicinal agent. In traditional Chinese medicine, it is used to treat various ailments like wasting-thirst syndrome and constipation. Studies suggest its extract fractions may alleviate metabolic syndrome symptoms by affecting gut microbiota. To explore this, fecal microbiota transplantation (FMT) was used in an experiment. Pseudo-germ-free mice were created with antibiotics and given a high-fat, high-sugar diet (HFD) to induce metabolic syndrome. Then, fecal bacterial infusions were transplanted. Results showed significant improvement in metabolic syndrome parameters in the FMT-MFPS(fecal microbiota transplantation-Mori Fructus polyphenols plus polysaccharides) group. Dyslipidemia, liver, and kidney injuries were modulated in treated mice. The PPARα/PGC-1α signaling pathway was activated. These findings indicate Mori Fructus extract fractions prevent metabolic syndrome via gut microbiota modulation, with effects sustained through FMT, providing a reference for prevention.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Metabolic Syndrome/metabolism/etiology
*Polyphenols/pharmacology
*Morus/chemistry
Mice
Signal Transduction/drug effects
*Polysaccharides/pharmacology/administration & dosage
*Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha/metabolism
Diet, High-Fat/adverse effects
*PPAR alpha/metabolism
Male
Fecal Microbiota Transplantation
Plant Extracts/pharmacology
Disease Models, Animal
Mice, Inbred C57BL

@article {pmid40750041,
year = {2025},
author = {Kenneth, MJ and Chen, JS and Fang, CY and Tsai, HC and Wu, CC and Hsu, TK and Chen, CC and Hsu, BM},
title = {Exploring the therapeutic potential of Bacteriophage-mediated modulation of Gut microbiota towards Colorectal Cancer.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107585},
doi = {10.1016/j.ijantimicag.2025.107585},
pmid = {40750041},
issn = {1872-7913},
abstract = {The rising incidence of colorectal cancer (CRC), particularly among young individuals, necessitates urgent preventive and therapeutic strategies to reduce mortality and financial burdens associated with CRC treatment. According to studies, gut dysbiosis is associated with CRC, indicating that restoration to a healthy gut microbiota can improve CRC outcomes. Conventional antibiotics can rapidly eliminate CRC-associated gut microbiota, however, their lack of taxonomic precision results in non-selective elimination of both pro-tumoral and antineoplastic bacteria. In this review, we explore the potential of phage therapy to specifically target and eliminate CRC-associated bacteria, thereby mitigating their role in CRC pathogenesis. Tailored phage therapy, including phage cocktails and Fecal Microbial Transplantation (FMT), has shown promise in treating various diseases. As the efficacy of FMT is met with safety concerns, we highlight in this review how fecal viral transplantation (FVT) offers a safer alternative by using filtered fecal samples devoid of intact bacteria that would cause adverse effects. As a relatively new field with complex host-phage interactions, FVT requires further research to fully understand its potential and safety profile. Despite its potential for modulating the gut microbiota and improving CRC treatment, phage therapy still requires more clinical studies and experimental evidence to further establish its efficacy and safety in CRC patients.},
}

@article {pmid40749821,
year = {2025},
author = {Tian, Y and Jin, W and Jin, X and Wang, Y and Wu, R and Yu, R and Jiang, J and Zhu, M},
title = {Fecal microbiota transplantation promotes hair growth through gut microbiome and metabolic regulation.},
journal = {Life sciences},
volume = {},
number = {},
pages = {123887},
doi = {10.1016/j.lfs.2025.123887},
pmid = {40749821},
issn = {1879-0631},
abstract = {BACKGROUND: Gut microbiota plays a role in the etiology of a number of skin illnesses. In this study, we aimed to determine the relationship between intestinal flora (and related metabolites) and Androgenetic Alopecia (AGA).

METHODS: Mendelian randomization (MR) analysis was used to explore the causal relationship between gut microbiota and AGA. Gut microbiota was detected by fecal 16S rRNA sequencing, and fecal metabolites were analyzed by non-targeted metabolomics. Senescence and inflammation levels in the colon and hair follicles of mice were detected by β-galactosidase assay kits and other staining methods. Hair growth was assessed by dermoscopy and hair growth scoring.

RESULTS: Mendelian randomization analysis revealed a significant correlation between Lactobacillaceae (OR = 0.981, 95 % CI: 0.969-0.992, p = 0.001) and Lactobacillus (OR = 0.985, 95 % CI: 0.973-0.997, p = 0.018) with AGA. A similar reduction in Lactobacillaceae and Lactobacillus was observed in the feces of AGA mice (p < 0.05). Fecal microbiota transplantation (FMT) increased Lactobacillaceae and Lactobacillus levels (p < 0.05), and Lactobacillus rhamnosus GG (LGG) reversed aging and inflammation in the gut and hair follicles, promoting hair growth.

CONCLUSION: There is an intestinal-skin axis regulation pattern in the pathological process of AGA, and the aging of intestinal tissues and the alteration of bacterial flora and related metabolites can affect hair follicle aging and inflammation.},
}

@article {pmid40747461,
year = {2025},
author = {Zhu, Z and Zhu, Y and Sun, Q and Xue, J and Xie, M and Yu, Y and Wang, B and Shangguan, W and Feng, Z and Wu, P},
title = {Pentosan polysulfate alleviates interstitial cystitis/bladder pain syndrome by modulating bile acid metabolism and activating the TGR5 receptor through gut microbiota regulation.},
journal = {Bladder (San Francisco, Calif.)},
volume = {12},
number = {2},
pages = {e21200036},
pmid = {40747461},
issn = {2327-2120},
abstract = {BACKGROUND: The disrupted gut microbiome has been found to be implicated in the development of interstitial cystitis/bladder pain syndrome (IC/BPS). Pentosan polysulfate (PPS) is an oral medication used for treating IC/BPS, acting as both an anti-inflammatory agent and a bladder barrier protector. However, the precise mechanisms by which the PPS-mediated modulation of the gut microbiome alleviates IC/BPS are not fully understood.

OBJECTIVE: This study aimed to identify the key gut microbiota species and metabolites involved in PPS's protective effects against IC/BPS.

METHODS: We employed a multifaceted approach, including 16S rDNA gene sequencing, antibiotic treatment, and fecal microbiota transplantation, to validate the dependency of PPS's protective effects on the gut microbiome. Furthermore, we performed a comprehensive metabolomic profiling using non-targeted metabolomics and liquid chromatography-tandem mass spectrometry.

RESULTS: PPS significantly elevated the abundance of the xylan-degrading bacteria, Eubacterium xylanophilum group, which, through its interaction with the gut microbiome, markedly reduced inflammation and barrier damage induced by cyclophosphamide in IC/BPS. In addition, PPS significantly increased the level of ursodeoxycholic acid (UDCA), a secondary bile acid, demonstrating a strong correlation with the abundance of the E. xylanophilum group. Ex vivo supplementation with UDCA mitigated lipopolysaccharide-induced inflammation and barrier disruption in SV-HUC-1 cells by activating the TGR5 receptor.

CONCLUSION: PPS exerts its protective effects against IC/BPS by modulating the gut microbiome and its metabolites.},
}

@article {pmid40747222,
year = {2025},
author = {Pamungkas, KMN and Lesmana Dewi, PIS and Alamsyah, AZ and Dewi, NLPY and Dewi, NNGK and Mariadi, IK and Sindhughosa, DA},
title = {Microbiome dysbiosis and immune checkpoint inhibitors: Dual targets in Hepatocellular carcinoma management.},
journal = {World journal of hepatology},
volume = {17},
number = {7},
pages = {106810},
pmid = {40747222},
issn = {1948-5182},
abstract = {Hepatocellular carcinoma (HCC), a primary malignancy of the liver and leading cause of cancer-related mortality worldwide, poses substantial therapeutic challenges, particularly in advanced and unresectable stages. Immune checkpoint inhibitors (ICIs) have emerged as critical therapeutic agents, targeting immune checkpoint pathways to restore antitumor immune responses. Combinations such as atezolizumab (anti-programmed cell death ligand 1 with bevacizumab (anti-vascular endothelial growth factor), as well as antibodies directed against cytotoxic T-lymphocyte associated protein 4 and programmed cell death protein 1 (e.g., ipilimumab and nivolumab), have demonstrated improved clinical outcome in selected patients. However, the overall efficacy of ICIs remains hindered by variable response rate and primary or acquired resistance. Recent evidence suggests that the gut microbiome plays a pivotal role in modulating host immune responses and may significantly influence the therapeutic efficacy of ICIs. Dysbiosis within the gut-liver axis has been implicated not only in pathogenesis and progression of HCC but also diminishing immunotherapy effectiveness. Emerging studies highlight the potential of microbiome-targeted interventions including dietary modulation, prebiotics, probiotics, and fecal microbiota transplantation to enhance ICIs responsiveness. This review explores the evolving interplay between the gut microbiota and immunotherapy in HCC, with a focus on microbiome-based strategies aimed at optimizing clinical outcomes.},
}

@article {pmid40745657,
year = {2025},
author = {Hu, J and Chen, H and Zhu, L and Tong, Y and Cheng, C and Yan, G and Shen, H},
title = {Baitouweng decoction modulates gut microbial production of indole-3-propionic acid and epithelial necroptosis to alleviate DSS-induced colitis in mice.},
journal = {Chinese medicine},
volume = {20},
number = {1},
pages = {119},
pmid = {40745657},
issn = {1749-8546},
support = {82205023//The National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: Ulcerative colitis (UC) is a kind of inflammatory disorder structuring in the colon. Baitouweng decoction (BD) derived from Treatise on Cold Damage (Shang-Han-Lun in Chinese) has been used for the treatment of UC in clinical practice for more than 2000 years. However, the clear mechanism of BD is still unknown. Our previous study revealed the regulation of BD on gut microbiota in colitis mice. This study aimed to investigate the crosstalk between intestinal flora and host immunity in the therapeutic effect of BD on colitis.

METHODS: The model of colitis in mice was established using dextran sulfate sodium in drinking water, and the treatment group received BD, 5-ASA, or indole-3-propionic acid (IPA). The disease symptoms were documented, and assessments were conducted on both local and systemic inflammation as well as intestinal barrier function. The gut microbiota structure was analyzed using 16S ribosomal RNA sequencing. The metabolomic assay was performed using ultra-high performance liquid chromatography and quadrupole time-of-flight mass spectrometry, and RNA-sequencing was used to explore the mechanism of IPA on colitis treatment.

RESULTS: BD could improve colitis mice's colonic injury and rebalance the gut microbiota dysbiosis. Fecal microbiota transplantation experiments confirmed that the therapeutic effects of BD depend on the intestinal flora, while antibiotic treatment abrogated the effect of BD. The concentration of IPA, a microbial tryptophan metabolite, was upregulated after BD-treated. IPA was further evaluated for its effect on the development of colitis and it was identified as an inhibitor of necroptosis of intestinal epithelial cells.

CONCLUSIONS: Our findings suggest that BD could alleviate colitis by regulating the gut microbiota-metabolism homeostasis to inhibit the necroptosis of intestinal epithelial cells.},
}

@article {pmid40743285,
year = {2025},
author = {Herman, C and Bolyen, E and Simard, A and Gehret, L and Caporaso, JG},
title = {Assessing microbiome engraftment extent following fecal microbiota transplant with q2-fmt.},
journal = {PLoS computational biology},
volume = {21},
number = {7},
pages = {e1013299},
doi = {10.1371/journal.pcbi.1013299},
pmid = {40743285},
issn = {1553-7358},
abstract = {We present q2-fmt, a QIIME 2 plugin that provides diverse methods for assessing the extent of microbiome engraftment following fecal microbiota transplant. The methods implemented here were informed by a recent literature review on approaches for assessing FMT engraftment, and cover aspects of engraftment including Community Coalescence, Indicator Features, and Resilience. q2-fmt is free for all use, and detailed documentation illustrating worked examples on a real-world data set are provided in the project's documentation.},
}

@article {pmid40742160,
year = {2025},
author = {Bo, T and Song, G and Zhang, M and Xu, X and Duan, J and She, H and Fang, Y and Li, W and Wen, J and Liu, J and Wang, D and Lei, F},
title = {Gut microbiota contribute to high-altitude adaptation in tree sparrows.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0063025},
doi = {10.1128/msystems.00630-25},
pmid = {40742160},
issn = {2379-5077},
abstract = {UNLABELLED: The intricate relationship between gut microbiota and various physiological functions in animals has emerged as a focal point in understanding host adaptability. Unlike the native birds of the Qinghai-Tibet Plateau (QTP), the tree sparrow (Passer montanus) is believed to have colonized the plateau within the last few thousand years. Given the vast expanse and harsh conditions of the plateau, the role of gut microbiota in facilitating the tree sparrow's adaptation to this high-altitude habitat remains largely unexplored and holds significant scientific interest. Therefore, we employed a multidisciplinary approach combining amplicon sequencing, transcriptome analysis, and fecal microbiota transplantation (FMT) to investigate the functional role of gut microbiota in high-altitude tree sparrows across different seasons. Results indicate that the gut microbiota of tree sparrows exhibits seasonal and altitude-dependent changes, with an increase in Lactobacillus in winter, which may promote heat production to cope with the cold. FMT experiments confirmed that "high-altitude gut microbiota" enhances the expression of heat-related proteins (avUCP) and upregulates heat-related genes syt1 and chodl. These findings suggest an adaptive strategy whereby tree sparrows utilize their gut microbiota to modulate energy metabolism, ultimately conserving energy in the resource-limited high-altitude environment.

IMPORTANCE: This study provides one evidence that gut microbiota mediates high-altitude adaptation in tree sparrow. By integrating multi-omics and fecal transplantation in tree sparrows (Passer montanus)-a species invading the Qinghai-Tibet Plateau within millennia-we reveal seasonally dynamic microbial strategies critical for survival in extreme environments. These findings establish gut microbiota as a key driver of rapid altitudinal adaptation, offering new insights into how microbial functions enable vertebrate range expansion into challenging ecosystems. The mechanistic framework also informs conservation strategies for wildlife facing climate-driven habitat shifts.},
}

@article {pmid40741477,
year = {2025},
author = {Ma, L and Zhang, MH and Xu, YF and Hao, YX and Niu, XX and Li, Y and Xing, HC},
title = {Fecal microbiota transplantation: A promising treatment strategy for chronic liver disease.},
journal = {World journal of gastroenterology},
volume = {31},
number = {28},
pages = {105089},
pmid = {40741477},
issn = {2219-2840},
mesh = {Humans ; *Fecal Microbiota Transplantation/adverse effects/methods ; *Gastrointestinal Microbiome ; Treatment Outcome ; Animals ; *Dysbiosis/therapy/microbiology ; *Liver Diseases/therapy/microbiology ; Liver/pathology/microbiology ; Chronic Disease ; Clinical Trials as Topic ; },
abstract = {Chronic liver disease has become a global health crisis, with increasing incidence and mortality rates placing a substantial burden on healthcare systems worldwide. A key factor in the progression of chronic liver disease is intestinal microbiota dysbiosis, which influences liver function via the intricate liver-gut axis. This axis plays a central role in various physiological processes, and disruptions in microbial composition can exacerbate liver pathology. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic strategy, with the potential to restore the composition and metabolic functions of the intestinal microbiota. Supported by encouraging findings from clinical trials and animal studies, FMT has demonstrated therapeutic benefits, including improvements in clinical symptoms, objective indicators, and long-term prognosis. These benefits encompass reductions in hepatic lipid deposition and inflammation, mitigation of complications in advanced liver disease, promotion of hepatitis B e antigen seroconversion, and enhancement of cognitive function. Although clinical evidence remains preliminary, current data underscore the transformative potential of FMT in managing chronic liver diseases. Nonetheless, challenges persist, including the need for standardized procedures, variability among donors, potential risks, and concerns regarding long-term safety. This review provides a comprehensive evaluation of the current literature on the efficacy and safety of FMT, while exploring future research directions to expand its application in liver disease management.},
}

Humans
*Fecal Microbiota Transplantation/adverse effects/methods
*Gastrointestinal Microbiome
Treatment Outcome
Animals
*Dysbiosis/therapy/microbiology
*Liver Diseases/therapy/microbiology
Liver/pathology/microbiology
Chronic Disease
Clinical Trials as Topic

@article {pmid40741168,
year = {2025},
author = {Gu, C and Du, H and Li, N and Zhou, Y and Li, S and Sun, Y and Han, Y and Xu, X and Li, X},
title = {The gut-bone axis in osteoporosis: a multifaceted interaction with implications for bone health.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1569152},
pmid = {40741168},
issn = {1664-2392},
mesh = {Humans ; *Osteoporosis/metabolism/microbiology ; *Gastrointestinal Microbiome/physiology ; *Bone and Bones/metabolism ; Animals ; },
abstract = {With the accelerated aging of the population, degenerative orthopedic diseases, particularly osteoporosis, have become a major public health challenge, threatening bone health and affecting the quality of life. Existing anti-osteoporosis regimens remain rather unitary or poorly adhered, which also limits the maintenance of bone health to some extent. Given the increasingly elucidated prominence of gut-related factors in osteoblasts/osteoclasts and bone formation/metabolism/maintenance, focusing on intestinal microecology and then targeting the distal bone tissue via the gut-bone axis have been recognized as a feasible intervention strategy. This review systematically summarized the interaction of the gut-bone axis while highlighting the physicochemical barriers formed by intestinal intrinsic structures, the gut microbiota, and related molecules for bone health maintenance through the immune and endocrine pathways. Meanwhile, we emphasized the ideal anti-osteoporotic property and individual achievability of methods like fecal microbiota transplantation, probiotic and prebiotic supplementation, and dietary pattern modification. The conceptual framework of the gut-bone axis plus X was innovatively proposed, given the potential synergy among different organs in disease characterization and pathogenesis, which may help better explain the etiology and manage other co-morbidities concurrent with or secondary to osteoporosis. Since the intersection of orthopedics with other subjects, we also supported the application of nano-biomaterials, bacterial synthetic biology, and novel small molecules in anti-osteoporosis, which is expected to unlock broader prospects for the multidisciplinary integration of the gut-bone axis.},
}

Humans
*Osteoporosis/metabolism/microbiology
*Gastrointestinal Microbiome/physiology
*Bone and Bones/metabolism
Animals

@article {pmid40739711,
year = {2025},
author = {Xu, Y and Zhu, Y and Wu, X and Peng, W and Zhong, Y and Cai, Y and Chen, W and Liu, L and Tan, B and Chen, T},
title = {Gut Microbiota-Derived Acetate Ameliorates Endometriosis via JAK1/STAT3-Mediated M1 Macrophage Polarisation.},
journal = {Microbial biotechnology},
volume = {18},
number = {8},
pages = {e70202},
doi = {10.1111/1751-7915.70202},
pmid = {40739711},
issn = {1751-7915},
support = {8216140922//National Natural Science Foundation of China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; Female ; *Endometriosis/therapy/microbiology/metabolism ; Mice ; Humans ; Fecal Microbiota Transplantation ; *STAT3 Transcription Factor/metabolism ; *Janus Kinase 1/metabolism ; *Macrophages/metabolism/immunology ; Disease Models, Animal ; *Acetates/metabolism ; Signal Transduction ; Feces/microbiology/chemistry ; },
abstract = {Endometriosis (EMs) is a common inflammatory disorder in women of reproductive age, severely impacting patients' quality of life and fertility. Current hormonal therapies offer limited efficacy, and surgical interventions often fail to prevent recurrence. Recent studies suggest a close association between gut microbiota and the pathophysiology of EMs, though the precise mechanisms remain unclear. To investigate the influence of gut microbiota on EMs, this study established an EMs mouse model and performed faecal microbiota transplantation (FMT) using samples from healthy donors (AH group) and EMs patients (AE group) into the model mice. Results demonstrated that compared to the model group (M group), FMT from healthy donors (AH group) significantly reduced ectopic lesion volume (658.3 ± 116.1 vs. 167.2 ± 112.8 mm[3], p < 0.01) and weight (0.7420 ± 0.1233 vs. 0.1885 ± 0.1239 mg, p < 0.01). Conversely, FMT from EMs patients exacerbated disease progression. Mechanistic studies revealed that healthy donor FMT attenuated EMs by remodelling the gut microbial composition (enhancing α-diversity and Lactobacillus abundance while suppressing Bacteroidetes), significantly elevating acetate levels in faeces and ectopic lesions, activating the JAK1/STAT3 signalling pathway within lesions, and thereby driving macrophage polarisation toward the M1 phenotype (by increased iNOS/CD86 expression and decreased Arg1/CD206 expression). Simultaneously, healthy donor FMT enhanced intestinal barrier integrity by upregulating tight junction proteins (ZO-1, Occludin, Claudin-1/5) and reducing levels of intestinal permeability markers (DAO, IFABP). In contrast, AE group FMT disrupted gut microbial ecology, reduced acetate production, failed to activate the JAK1/STAT3 pathway, promoted M2 macrophage polarisation and impaired intestinal barrier function. Collectively, this study elucidates for the first time that acetate, as a key gut microbiota metabolite, exerts anti-EMs effects by activating the JAK1/STAT3 signalling pathway to drive macrophage reprogramming toward the M1 phenotype, thereby positioning gut microbiota reconstruction as a novel therapeutic strategy for endometriosis.},
}

Animals
*Gastrointestinal Microbiome/physiology
Female
*Endometriosis/therapy/microbiology/metabolism
Mice
Humans
Fecal Microbiota Transplantation
*STAT3 Transcription Factor/metabolism
*Janus Kinase 1/metabolism
*Macrophages/metabolism/immunology
Disease Models, Animal
*Acetates/metabolism
Signal Transduction
Feces/microbiology/chemistry

@article {pmid40739580,
year = {2025},
author = {Song, J and Zhang, W and Wang, D},
title = {Gut microbiome in gastrointestinal neoplasms: from mechanisms to precision therapeutic strategies.},
journal = {Gut pathogens},
volume = {17},
number = {1},
pages = {57},
pmid = {40739580},
issn = {1757-4749},
abstract = {BACKGROUND: The incidence of Gastrointestinal Neoplasms (GI neoplasms) continues to increase globally. Colorectal cancer (CRC), in particular, has emerged as the second leading cause of cancer-related mortality worldwide. Now, Specific pathogenic bacteria, such as Fusobacterium nucleatum (F. nucleatum) and Helicobacter pylori (H. pylori), critically promote tumorigenesis through multiple mechanisms, including the induction of genotoxic damage, host metabolic reprogramming, and remodeling of the tumor immune microenvironment. Notably, a dysbiotic Gut Microbiome (GM) state significantly compromises patient response rates to cancer therapeutics. This review aims to systematically analyze the core molecular mechanism of GM affecting tumor development and explore the precise intervention strategies guided by clinical translation.

METHODS: This systematic review adhered to the PRISMA-2020 guidelines. We conducted a comprehensive literature search in PubMed (2008-2025) using key terms including "Gut Microbiome", "Gastrointestinal Neoplasms", "Fecal Microbiota Transplantation (FMT)", "immunotherapy resistance", "precision-based interventions", and "emerging research frontiers". Preclinical and clinical studies investigating the mechanisms, diagnostic applications, and therapeutic interventions of the GM in GI neoplasms were included.

RESULTS: This review systematically elucidates the tripartite mechanisms by which the GM influences the initiation and progression of GI neoplasms. And we innovatively proposed the "Proinflammation-metabolism-Immune framework (Dysbiosis of the GM jointly leads to the occurrence, development and metastasis of GI neoplasms by driving three interrelated processes: chronic inflammation (Proinflammation), reshaping the Metabolism of the host and TME(Metabolism), and inhibiting or altering the host Immune surveillance (Immune))" To deepen the understanding of host-microbe interactions. Based on this framework, we focused on discussing the therapeutic strategy targeting GM and confirmed its significant impact on the efficacy of anti-cancer treatment. Although these strategies have demonstrated clinical potential, current research is still mainly confined to preclinical models and the early clinical trial stage. To address this, we outline future directions: Integrating emerging technologies like multi-omics and artificial intelligence will enable dynamic monitoring and real-time modulation of microbial activity. This integration aims to establish a novel paradigm for microbiome-based personalized precision medicine.

DISCUSSION: This review systematically clarifies that GM is a key target for optimizing the treatment of GI neoplasms. Future research should integrate multi-omics and AI technologies for dynamic microbial monitoring and modulation, paving the way for microbiome-based precision medicine. Overcoming challenges in standardization and clinical translation is essential.},
}

@article {pmid40737908,
year = {2025},
author = {An, K and Yan, D and Lv, X and Liu, Y and Xia, Z},
title = {T-2 toxin induces gut and liver injury through triggering gut microbiota dysbiosis.},
journal = {Poultry science},
volume = {104},
number = {10},
pages = {105577},
doi = {10.1016/j.psj.2025.105577},
pmid = {40737908},
issn = {1525-3171},
abstract = {T-2 toxin (T-2), a foodborne mycotoxin, causes gut and liver injury in organisms. However, its effects on intestine in ducks and the mediating role of gut microbiota in pathogenesis remain unclear. This study investigated the involvement of gut microbiota in T-2-induced enterotoxicity and hepatotoxicity in ducks. Thirty 1-day-old ducklings were divided into control (CON) and T-2-exposed (400 μg/kg BW/day via oral gavage) groups for two weeks. Alterations in gut microbiota composition and barrier function were assessed. To further elucidate the role of microbiota, antibiotics mixture (ABX) treatment and fecal microbiota transplantation (FMT) were employed. Results revealed that T-2 exposure induced ileal dysbiosis characterized by increased relative abundance of Firmicutes, Candidatus Arthromitus, and Lactococcus, decreased Corynebacterium abundance with diminished α-diversity. For gut physical barrier function, ileal villi heights and mRNA levels of mucin2, Occludin, zonula occludens-1 were significantly downregulated by T-2, and serum concentration of lipopolysaccharide was increased. Notably, ABX treatment prevented T-2-induced gut barrier disruption, completely suppressed hepatic inflammation via toll-like receptor 4 (TLR4) pathway inhibition. Hepatic lipid accumulation induced by T-2 was significantly attenuated by ABX treatment. Furthermore, FMT confirmed the essential role of T-2-altered microbiota in recapitulating pathological features including intestinal leakage, hepatic inflammation and steatosis, and upregulated TLR4 pathway and lipid metabolism genes (angiopoietin-like 4, carnitine palmitoyltransferase 1B, perilipin 1) expression. These findings establish gut microbiota as a critical mediator in T-2-induced multiorgan toxicity, providing new insights into the potential therapeutic strategies.},
}

@article {pmid40736248,
year = {2025},
author = {Huang, X and Wu, R and Liang, X and Yu, Z and Qin, P and Wang, Z and Guo, P and Zeng, Y and Yan, Z and Xiao, W and Ma, Y},
title = {Streptococcus salivarius-derived ilexgenin A alleviates pneumonia through the gut-lung axis.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0073125},
doi = {10.1128/msystems.00731-25},
pmid = {40736248},
issn = {2379-5077},
abstract = {The alteration of gut microbiota during critical illness is associated with adverse clinical outcomes. This connection between intestinal dysbiosis and poor outcomes has prompted the idea that restoring healthy microbial communities could offer a novel approach to life-support treatment for patients with severe pneumonia. In this study, using 16S rRNA sequencing and fecal microbiota transplantation (FMT), we demonstrated that alterations in intestinal microbiota structure during pneumonia exacerbate disease outcomes. A notable feature of these alterations is the reduction in the relative levels of Streptococcus salivarius (S. salivarius). In combination with metabolomics analysis, we found that the administration of S. salivarius increased the level of ilexgenin A (IA) in mice, which enhances the resistance of mice to Pseudomonas aeruginosa (P. aeruginosa)-induced pneumonia. Mechanistically, IA regulates lipopolysaccharide-induced overexpression of macrophage inflammation through Toll-like receptor 4 (TLR4)-mediated NF-κB and MAPK signaling pathways. Our findings reveal the role of the microbial-immune axis in pneumonia, highlighting the potential of S. salivarius and IA in providing promising treatment strategies for pneumonia.IMPORTANCEOne of the major challenges faced by the clinical microbiome research community is to convert the connections between dysbiosis and negative clinical outcomes into rationalized and targeted therapeutic interventions. In the present work, 30 fecal samples from pneumonia and non-pneumonia patients were subjected to FMT and 16S rRNA analysis. The results revealed that a characteristic feature of gut microbiota dysbiosis in pneumonia hosts is the reduction of S. salivarius. Supplementation with S. salivarius can effectively enhance the resistance of mice to P. aeruginosa pneumonia. Moreover, we confirmed the anti-inflammatory effects of IA derived from S. salivarius both in vivo and in vitro. Thus, these findings enhance our understanding of how gut microbiota influences the outcomes of pneumonia and underscore the potential of S. salivarius as a precision microbial therapeutic for combating pneumonia.},
}

@article {pmid40741483,
year = {2024},
author = {Hunter, C and Dia, K and Boykins, J and Perry, K and Banerjee, N and Cuffee, J and Armstrong, E and Morgan, G and Banerjee, HN and Banerjee, A and Bhattacharya, S},
title = {An investigation for phylogenetic characterization of human pancreatic cancer microbiome by 16S rDNA sequencing and bioinformatics techniques.},
journal = {Journal of solid tumors},
volume = {14},
number = {1},
pages = {1-9},
pmid = {40741483},
issn = {1925-4067},
abstract = {Pancreatic cancer is a significant public health concern, with increasing incidence rates and limited treatment options. Recent studies have highlighted the role of the human microbiome, particularly the gut microbiota, in the development and progression of this disease. Microbial dysbiosis, characterized by alterations in the composition and function of the gut microbiota, has been implicated in pancreatic carcinogenesis through mechanisms involving chronic inflammation, immune dysregulation, and metabolic disturbances. Researchers have identified specific microbial signatures associated with pancreatic cancer, offering potential biomarkers for early detection and prognostication. By leveraging advanced sequencing and bioinformatics tools, scientists have delineated differences in the gut microbiota between pancreatic cancer patients and healthy individuals, providing insights into disease pathogenesis and potential diagnostic strategies. Moreover, the microbiome holds promise as a therapeutic target in pancreatic cancer treatment. Interventions aimed at modulating the microbiome, such as probiotics, prebiotics, and fecal microbiota transplantation, have demonstrated potential in enhancing the efficacy of existing cancer therapies, including chemotherapy and immunotherapy. These approaches can influence immune responses, alter tumor microenvironments, and sensitize tumors to treatment, offering new avenues for improving patient outcomes and overcoming therapeutic resistance. Overall, understanding the complex interplay between the microbiome and pancreatic cancer is crucial for advancing our knowledge of disease mechanisms and identifying innovative therapeutic strategies. Here we report phylogenetic analysis of the 16S rDNA microbial sequences of the pancreatic cancer mice microbiome and corresponding age matched healthy mice microbiome. We successfully identified differentially abundant microbiota in pancreatic cancer.},
}

@article {pmid40735439,
year = {2025},
author = {Wang, Q and Han, Y and Pang, L and Zhou, Z and Dai, L},
title = {Gut microbiome remodeling in chronic kidney disease: implications of kidney replacement therapies and therapeutic interventions.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1620247},
pmid = {40735439},
issn = {2296-858X},
abstract = {The escalating global burden of end-stage renal disease (ESRD), driven by aging populations and rising metabolic comorbidities, underscores the urgent need for innovative therapeutic strategies. Emerging evidence highlights the gut microbiome as a pivotal modulator of renal pathophysiology through the gut-kidney axis, with microbial dysbiosis exacerbating gut microbial metabolites (e.g., uremic toxins), systemic inflammation, and multi-organ damage. This narrative review explores the divergent impacts of kidney replacement therapies (KRT)-hemodialysis (HD) and peritoneal dialysis (PD)-on gut microbiota dynamics: HD is associated with Firmicutes and Proteobacteria enrichment, reduced butyrate-producing taxa (e.g., Faecalibacterium, Roseburia), and systemic microbial translocation; whereas PD-driven glucose absorption and iron supplementation foster pathogenic proliferation (e.g., Enterobacteriaceae) and impair short-chain fatty acid (SCFA) metabolism. Current interventions, including probiotics, prebiotics, plant-based diets (PBDs), and fecal microbiota transplantation (FMT), demonstrate potential in mitigating dysbiosis and uremic toxin accumulation. PBDs reduce inflammatory markers (IL-6, CRP) and lower all-cause mortality risk by 24% in PD patients; synbiotics (e.g., Lactobacillus casei + galactooligosaccharides) reduce serum p-cresyl sulfate by 20% in HD patients; and FMT increases levels of short-chain fatty acids (propionate, butyrate) and lowers trimethylamine N-oxide (TMAO) concentrations in streptozotocin-induced diabetic nephropathy mouse models. However, clinical translation remains challenged by small sample sizes, heterogeneous outcomes, and a lack of hard endpoints. Future research must prioritize standardized protocols, personalized microbial profiling, and synergistic integration of dietary and microbiome-targeted therapies. Bridging mechanistic insights with clinical validation will advance precision medicine in ESRD management, offering transformative potential for patients burdened by this therapeutic impasse.},
}

@article {pmid40735351,
year = {2025},
author = {Dean, EA and Roy, A and Lin, RY and Gharaibeh, RZ and Li, DM and Gauthier, J and Jobin, C and Wingard, JR},
title = {Gut Faecalibacterium abundance in patients with plasma cell disorders is associated with survival after autologous HSCT.},
journal = {Blood neoplasia},
volume = {2},
number = {3},
pages = {100114},
pmid = {40735351},
issn = {2950-3280},
abstract = {The gut microbiota (GM) has been linked to the development, progression, and response to therapy in plasma cell neoplasms (PCNs). The primary goal of this study was to investigate the relationship between the composition of the GM before and during autologous hematopoietic stem cell transplant (HSCT) with clinical outcomes of patients with PCNs. We focused on the genus Faecalibacterium, which includes the most abundant anaerobic commensal bacterium in the GM. Fecal samples were collected prospectively before, mid (at 1 week from the start of intervention), and end (at engraftment) of intervention (liberalized vs neutropenic diet) and subjected to 16S ribosomal DNA sequencing. Eighty-three patients were enrolled. Their median age was 64 (range, 31-79) years. Fifty-four patients received HSCT as part of frontline therapy and 29 for relapsed/refractory disease. With median follow-up time for survivors (n = 82) of 32 (range, 0.7-61) months, the median progression-free survival (PFS) was 40 months. Higher preintervention Faecalibacterium abundance was associated with improved PFS (hazard ratio [HR], 0.92; 95% confidence interval [CI], 0.86-0.99; P = .02). Faecalibacterium abundance was found to decrease early after transplant (P < .01). Although the administration of high-dose melphalan (200 mg/m[2]) was significantly associated with PFS in both univariable (HR, 0.38, 95% CI, 0.19-0.75; P = .006) and multivariable (HR, 0.42; 95% CI, 0.20-0.87; P = .02) analyses, preintervention Faecalibacterium abundance remained independently associated with PFS (HR, 0.93; 95% CI, 0.86-0.99; P = .04) on multivariable analysis. In conclusion, lower preintervention Faecalibacterium abundance was associated with inferior PFS.},
}

@article {pmid40733607,
year = {2025},
author = {Shrivastav, K and Nasser, H and Ikeda, T and Nema, V},
title = {Possible Crosstalk and Alterations in Gut Bacteriome and Virome in HIV-1 Infection and the Associated Comorbidities Related to Metabolic Disorder.},
journal = {Viruses},
volume = {17},
number = {7},
pages = {},
doi = {10.3390/v17070990},
pmid = {40733607},
issn = {1999-4915},
mesh = {Humans ; *Gastrointestinal Microbiome ; *HIV Infections/virology/complications/microbiology ; *Virome ; *Metabolic Diseases/virology/microbiology ; Dysbiosis ; HIV-1 ; Comorbidity ; },
abstract = {Improved antiretroviral therapy (ART) has significantly increased the life expectancy of people living with HIV (PLWH). At the same time, other complications like metabolic syndrome (MetS) are coming up as new challenges to handle. This review aims to explore the emerging evidence of gut microbiome and virome alterations in human immunodeficiency virus-1 (HIV-1) infection and associated metabolic disorders, such as type-2 diabetes (T2DM) and cardiovascular disease (CVD), with a focus on their interplay, contribution to immune dysfunction, and potential as therapeutic targets. We conducted a comprehensive review of the current literature on gut bacteriome and virome changes in HIV-1-infected individuals and those with metabolic comorbidities emphasizing their complex interplay and potential as biomarkers or therapeutic targets. HIV-1 infection disrupts gut microbial homeostasis, promoting bacterial translocation, systemic inflammation, and metabolic dysregulation. Similarly, metabolic disorders are marked by reduced beneficial short-chain fatty acid-producing bacteria and an increase in pro-inflammatory taxa. Alterations in the gut virome, particularly involving bacteriophages, may exacerbate bacterial dysbiosis and immune dysfunction. Conversely, some viral populations have been associated with immune restoration post-ART. These findings point toward a dynamic and bidirectional relationship between the gut virome, bacteriome, and host immunity. Targeted interventions such as microbiome modulation and fecal virome transplantation (FVT) offer promising avenues for restoring gut homeostasis and improving long-term outcomes in PLWH.},
}

Humans
*Gastrointestinal Microbiome
*HIV Infections/virology/complications/microbiology
*Virome
*Metabolic Diseases/virology/microbiology
Dysbiosis
HIV-1
Comorbidity

@article {pmid40732941,
year = {2025},
author = {Marano, G and Rossi, S and Sfratta, G and Acanfora, M and Anesini, MB and Traversi, G and Lisci, FM and Rinaldi, L and Pola, R and Gasbarrini, A and Sani, G and Gaetani, E and Mazza, M},
title = {Gut Microbiota in Women with Eating Disorders: A New Frontier in Pathophysiology and Treatment.},
journal = {Nutrients},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/nu17142316},
pmid = {40732941},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Female ; *Feeding and Eating Disorders/microbiology/physiopathology/therapy ; Dysbiosis/microbiology/physiopathology/therapy ; Probiotics/therapeutic use ; Prebiotics/administration & dosage ; Fecal Microbiota Transplantation ; },
abstract = {Emerging evidence highlights the critical role of the gut microbiota in the development and progression of eating disorders (EDs), particularly in women, who are more frequently affected by these conditions. Women with anorexia nervosa, bulimia nervosa, and binge eating disorder exhibit distinct alterations in gut microbiota composition compared to healthy controls. These alterations, collectively termed dysbiosis, involve reduced microbial diversity and shifts in key bacterial populations responsible for regulating metabolism, inflammation, and gut-brain signaling. The gut microbiota is known to influence appetite regulation, mood, and stress responses-factors closely implicated in the pathogenesis of EDs. In women, hormonal fluctuations related to menstruation, pregnancy, and menopause may further modulate gut microbial profiles, potentially compounding vulnerabilities to disordered eating. Moreover, the restrictive eating patterns, purging behaviors, and altered dietary intake often observed in women with EDs exacerbate microbial imbalances, contributing to intestinal permeability, low-grade inflammation, and disturbances in neurotransmitter production. This evolving understanding suggests that microbiota-targeted therapies, such as probiotics, prebiotics, dietary modulation, and fecal microbiota transplantation (FMT), could complement conventional psychological and pharmacological treatments in women with EDs. Furthermore, precision nutrition and personalized microbiome-based interventions tailored to an individual's microbial and metabolic profile offer promising avenues for improving treatment efficacy, even though these approaches remain exploratory and their clinical applicability has yet to be fully validated. Future research should focus on sex-specific microbial signatures, causal mechanisms, and microbiota-based interventions to enhance personalized treatment for women struggling with eating disorders.},
}

Humans
*Gastrointestinal Microbiome/physiology
Female
*Feeding and Eating Disorders/microbiology/physiopathology/therapy
Dysbiosis/microbiology/physiopathology/therapy
Probiotics/therapeutic use
Prebiotics/administration & dosage
Fecal Microbiota Transplantation

@article {pmid40732937,
year = {2025},
author = {Zhang, G and Dou, Y and Xie, H and Pu, D and Wang, L and Wang, R and Han, X},
title = {Sea Cucumber Egg Oligopeptides Ameliorate Cognitive Impairments and Pathology of Alzheimer's Disease Through Regulating HDAC3 and BDNF/NT3 via the Microbiota-Gut-Brain Axis.},
journal = {Nutrients},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/nu17142312},
pmid = {40732937},
issn = {2072-6643},
support = {DLUXK-2024-YB-006//Dalian University/ ; },
mesh = {Animals ; *Alzheimer Disease/pathology/metabolism ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Brain-Derived Neurotrophic Factor/metabolism ; *Cognitive Dysfunction/drug therapy ; *Histone Deacetylases/metabolism ; *Oligopeptides/pharmacology ; *Sea Cucumbers/chemistry ; Disease Models, Animal ; Brain/metabolism/pathology/drug effects ; Male ; Fecal Microbiota Transplantation ; Neuroprotective Agents/pharmacology ; Fatty Acids, Volatile/metabolism ; Mice, Inbred C57BL ; *Eggs ; *Brain-Gut Axis/drug effects ; Feces/microbiology ; },
abstract = {BACKGROUND: Oligopeptides from sea cucumber eggs (SCEPs) are rarely studied for their neuroprotective effects.

METHODS: Therefore, we prepared SCEPs via simulated gastrointestinal digestion and then administered them to an Alzheimer's disease (AD) mouse model via gavage. Behavior tests, gut-brain histopathology and fecal microbiota transplantation (FMT) experiments were conducted, and gut microbiota and metabolite short-chain fatty acids (SCFAs) were evaluated via 16sRNA gene sequencing and LC-MS.

RESULTS: The results showed that both the SCEP and FMT groups experienced improvements in the cognitive impairments of AD and showed reduced levels of Aβ, P-Tau, GFAP, and NFL in the brain, especially in the hippocampus. SCEP remodeled the gut microbiota, increasing the relative abundances of Turicibacter and Lactobacillus by 2.7- and 4.8-fold compared with the model at the genus level. In the SCEP and FMT treatments, four SCFA-producing bacteria obtained from gut microbiota profiling showed consistent trends, indicating that they may be involved in mediating the neuroprotective effects of SCEP. Mechanically, SCEP regulated the SCFA distribution in feces, blood, and the brain, greatly increased the content of SCFAs in the brain up to 2000 μg/mg, eased gut-brain barrier dysfunction, inhibited HDAC3 overexpression, and upregulated BDNF/NT3 levels.

CONCLUSIONS: This study provides a promising candidate for preventing AD and a reference for applying SCEP.},
}

Animals
*Alzheimer Disease/pathology/metabolism
*Gastrointestinal Microbiome/drug effects
Mice
*Brain-Derived Neurotrophic Factor/metabolism
*Cognitive Dysfunction/drug therapy
*Histone Deacetylases/metabolism
*Oligopeptides/pharmacology
*Sea Cucumbers/chemistry
Disease Models, Animal
Brain/metabolism/pathology/drug effects
Male
Fecal Microbiota Transplantation
Neuroprotective Agents/pharmacology
Fatty Acids, Volatile/metabolism
Mice, Inbred C57BL
*Eggs
*Brain-Gut Axis/drug effects
Feces/microbiology

@article {pmid40732886,
year = {2025},
author = {Dipalma, G and Marinelli, G and Ferrante, L and Di Noia, A and Carone, C and Colonna, V and Marotti, P and Inchingolo, F and Palermo, A and Tartaglia, GM and Del Fabbro, M and Inchingolo, AM and Inchingolo, AD},
title = {Modulating the Gut Microbiota to Target Neuroinflammation, Cognition and Mood: A Systematic Review of Human Studies with Relevance to Fibromyalgia.},
journal = {Nutrients},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/nu17142261},
pmid = {40732886},
issn = {2072-6643},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; *Fibromyalgia/therapy/microbiology/psychology ; Probiotics/administration & dosage/therapeutic use ; *Cognition ; Prebiotics/administration & dosage ; *Affect ; *Neuroinflammatory Diseases/therapy/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {AIM: This systematic review aims to evaluate the effectiveness of microbiota-modulating interventions (such as probiotics, prebiotics, and fecal microbiota transplantation) in reducing cognitive symptoms, pain, and neuroinflammation in human studies relevant to fibromyalgia (FM). The review will investigate the role of gut-brain axis modulation through these interventions and explore the potential therapeutic benefits for FM management.

MATERIALS AND METHODS: A comprehensive search was conducted in electronic databases including PubMed, Scopus, and the Cochrane Library for studies published from 1 January 2015 to 30 April 2025. Studies were eligible if they were randomized controlled trials (RCTs), pilot studies, or observational studies assessing the impact of microbiota-targeted interventions (probiotics, prebiotics, fecal microbiota transplantation) on cognitive function, pain, or neuroinflammation in patients with FM. Studies were excluded if they involved animal models, lacked relevant outcome measures, or were not peer-reviewed. Although only a subset of the included studies directly involved FM patients, all were selected for their relevance to symptom domains (e.g., pain, cognition, mood) and mechanisms (e.g., neuroinflammation, gut-brain axis dysfunction) that are central to FM. A total of 11 human studies were included in the final qualitative synthesis.

RESULTS: Preliminary findings from the included studies suggest that microbiota-targeted interventions, particularly probiotics and prebiotics, show promise in reducing cognitive symptoms, pain, and neuroinflammation in FM patients. Improvements in mood and quality of life were also reported, indicating potential benefits for overall well-being. However, heterogeneity in study designs, sample sizes, and outcome measures limit the ability to draw definitive conclusions.

CONCLUSIONS: This systematic review highlights the potential of microbiota modulation as a therapeutic strategy for managing FM symptoms, particularly cognitive dysfunction and neuroinflammation.},
}

Humans
*Gastrointestinal Microbiome/physiology
*Fibromyalgia/therapy/microbiology/psychology
Probiotics/administration & dosage/therapeutic use
*Cognition
Prebiotics/administration & dosage
*Affect
*Neuroinflammatory Diseases/therapy/microbiology
Fecal Microbiota Transplantation

@article {pmid40732657,
year = {2025},
author = {Maisetta, G and Moneta, S and Tuvo, B and Giordano, C and Petrocelli, PA and Tincani, G and Campani, D and Ghinolfi, D and Falcone, M and Bruschi, F and Lupetti, A},
title = {Three Autochthonous Cases of Amoebic Liver Abscess Clustered in a Small Village of Tuscany (Central Italy), a Non-Endemic Area.},
journal = {Pathogens (Basel, Switzerland)},
volume = {14},
number = {7},
pages = {},
doi = {10.3390/pathogens14070609},
pmid = {40732657},
issn = {2076-0817},
mesh = {Humans ; *Liver Abscess, Amebic/diagnosis/parasitology/epidemiology/pathology ; Italy/epidemiology ; Male ; Middle Aged ; *Entamoeba histolytica/isolation & purification/genetics ; Female ; Adult ; Feces/parasitology ; Aged ; },
abstract = {Amebiasis is a rare condition in industrialised countries but is epidemiologically growing. Clinical manifestations may range from asymptomatic to invasive disease. An amebic abscess can be the result of extraintestinal amebiasis, and it is associated with relatively high morbidity and mortality. We present three indigenous cases of amoebic liver abscesses observed within a few weeks (October-November 2023) in patients living in a small area near Lucca in Tuscany, Central Italy. Fever accompanied by abdominal pain and liver abscess was observed in all three patients, and one of them presented necrotising colitis and pleural effusion, too. The parasitological diagnosis was performed by microscopy and confirmed with real-time PCR in liver abscess drainage fluid and stools.},
}

Humans
*Liver Abscess, Amebic/diagnosis/parasitology/epidemiology/pathology
Italy/epidemiology
Male
Middle Aged
*Entamoeba histolytica/isolation & purification/genetics
Female
Adult
Feces/parasitology
Aged

@article {pmid40732223,
year = {2025},
author = {Li, W and Huang, D and Luo, Z and Zhou, T and Jin, Z},
title = {Yinchenhao Decoction Mitigates Cholestatic Liver Injury in Mice via Gut Microbiota Regulation and Activation of FXR-FGF15 Pathway.},
journal = {Pharmaceuticals (Basel, Switzerland)},
volume = {18},
number = {7},
pages = {},
doi = {10.3390/ph18070932},
pmid = {40732223},
issn = {1424-8247},
support = {82004417//National Natural Science Foundation of China/ ; 2021M702214//China Postdoctoral Science Foundation/ ; 2024//the 2024 Shanghai Public Health Research Special Project/ ; },
abstract = {Objective: Yinchenhao decoction (YCHD), a classical herbal formula comprising Artemisia capillaris, Gardenia jasminoides, and Rheum palmatum, has been clinically used for over 1000 years to treat cholestasis. However, its mechanism of action remains undefined. This study aimed to elucidate YCHD's therapeutic mechanisms against cholestasis, with a focus on the gut microbiota-mediated regulation of the farnesoid X receptor (FXR)-fibroblast growth factor 15 (FGF15) pathway. Methods: An alpha-naphthyl isothiocyanate (ANIT)-induced cholestasis mouse model was established. Mice received YCHD (3/9 g/kg) for 7 days. 16S rRNA sequencing, targeted LC/MS (bile acid (BA) quantification), untargeted GC/MS (fecal metabolite detection), qPCR/Western blot (FXR pathway analysis), fecal microbiota transplantation (FMT), and antibiotic depletion were employed to dissect the gut-liver axis interactions. Results: YCHD alleviated cholestatic liver injury by reducing serum biomarkers, restoring BA homeostasis via FXR-FGF15 activation, and suppressing hepatic Cyp7a1-mediated BA synthesis. It remodeled gut microbiota, enriched FXR-activating secondary BAs (CDCA, DCA, CA), and restored the intestinal barrier integrity. Antibiotic cocktail abolished YCHD's efficacy, while FMT from YCHD-treated mice enhanced its therapeutic effects, confirming microbiota dependency. Conclusions: YCHD mitigates cholestasis through gut microbiota-driven FXR activation and direct hepatobiliary regulation. These findings bridge traditional medicine and modern pharmacology, highlighting microbiome modulation as a therapeutic strategy for cholestatic liver diseases.},
}

@article {pmid40730543,
year = {2025},
author = {Du, L and Ding, X and Zhang, W and Huang, L and Lü, H and Jian, T and Li, J and Gai, Y and Meng, X and Niu, G and Chen, J and Li, W},
title = {Anthocyanins from blueberry and blackberry ameliorate metabolic syndrome by Prevotella histicola and acetic acid.},
journal = {NPJ science of food},
volume = {9},
number = {1},
pages = {158},
doi = {10.1038/s41538-025-00526-4},
pmid = {40730543},
issn = {2396-8370},
support = {KYCX24-1240//Postgraduate Research & Practice Innovation Program of Jiangsu Province/ ; 82004018//National Natural Science Foundation of China/ ; 81973463//National Natural Science Foundation of China/ ; 32170377//National Natural Science Foundation of China/ ; },
abstract = {Metabolic syndrome (MetS) is a globally prevalent disorder and poses a significant threat to human health and social harmony. Consumption of anthocyanins has been proven to improve disrupted gut microbiota and obesity in mice and humans. However, the potential specific gut microbiota and metabolites that might mediate these beneficial effects on MetS remain unknown. Here, the MetS-mice model, induced by a high-fat diet (HFD), was employed to investigate the specific effects of ACNs. Additionally, 16S rRNA sequencing and targeted metabolomics analysis of short-chain fatty acids (SCFAs) were utilized to evaluate the influence on gut microbiota composition and SCFAs levels. More importantly, we also utilized antibiotics to construct a pseudo-germ-free mouse model for fecal microbiota transplantation (FMT) to further confirm the regulation of gut microbiota by ACNs and demonstrating that the related effects on MetS could be transferable through FMT. Our data demonstrated that the amelioration of MetS by ACNs might be achieved through modulation of the gut microbiota, which was validated through FMT, and the related benefits could be transferable by FMT. Furthermore, acetic acid and Prevotella histicola might be key microbial metabolites and bacteria, respectively, in this process. These findings highlight the diet-gut-metabolites-diseases system crosstalk and provide new research perspectives for plant-derived ingredients with poor bioavailability.},
}

@article {pmid40728956,
year = {2025},
author = {Qiao, Y and Cheng, R and Li, X and Zheng, H and Guo, J and Wei, L and Gao, T and Bi, H},
title = {Plateau Environment, Gut Microbiota, and Depression: A Possible Concealed Connection?.},
journal = {Current issues in molecular biology},
volume = {47},
number = {7},
pages = {},
doi = {10.3390/cimb47070487},
pmid = {40728956},
issn = {1467-3045},
support = {Grant No. 82171863//the Natural Science Foundation of China/ ; 2020-ZJ-T08//the Innovation Platform Program of Qinghai Province/ ; None//the Tianfu Emei Project of Sichuan Province/ ; },
abstract = {Plateau environments present unique mental health challenges owing to stressors including hypoxia, low temperatures, and intense ultraviolet (UV) radiation. These factors induce structural and functional alterations in the gut microbiota, disrupting gut-brain axis homeostasis and contributing to the higher prevalence of depression in plateau regions relative to flatland areas. For example, studies report that 28.6% of Tibetan adults and 29.2% of children/adolescents on the Qinghai-Tibet Plateau experience depression, with increasing evidence linking this trend to alterations in the gut microbiota. Dysbiosis contributes to depression through three interconnected mechanisms: (1) Neurotransmitter imbalance: Reduced bacterial diversity impairs serotonin synthesis, disrupting emotional regulation. (2) Immune dysregulation: Compromised gut barrier function allows bacterial metabolites to trigger systemic inflammation via toll-like receptor signaling pathways. (3) Metabolic dysfunction: Decreased short-chain fatty acid levels weaken neuroprotection and exacerbate hypothalamic-pituitary-adrenal axis stress responses. Current interventions-including dietary fiber, probiotics, and fecal microbiota transplantation-aim to restore microbiota balance and increase short-chain fatty acids, alleviating depressive symptoms. However, key knowledge gaps remain in understanding the underlying mechanisms and generating population-specific data. In conclusion, existing evidence indicates an association between plateau environments, the gut microbiota, and depression, but causal relationships and underlying mechanisms require further empirical investigation. Integrating multiomics technologies to systematically explore interactions among high-altitude environments, the microbiota and the brain will facilitate the development of precision therapies such as personalized nutrition and tailored probiotics to protect mental health in high-altitude populations.},
}

@article {pmid40693962,
year = {2025},
author = {Mutengo, M and Dashti, A and Liptáková, M and Mulunda, NR and Chabala, FW and Hayashida, K and Chinyanta, S and Chisanga, K and Mwansa, J and Köster, PC and Santín, M and Sotillo, J and Sánchez, S and Carmena, D},
title = {High prevalence of Enterocytozoon bieneusi (microsporidia) in asymptomatic schoolchildren, Zambia.},
journal = {Medical mycology},
volume = {63},
number = {7},
pages = {},
doi = {10.1093/mmy/myaf065},
pmid = {40693962},
issn = {1460-2709},
support = {//Health Institute Carlos III (ISCIII)/ ; PI19CIII/00029//Spanish Ministry of Economy and Competitiveness/ ; FI20CIII/00002//PFIS/ ; //Spanish Ministry of Science and Innovation and Universities/ ; //Women Program of the Women for Africa Foundation/ ; },
mesh = {Humans ; Zambia/epidemiology ; *Enterocytozoon/genetics/isolation & purification/classification ; Child ; Male ; *Microsporidiosis/epidemiology/microbiology ; Female ; Adolescent ; Prevalence ; Feces/microbiology ; Child, Preschool ; Genetic Variation ; DNA, Fungal/genetics ; *Asymptomatic Infections/epidemiology ; Genotype ; Sequence Analysis, DNA ; Polymerase Chain Reaction ; },
abstract = {Microsporidia are single-celled, fungi-related eukaryotic intracellular parasites able to infect a wide diversity of invertebrate and vertebrate hosts. Among them, Enterocytozoon bieneusi and Encephalitozoon spp. (including Enc. cuniculi, Enc. hellem, and Enc. intestinalis) are known causative agents of infectious diseases in immunocompromised individuals, including HIV/AIDS patients and organ transplant recipients. Additionally, asymptomatic microsporidial infections seem more frequent than initially anticipated and might represent an overlooked public health threat. Here, we provide novel data on the occurrence and genetic diversity of microsporidial infections in individual stool samples (n = 247) collected from apparently healthy schoolchildren (age range: 5-18 years; male/female ratio: 1.1) in Lusaka, Zambia. Stool DNA samples were analysed by PCR and Sanger sequencing methods. A basic epidemiological questionnaire was used to retrieve data on variables potentially linked with higher odds of harbouring E. bieneusi infections. A high prevalence rate was found for E. bieneusi (9.3%, 23/247; 95% CI: 6.0-13.6), whereas Enc. intestinalis was much less frequent (0.4%, 1/247; 95% CI: 0.01-2.2). Four known (D, S2, S6, and Type IV) and three novel (HhZbEb1, HhZbEb2, and HhZbEb3) genotypes were identified within E. bieneusi. Genotype D was the predominant genotype found (30.8%, 4/13), followed by genotypes Type IV, HhZbEb2, and HhZbEb3 (15.4%, 2/13 each), and genotypes S2, S6, and HhZbEb1 (7.7%, 1/13 each). The only Encephalitozoon-positive sample was identified as Enc. intestinalis. Subclinical infections by E. bieneusi were common in the investigated paediatric population. Infected children could act as disregarded spreaders of microsporidial pathogens at the community level, thus representing a potential public health concern.},
}

Humans
Zambia/epidemiology
*Enterocytozoon/genetics/isolation & purification/classification
Child
Male
*Microsporidiosis/epidemiology/microbiology
Female
Adolescent
Prevalence
Feces/microbiology
Child, Preschool
Genetic Variation
DNA, Fungal/genetics
*Asymptomatic Infections/epidemiology
Genotype
Sequence Analysis, DNA
Polymerase Chain Reaction

@article {pmid40734779,
year = {2024},
author = {Lo, K and Kavarian, P and Wang, B and Parsana, R and Durazo-Arvizu, R and Sun, F and Michail, S},
title = {Fecal bile acid profiles before and after fecal microbial transplant in pediatric onset ulcerative colitis.},
journal = {Gut microbes reports},
volume = {1},
number = {1},
pages = {},
pmid = {40734779},
issn = {2993-3935},
abstract = {Fecal bile acids (BAs) are key metabolites altered in patients with inflammatory bowel disease (IBD), therefore serving as potential targets of fecal microbial transplant (FMT). To compare changes in fecal BA composition and corresponding microbial transformation pathways in pediatric ulcerative colitis (UC) patients before and after FMT for up to 48 weeks. Fecal BAs, as well as enzymes and bacteria related to BA metabolism were measured in 28 healthy children, and 48 children with mild to moderate UC before and after FMT. Several primary BAs were higher in UC patients at baseline, and subsequently decreased over the 48 weeks following FMT. In particular, the primary BA cholic acid (CA) was higher in UC children at baseline (11.73 pg/mg) compared to healthy controls (8.47 pg/mg), decreased to 10.82 pg/mg at 4 weeks post FMT (p = 0.001) then 10.07 pg/mg at 48 weeks (p = 0.077). Following FMT, the ratio of secondary to primary BAs became more similar to healthy children. The genes coding for bile salt hydrolase, 7α/β-hydroxysteroid dehydrogenase, and bile acid induced operon enzymes were lower in UC patients at baseline, with the majority of them increasing following FMT. Similarly, many of the bacterial genera involved in bile acid metabolism had corresponding increases after FMT.},
}

@article {pmid40728532,
year = {2025},
author = {Zhu, L and Song, B and Zhang, R and Wang, C and He, X and Cao, Y and Li, G},
title = {Gut microbiota in sexual function: exploring new avenues.},
journal = {Sexual medicine reviews},
volume = {},
number = {},
pages = {},
doi = {10.1093/sxmrev/qeaf039},
pmid = {40728532},
issn = {2050-0521},
support = {2022xkjT020//Basic and Clinical Collaborative Research Program of Anhui Medical University/ ; 82201777//The National Natural Science Foundation of China/ ; },
abstract = {INTRODUCTION: The gut microbiota, which is recognized for its crucial role in regulating numerous physiological processes, harbors a relationship with sexual function that has remained relatively understudied.

OBJECTIVES: This narrative review aims to integrate the existing evidence regarding the association between the gut microbiota and sexual function. Additionally, it endeavors to discuss the research challenges and delineate the future directions within this burgeoning field.

METHODS: A comprehensive analysis was carried out on both pre-clinical and clinical studies. The scope of the analysis encompassed: (1) the associations between the composition of the gut microbiota and various forms of sexual dysfunctions, (2) the risk factors for sexual dysfunction that are associated with alterations in the microbiota, and (3) the potential interventions that target the regulation of the gut microbiota.

RESULTS: In the context of erectile dysfunction and hypoactive sexual desire disorder, several investigations have identified specific changes in the gut microbiota. Additionally, risk factors for sexual dysfunction, such as mental health disorders, obesity, diabetes, hypertension, and thyroid dysfunction, are also influenced by the gut microbiota. Promising intervention strategies include dietary modification, supplementation with probiotics or prebiotics, fecal microbiota transplantation, and bioengineering approaches.

CONCLUSION: The current body of evidence has established a link between gut microbial dysbiosis and the pathophysiology of various sexual health issues. Despite the fact that our understanding and assessment of the impact of gut microbes on the sexual function of the host are still in their infancy, continued advancements may unveil novel potential targets for the management of sexual health.},
}

@article {pmid40727459,
year = {2025},
author = {Xue, J and Zhou, Q},
title = {Effects of Emodin on Lung Inflammation and Intestinal Microbes in Chronic Obstructive Pulmonary Disease.},
journal = {Journal of inflammation research},
volume = {18},
number = {},
pages = {9795-9809},
pmid = {40727459},
issn = {1178-7031},
abstract = {INTRODUCTION: The impact of COPD on human health is enormous. Emodin, which has anti-inflammatory, anti-cancer, spasmolysis, and laxative effects, has not been systematically investigated within a study with regard to the treatment of COPD.

METHODS: In this study, we conducted Experiment 1 to evaluate the effects of emodin on COPD. Emodin was purchased from Shanghai Yuanye Biotechnology Co. Ltd. (batch number: T17A10F95418). Pathological changes in lung tissue and the average lung lining interval were used to evaluate the severity of emphysema. Inflammatory cell counts in alveolar lavage fluid and the ratio of neutrophils and lymphocytes were used to observe the level of inflammation. The level of HMGB1-RAGE expression was determined via PCR. Moreover, we compared changes in the metabolites of the intestinal microbial community following an intervention with emodin. In Experiment 2, we observed the effect of fecal on the inflammatory response in COPD mice. A mouse dual intervention model was established using flora depletion and COPD modeling. We evaluated the general health of the model mice, specific pathological changes in lung tissue, the average lung lining interval, inflammatory cell counts within the alveolar lavage fluid, and HMGB1-RAGE pathway expression.

RESULTS: Our results demonstrated that emodin statistically significantly improved lung tissue inflammation in COPD mice, and that butanoic acid was the main differential metabolite in intestinal bacteria. Transplanting the feces of the emodin group mice in Experiment 1 to the model mice evaluated in Experiment 2 reduced the infiltration of inflammatory cells and down-regulated the HMGB1-RAGE inflammation pathway.

CONCLUSION: Our findings provide important information for guiding future research directions.},
}

@article {pmid40725913,
year = {2025},
author = {Ugwu, OP and Okon, MB and Alum, EU and Ugwu, CN and Anyanwu, EG and Mariam, B and Ogenyi, FC and Eze, VHU and Anyanwu, CN and Ezeonwumelu, JOC and Egba, SI and Uti, DE and Onohuean, H and Aja, PM and Ugwu, MN},
title = {Unveiling the therapeutic potential of the gut microbiota-brain axis: Novel insights and clinical applications in neurological disorders.},
journal = {Medicine},
volume = {104},
number = {30},
pages = {e43542},
doi = {10.1097/MD.0000000000043542},
pmid = {40725913},
issn = {1536-5964},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology ; Probiotics/therapeutic use ; *Nervous System Diseases/therapy/microbiology ; *Dysbiosis/therapy/complications ; *Brain ; Fecal Microbiota Transplantation/methods ; Prebiotics/administration & dosage ; *Brain-Gut Axis/physiology ; },
abstract = {Over the last several years, the gut microbiota-brain axis has been the focus of medical study, demonstrating the bidirectional nature of gut and brain communication and the resulting influence on neurological and mental health. Trillions of microorganisms, particularly those found in the gastrointestinal tract, contribute the most to the pathophysiology recovery of organs that are critical to human health, such as digestive processes and metabolism, immune responses, and even cognitive function. Dysbiosis (a disturbance in the microbiome balance) has been identified as one of the risk factors for neuropsychiatric illnesses such as depression, anxiety, autism spectrum disorder, Parkinson's disease, and Alzheimer's disease. Therapeutic strategies aimed at the gut microbiota, such as probiotics, dietary modifications, prebiotics, and fecal microbiota transplantation, will eventually offer ways to alleviate symptoms associated with these disorders by restoring microbial balance, modulating the immune response, and influencing the production of major neurotransmitters. Innovative drug carriers, such as microbially-derived nanoparticles and probiotics that target particular parts of the gut or microbial communities, may improve pharmaceutical treatment efficacy and specificity. The resolution of difficulties such as ethical concerns, unexpected repercussions, and peak performance optimization in a clinical setting is critical for the advancement of this subject.},
}

Humans
*Gastrointestinal Microbiome/physiology
Probiotics/therapeutic use
*Nervous System Diseases/therapy/microbiology
*Dysbiosis/therapy/complications
*Brain
Fecal Microbiota Transplantation/methods
Prebiotics/administration & dosage
*Brain-Gut Axis/physiology

@article {pmid40725626,
year = {2025},
author = {Augustynowicz, G and Lasocka, M and Szyller, HP and Dziedziak, M and Mytych, A and Braksator, J and Pytrus, T},
title = {The Role of Gut Microbiota in the Development and Treatment of Obesity and Overweight: A Literature Review.},
journal = {Journal of clinical medicine},
volume = {14},
number = {14},
pages = {},
doi = {10.3390/jcm14144933},
pmid = {40725626},
issn = {2077-0383},
abstract = {The gut microbiota, dominated by bacteria from the Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria phyla, plays an essential role in fermenting indigestible carbohydrates, regulating metabolism, synthesizing vitamins, and maintaining immune functions and intestinal barrier integrity. Dysbiosis is associated with obesity development. Shifts in the ratio of Firmicutes to Bacteroidetes, particularly an increase in Firmicutes, may promote enhanced energy storage, appetite dysregulation, and increased inflammatory processes linked to insulin resistance and other metabolic disorders. The purpose of this literature review is to summarize the current state of knowledge on the relationship between the development and treatment of obesity and overweight and the gut microbiota. Current evidence suggests that probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) can influence gut microbiota composition and metabolic parameters, including body weight and BMI. The most promising effects are observed with probiotic supplementation, particularly when combined with prebiotics, although efficacy depends on strain type, dose, and duration. Despite encouraging preclinical findings, FMT has shown limited and inconsistent results in human studies. Diet and physical activity are key modulators of the gut microbiota. Fiber, plant proteins, and omega-3 fatty acids support beneficial bacteria, while diets low in fiber and high in saturated fats promote dysbiosis. Aerobic exercise increases microbial diversity and supports growth of favorable bacterial strains. While microbiota changes do not always lead to immediate weight loss, modulating gut microbiota represents an important aspect of obesity prevention and treatment strategies. Further research is necessary to better understand the mechanisms and therapeutic potential of these interventions.},
}

@article {pmid40724502,
year = {2025},
author = {Lazăr, DC and Chiriac, SD and Drăghici, GA and Moacă, EA and Faur, AC and Avram, MF and Turi, VR and Nicolin, MR and Goldiș, A and Salehi, MA and Jipa, R},
title = {Gastric Cancer and Microbiota: Exploring the Microbiome's Role in Carcinogenesis and Treatment Strategies.},
journal = {Life (Basel, Switzerland)},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/life15070999},
pmid = {40724502},
issn = {2075-1729},
abstract = {Gastric cancer (GC) remains a major global health burden, with high morbidity and mortality rates, particularly in regions with prevalent Helicobacter pylori (H. pylori) infection. While H. pylori has long been recognized as a primary carcinogenic agent, recent research has underscored the broader contribution of the gastric microbiota to gastric carcinogenesis. Alterations in the microbial community, or dysbiosis, contribute to chronic inflammation, immune modulation, and epithelial transformation through a range of mechanisms, including disruption of mucosal integrity, activation of oncogenic signaling pathways (e.g., PI3K/Akt, NF-κB, STAT3), and epigenetic alterations. Furthermore, microbial metabolites, such as short-chain fatty acids, secondary bile acids, and lactate, play dual roles in either promoting or suppressing tumorigenesis. Oral and gut-derived microbes, translocated to the gastric niche, have been implicated in reshaping the gastric microenvironment and exacerbating disease progression. The composition of the microbiota also influences responses to cancer immunotherapy, suggesting that microbial profiles can serve as both prognostic biomarkers and therapeutic targets. Emerging strategies, such as probiotics, dietary interventions, and fecal microbiota transplantation (FMT), offer new avenues for restoring microbial balance and enhancing therapy response. This review synthesizes current knowledge on the complex interplay between microbiota and gastric cancer development and emphasizes the potential of microbiome modulation in both preventive and therapeutic frameworks.},
}

@article {pmid40723882,
year = {2025},
author = {Neagu, AI and Bostan, M and Ionescu, VA and Gheorghe, G and Hotnog, CM and Roman, V and Mihaila, M and Stoica, SI and Diaconu, CC and Diaconu, CC and Ruta, SM and Bleotu, C},
title = {The Impact of the Microbiota on the Immune Response Modulation in Colorectal Cancer.},
journal = {Biomolecules},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/biom15071005},
pmid = {40723882},
issn = {2218-273X},
mesh = {Humans ; *Colorectal Neoplasms/immunology/microbiology/therapy ; *Gastrointestinal Microbiome/immunology ; Animals ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; },
abstract = {Colorectal cancer (CRC) is a multifactorial disease increasingly recognized for its complex interplay with the gut microbiota. The disruption of microbial homeostasis-dysbiosis-has profound implications for intestinal barrier integrity and host immune function. Pathogenic bacterial species such as Fusobacterium nucleatum, Escherichia coli harboring polyketide synthase (pks) island, and enterotoxigenic Bacteroides fragilis are implicated in CRC through mechanisms involving mucosal inflammation, epithelial barrier disruption, and immune evasion. These pathogens promote pro-tumorigenic inflammation, enhance DNA damage, and suppress effective anti-tumor immunity. Conversely, commensal and probiotic bacteria, notably Lactobacillus and Bifidobacterium species, exert protective effects by preserving epithelial barrier function and priming host immune responses. These beneficial microbes can promote the maturation of dendritic cells, stimulate CD8[+] T cell cytotoxicity, and modulate regulatory T cell populations, thereby enhancing anti-tumor immunity. The dichotomous role of the microbiota underscores its potential as both a biomarker and a therapeutic target in CRC. Recent advances in studies have explored microbiota-modulating strategies-ranging from dietary interventions and prebiotics to fecal microbiota transplantation (FMT) and microbial consortia-as adjuncts to conventional therapies. Moreover, the composition of the gut microbiome has been shown to influence the responses to immunotherapy and chemotherapy, raising the possibility of microbiome-informed precision oncology therapy. This review synthesizes the current findings on the pathogenic and protective roles of bacteria in CRC and evaluates the translational potential of microbiome-based interventions in shaping future therapeutic paradigms.},
}

Humans
*Colorectal Neoplasms/immunology/microbiology/therapy
*Gastrointestinal Microbiome/immunology
Animals
Probiotics/therapeutic use
Fecal Microbiota Transplantation

@article {pmid40723792,
year = {2025},
author = {Guo, H and Tang, X and He, X and Weng, Y and Zhang, Q and Fang, Q and Zhang, L},
title = {A Comprehensive Review of the Role of the Microbiota-Gut-Brain Axis via Neuroinflammation: Advances and Therapeutic Implications for Ischemic Stroke.},
journal = {Biomolecules},
volume = {15},
number = {7},
pages = {},
doi = {10.3390/biom15070920},
pmid = {40723792},
issn = {2218-273X},
support = {KJXW2023013//Xingwei Kejiao science and technology project of Suzhou/ ; SSD2024058//Suzhou Basic Research Pilot Project/ ; 82001125//National Natural Science Foundation of China/ ; BK20180201//Natural Science Foundation of Jiangsu Province/ ; 23KJB320016//The Natural Science Foundation of the Jiangsu Higher Education Institutions of China/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome ; *Ischemic Stroke/microbiology/therapy/metabolism ; Animals ; *Brain/metabolism ; *Neuroinflammatory Diseases/microbiology/metabolism/therapy ; Probiotics/therapeutic use ; *Brain-Gut Axis ; Fecal Microbiota Transplantation ; },
abstract = {The human gastrointestinal tract harbors a complex and diverse microbial community. Emerging evidence has revealed bidirectional communication between the gut microbiome and the central nervous system, termed the "microbiota-gut-brain axis". This axis serves as a critical regulator of glial cell function, positioning it as an essential target for ameliorating the onset and progression of ischemic stroke. In this review, we discuss the developments in the relationship between ischemic stroke and neuroinflammation via MGBA. The gut microbiome plays a critical role in signaling to microglia, astrocytes, and other immune components within this axis. We also summarize the interactions between the gut microbiota and glial cells under both healthy and ischemic stroke conditions. Additionally, we also focus on the role of microbiota-derived metabolites and neurotransmitters in ischemic stroke. Furthermore, we investigate the potential of targeting the intestinal and blood-brain barriers to improve MGBA. Finally, we evaluate the preclinical and clinical evidence for dietary interventions, probiotics, prebiotics, and fecal microbiota transplantation in ischemic stroke. A comprehensive understanding of the MGBA is essential for developing MGBA-based treatment for ischemic stroke.},
}

Humans
*Gastrointestinal Microbiome
*Ischemic Stroke/microbiology/therapy/metabolism
Animals
*Brain/metabolism
*Neuroinflammatory Diseases/microbiology/metabolism/therapy
Probiotics/therapeutic use
*Brain-Gut Axis
Fecal Microbiota Transplantation

@article {pmid40723178,
year = {2025},
author = {Tudorache, M and Treteanu, AR and Gradisteanu Pircalabioru, G and Lixandru-Petre, IO and Bolocan, A and Andronic, O},
title = {Gut Microbiome Alterations in Colorectal Cancer: Mechanisms, Therapeutic Strategies, and Precision Oncology Perspectives.},
journal = {Cancers},
volume = {17},
number = {14},
pages = {},
doi = {10.3390/cancers17142294},
pmid = {40723178},
issn = {2072-6694},
abstract = {Colorectal cancer (CRC) is one of the most prevalent and lethal oncological diseases worldwide, with a concerning rise in incidence, particularly in developing countries. Recent advances in genetic sequencing have revealed that the gut microbiome plays a crucial role in CRC development. Mechanisms such as chronic inflammation, metabolic alterations, and oncogenic pathways have demonstrated that dysbiosis, a disruption of the gut microbiome, is linked to CRC. Associations have been found between tumor progression, treatment resistance, and pathogenic microbes such as Fusobacterium nucleatum and Escherichia coli. A promising approach for CRC prevention and treatment is microbiome manipulation through interventions such as probiotics, prebiotics, fecal microbiota transplantation, and selective antibiotics. This article explores how gut microbiome alterations influence CRC pathogenesis and examines microbiome modulation strategies currently used as adjuncts to traditional treatments. Advances in artificial intelligence, single-cell and spatial transcriptomics, and large-scale initiatives such as the ONCOBIOME Project are paving the way for the identification of microbiome-derived biomarkers for early CRC detection and personalized treatment. Despite promising progress, challenges such as interindividual variability, causal inference, and regulatory hurdles must be addressed. Future integration of microbiome analysis into multi-omics frameworks holds great potential to revolutionize precision oncology in CRC management.},
}

@article {pmid40722867,
year = {2025},
author = {Akinrimisi, OI and Maasen, K and Scheijen, JLJM and Nemet, I and Nieuwdorp, M and Schalkwijk, CG and Hanssen, NMJ},
title = {Does Gut Microbial Methylglyoxal Metabolism Impact Human Physiology?.},
journal = {Antioxidants (Basel, Switzerland)},
volume = {14},
number = {7},
pages = {},
doi = {10.3390/antiox14070763},
pmid = {40722867},
issn = {2076-3921},
support = {09150172210019/NWO_/Dutch Research Council/Netherlands ; 2021T055//Hartstichting/ ; },
abstract = {Methylglyoxal (MGO) is a highly reactive dicarbonyl associated with oxidative stress, inflammation, and chronic diseases, particularly diabetic vascular complications and atherosclerosis through the formation of advanced glycation end products (AGEs). In the setting of human/host diseases, the formation of MGO has mainly been considered as the byproduct of glycolysis. Gut microbes play an important role in the development of cardiometabolic diseases. Here, we discuss a possibility that gut microbes can modulate the MGO pool within the host through (i) the alternation of the host metabolism, and (ii) direct MGO synthesis and/or detoxification by human commensal microorganisms. We also explore how dietary MGO impacts the composition of the gut microbiota and their potential role in modulating host health. This paradigm is highly innovative, with the current literature providing observations supporting this concept. Targeting the gut microbiome is emerging as an approach for treating cardiometabolic diseases through dietary, pre-, pro-, and postbiotic interventions, faecal microbiota transplantations, and the use of small molecule inhibitors of microbial enzymes. This can be a novel strategy to reduce MGO stress in the setting of cardiometabolic diseases and lowering the burden of diabetic complications and cardiovascular disease.},
}

@article {pmid40722839,
year = {2025},
author = {Carrossa, G and Misenti, V and Faggin, S and Giron, MC and Antonini, A},
title = {The Small Intestinal Microbiota and the Gut-Brain Axis in Parkinson's Disease: A Narrative Review.},
journal = {Biomedicines},
volume = {13},
number = {7},
pages = {},
doi = {10.3390/biomedicines13071769},
pmid = {40722839},
issn = {2227-9059},
abstract = {Researchers are increasingly focusing on understanding the microbiota's influence on disease susceptibility and overall health. The vast number of microorganisms in our gastrointestinal tract and their extensive surface area underscore their undeniable impact on well-being. Viewing the gut microbiome as a distinct pool of microbial genetic information that interacts with the human genome highlights its pivotal role in genetically predisposed diseases. Investigating this complex crosstalk may lead to the development of novel therapeutic strategies-such as targeting dysbiosis-to complement conventional treatments and improve patient care. Parkinson's disease (PD) is a multifactorial condition originating from a combination of genetic and environmental risk factors. Compelling evidence points to the enteric nervous system as an initial site of pathological processes that later extend to the brain-a pattern known as the 'body-first' model. Furthermore, most patients with PD exhibit both qualitative and quantitative alterations in the composition of the gut microbiota, including dysbiosis and small intestinal overgrowth. Nonetheless, the existing literature predominantly addresses fecal microbiota, while knowledge of upper intestinal sections, like the duodenum, remains scarce. Given the potential for microbiota modulation to impact both motor and gastrointestinal symptoms, further research exploring the therapeutic roles of balanced diets, probiotics, and fecal transplants in PD is warranted.},
}

@article {pmid40722483,
year = {2025},
author = {Dragasevic, S and Nikolic, A and Zgradic, S and Stojkovic Lalosevic, M and Stojkovic, S and Matovic Zaric, V and Lukic, S and Glisic, T and Kmezic, S and Saponjski, D and Popovic, D},
title = {Dysbiosis of Gut Microbiota in Microscopic Colitis: Diagnostic and Therapeutic Implications.},
journal = {Diagnostics (Basel, Switzerland)},
volume = {15},
number = {14},
pages = {},
doi = {10.3390/diagnostics15141733},
pmid = {40722483},
issn = {2075-4418},
abstract = {Microscopic colitis (MC) is an idiopathic inflammatory bowel disease characterized by watery, non-bloody diarrhea and histopathological changes but normal endoscopic findings. Increasing evidence now suggests that alterations in the gut microbiota contribute to the pathogenesis of MC. In this narrative review, we summarize evidence from nine case-control studies examining microbial composition using sequencing technology. The research presented here illustrates reduced alpha diversity, high dysbiosis, and pro-inflammatory oral-associated taxa enrichment, such as Veillonella dispar, and loss of protective microbes such as Akkermansia muciniphila and Bacteroides stercoris. These microbial changes have the potential to be non-invasive diagnostic biomarkers that can differentiate MC from other etiologies. In addition, the characterization of gut microbiota in MC can guide personalized therapeutic strategies, such as directed probiotic therapy or fecal microbiota transplantation, to help restore microbial balance. These microbial patterns can be applied to guide the creation of diagnostic biomarkers and personalized therapy. Despite differences in sample types and sequencing methods, general microbial trends highlight the need for further longitudinal and standardized investigations.},
}

@article {pmid40721426,
year = {2025},
author = {Yang, Y and Ye, M and Song, Y and Xing, W and Zhao, X and Li, Y and Shen, J and Zhou, J and Arikawa, K and Wu, S and Song, Y and Xu, N},
title = {Gut microbiota and SCFAs improve the treatment efficacy of chemotherapy and immunotherapy in NSCLC.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {146},
doi = {10.1038/s41522-025-00785-9},
pmid = {40721426},
issn = {2055-5008},
support = {2020YFC2003700//National Key R&D Plan/ ; ZD2021CY001//Shanghai Municipal Science and Technology Major Project/ ; 20Z11901000, 20DZ2261200, 20XD1401200, 22Y11900800//Science and Technology Commission of Shanghai Municipality/ ; SHDC2020CR5010-002//Clinical Research Plan of SHDC/ ; shslczdzk02201//Shanghai Municipal Key Clinical Specialty/ ; ZY(2021-2023)-0207-01//Shanghai Municipal Health Commission and Shanghai Municipal Administrator of Traditional Chinese Medicine/ ; 81401877, 82130001, and 82272243//National Natural Science Foundation of China/ ; 81401877, 82130001, and 82272243//National Natural Science Foundation of China/ ; },
mesh = {*Gastrointestinal Microbiome ; Humans ; *Carcinoma, Non-Small-Cell Lung/therapy/microbiology/drug therapy ; *Immunotherapy/methods ; Animals ; *Lung Neoplasms/therapy/microbiology/drug therapy ; Mice ; *Fatty Acids, Volatile/metabolism ; Fecal Microbiota Transplantation ; RNA, Ribosomal, 16S/genetics ; Treatment Outcome ; *Bacteria/classification/genetics/isolation & purification/metabolism ; Female ; Male ; Metagenomics ; Middle Aged ; Aged ; Dysbiosis/microbiology ; Antineoplastic Agents/therapeutic use ; },
abstract = {The role of gut dysbiosis in shaping immunotherapy responses is well-recognized, yet its effect on the therapeutic efficacy of chemotherapy and immunotherapy combinations remains poorly understood. We analyzed gut microbiota in non-small cell lung cancer (NSCLC) patients treated with chemo-immunotherapy, comparing responders and non-responders using 16S rRNA sequencing. Responders showed higher microbial richness and abundance of specific genera like Faecalibacterium and Subdoligranulum, and the phylum Firmicutes. Support vector machine (SVM), a machine learning model based on microbial composition, predicted treatment efficacy with the area under the curve (AUC) values of 0.763 for genera and 0.855 for species. Metagenomic analysis revealed significant differences in metabolic pathways, with responders exhibiting higher short-chain fatty acids (SCFAs) production. Fecal microbiota transplantation (FMT) and SCFAs supplementation in mouse models enhanced treatment efficacy by promoting effector T cell activity in tumors. Our study suggests that gut microbiota, through SCFAs production, regulates chemo-immunotherapy efficacy, offering new strategies to improve NSCLC treatment outcomes.},
}

*Gastrointestinal Microbiome
Humans
*Carcinoma, Non-Small-Cell Lung/therapy/microbiology/drug therapy
*Immunotherapy/methods
Animals
*Lung Neoplasms/therapy/microbiology/drug therapy
Mice
*Fatty Acids, Volatile/metabolism
Fecal Microbiota Transplantation
RNA, Ribosomal, 16S/genetics
Treatment Outcome
*Bacteria/classification/genetics/isolation & purification/metabolism
Female
Male
Metagenomics
Middle Aged
Aged
Dysbiosis/microbiology
Antineoplastic Agents/therapeutic use

@article {pmid40716617,
year = {2025},
author = {Yi, D and Li, T and Xiao, Y and Li, X and Shao, B and Wu, Z and Hao, Q and Zhang, F and Zhang, X and Yang, G and Zhang, C and Deng, H and Sun, X and Wang, N},
title = {Hydroxytyrosol improved insulin resistance in male offspring born to high-fat diet dams by remodeling gut microbiota.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110041},
doi = {10.1016/j.jnutbio.2025.110041},
pmid = {40716617},
issn = {1873-4847},
abstract = {Maternal obesity during pregnancy and lactation critically influences offspring metabolic programming, increasing insulin resistance (IR) risk through gut microbiome alterations. This study investigated whether hydroxytyrosol (HT), a polyphenol, could exert metabolic benefits through intergenerational regulation of gut microbiota. Through dietary intervention and fecal microbiota transplantation experiments in pregnant and lactating C57BL/6J dams, combined with 16S rRNA sequencing and interaction analysis, we found that maternal high-fat diet (60% fat for energy) during gestation and lactation caused obesity and IR associated phenotypes in male offspring at 4 weeks of age, but not in female young pups. Oral gavage of HT (50 mg/kg) during pregnancy and lactation alleviated abnormal adipocyte hypertrophy, hyperplasia, and excessive leptin secretion in male offspring born to obese dams. Additionally, HT reduced systemic insulin intolerance, hyperglycemia, and hyperinsulinemia, decreased liver index and liver injury, attenuated hepatocyte ballooning, hepatic oxidative stress, and systemic inflammation, and restored hepatic PI3K/AKT signaling in male offspring. Furthermore, HT recovered intestinal barrier function and gut microbiota homeostasis in male offspring, especially the community structure represented by β-diversity, microbial dysbiosis index and SCFAs content. Importantly, the beneficial effects of maternal HT ingestion on offspring IR were closely associated with gut microbiota remodeling and could be transmitted through intergenerational microbial inheritance between mothers and offspring. Together, our study indicated that the intergenerational transmission of microbiota may underlie maternal obesity-induced IR and that HT intake could be a promising intervention.},
}

@article {pmid40716471,
year = {2025},
author = {Mkilima, T},
title = {Synthetic Biology Approaches for Restoring Gut Microbial Balance and Engineering Disease-Specific Microbiome Therapeutics.},
journal = {Microbial pathogenesis},
volume = {},
number = {},
pages = {107931},
doi = {10.1016/j.micpath.2025.107931},
pmid = {40716471},
issn = {1096-1208},
abstract = {The human gut microbiome plays a pivotal role in regulating digestion, immune function, and metabolic homeostasis. Disruption of this microbial equilibrium, known as dysbiosis, is increasingly linked to chronic conditions including inflammatory bowel disease (IBD), obesity, diabetes, and neurodegenerative disorders. Conventional interventions, such as probiotics and faecal microbiota transplantation (FMT), often yield inconsistent results due to individual microbiome variability and limited ecological stability. Engineered artificial microbial consortia (AMCs) have emerged as a next-generation strategy for precision modulation of the gut microbiome. This review critically examines cutting-edge advances in synthetic biology, CRISPR-based genome editing, metabolic engineering, and multi-omics integration that underpin the rational design of AMCs targeted to disease-specific microbial dysfunctions. Notably, this work presents an ecological precision engineering framework that integrates regional microbiome ecotypes, diet-responsive modular design, and adaptive metabolic modelling to ensure cross-population compatibility and stability. Enabling technologies, such as gut-on-a-chip platforms, high-throughput co-culture screening, and ecological modelling, are explored in the context of optimising AMC performance across diverse host environments. Furthermore, the review highlights the potential for AMC-based therapeutics to be equitably scaled through regionally adapted templates, thereby extending microbiome-based healthcare to low-resource settings. By bridging ecological diversity and therapeutic specificity, this review presents a globally relevant roadmap for developing reproducible, adaptable, and inclusive microbiome interventions within the broader framework of precision medicine.},
}

@article {pmid40720392,
year = {2025},
author = {Solis, AJ and Zucchi, P and Romo, JA},
title = {Biofilm Assay for Clostridioides difficile with Applications for Drug Discovery.},
journal = {Journal of visualized experiments : JoVE},
volume = {},
number = {221},
pages = {},
doi = {10.3791/67913},
pmid = {40720392},
issn = {1940-087X},
mesh = {*Biofilms/drug effects/growth & development ; *Clostridioides difficile/drug effects/physiology ; *Drug Discovery/methods ; *Anti-Bacterial Agents/pharmacology ; Humans ; Clostridium Infections/microbiology/drug therapy ; },
abstract = {Clostridioides difficile is a gastrointestinal bacterial pathogen able to take advantage of a dysbiotic microbiota environment to proliferate, secrete toxins, and damage the intestinal epithelium. A subset of C. difficile infection (CDI) patients will experience antibiotic (15%-30%) or fecal microbiota transplant (FMT) (<10%) treatment failure. Therefore, the development of additional therapeutic interventions is of critical importance. The role of C. difficile biofilms in recurrence is unclear. However, biofilms in other organisms are responsible for chronic and relapsing disease, suggesting this could also be the case in recurrent CDI. We hypothesize that biofilms of C. difficile present a valuable therapeutic target. The goal of the protocol presented here is to adapt a biofilm formation assay for the identification of repositionable compounds with activity against established C. difficile biofilms. The protocol refines a robust and reproducible assay for forming biofilms, couples it to a metabolic assay, and applies it to drug discovery. This protocol outlines the biofilm formation assay, biomass and metabolic activity readouts, drug susceptibility testing, drug screening of a repositioning library, and representative results.},
}

*Biofilms/drug effects/growth & development
*Clostridioides difficile/drug effects/physiology
*Drug Discovery/methods
*Anti-Bacterial Agents/pharmacology
Humans
Clostridium Infections/microbiology/drug therapy

@article {pmid40715107,
year = {2025},
author = {Lei, W and Zhou, K and Lei, Y and Li, Q and Zhu, H},
title = {Gut microbiota shapes cancer immunotherapy responses.},
journal = {NPJ biofilms and microbiomes},
volume = {11},
number = {1},
pages = {143},
pmid = {40715107},
issn = {2055-5008},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; *Neoplasms/therapy/immunology/microbiology ; *Immunotherapy/methods ; Tumor Microenvironment/immunology ; Probiotics/therapeutic use ; Animals ; Fecal Microbiota Transplantation ; },
abstract = {The gut microbiota significantly influences cancer immunotherapy efficacy by modulating immune responses, remodeling the tumor microenvironment (TME), and producing key metabolites. Strategies such as FMT, probiotics, and dietary interventions show promise in enhancing responses to ICIs and ACTs while reducing immune-related adverse events (irAEs). This review summarizes clinical and preclinical findings and discusses microbiota-based interventions and future directions for precision immunotherapy.},
}

Humans
*Gastrointestinal Microbiome/immunology
*Neoplasms/therapy/immunology/microbiology
*Immunotherapy/methods
Tumor Microenvironment/immunology
Probiotics/therapeutic use
Animals
Fecal Microbiota Transplantation

@article {pmid40719366,
year = {2025},
author = {Wang, X and Wang, N and Gao, T and Zhang, Y and Fu, Z and Zhao, Y and Huang, Y and Zheng, X and Gao, X and Lu, L and Yang, L},
title = {Symptom-specific gut microbial and metabolic profiles in ADHD reveal SCFA deficiency as a Key pathogenic mechanism.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2537755},
doi = {10.1080/19490976.2025.2537755},
pmid = {40719366},
issn = {1949-0984},
abstract = {Previous evidence links gut microbiota to attention-deficit/hyperactivity disorder (ADHD) through the gut-brain axis. However, the specific microbiota contributing to symptoms remain unclear. To characterize the gut microbial profile related to different symptoms and explore the mediation mechanism between microbiota alterations and the core ADHD symptoms, we conducted shotgun metagenomic sequencing and fecal metabolomics analysis on 94 ADHD patients and 94 age- and gender-matched controls. Microbial characteristics of three subgroups exhibiting different ADHD core symptom presentations were analyzed. We developed a metabolic model and conducted causal mediation analyses to examine how metabolites connect the microbiota to the symptoms. Fecal microbiota transplantation in mice was employed to validate the findings. The redundancy analysis identified ADHD symptoms as environmental gradients and explained the changes in beta diversity (F = 1.345, pFDR = 0.015). Greater gut microbial alterations were observed in combined presentations (ADHD-C). Several beneficial bacteria involved in short-chain fatty acid synthesis were found to be downregulated, with Lactobacillus sanfranciscensis notably linked to all three core symptoms (p.adj = 1.04E-13; p.adj = 5.07E-07; p.adj = 2.61E-05). Various taxa, functional pathways, and metabolites associated with specific ADHD symptom domains were identified. Imidazoleacetic acid partially mediated the effects between Lactobacillus sanfranciscensis and inattention (p = 0.012). In mice subjected to feces from ADHD patients with a low abundance of Lactobacillus sanfranciscensis, treatment with this strain greatly improved both hyperactivity (t = 2.665, p = 0.0237) and inattention (t = 2.389, p = 0.0380), while acetate supplementation only alleviated inattention (t = 2.362, p = 0.0398). Our findings suggest that different ADHD symptoms were related to common and different gut microbiota and metabolites. Fecal microbiota transplantation in mice validated the hypothesis that gut microbial composition affects ADHD symptoms through metabolic alterations. This study provides more insight into the mechanisms underlying metabolic disturbances in ADHD and elucidates the role of gut microbiota in these processes.},
}

@article {pmid40717663,
year = {2025},
author = {Liu, Y and Wang, Z and Zhang, Y and Zhao, T and Zhang, Q and Huang, W and Lu, B},
title = {Dietary cholesterol impairs cognition via gut microbiota-derived deoxycholic acid in obese mice.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2537753},
doi = {10.1080/19490976.2025.2537753},
pmid = {40717663},
issn = {1949-0984},
abstract = {Dietary cholesterol is often found in a high-fat diet (HFD) and excessive intake is harmful to cognitive function. The gut microbiome constitutes an environmental factor influenced by diet, which regulates cognitive function via the gut-brain axis. The present study explored the role of dietary cholesterol in HFD-induced cognitive impairment and the participation of the gut microbiota and metabolites. Here, we found that dietary cholesterol promoted cognitive impairment in HFD-fed mice, which was associated with an increase in gut microbiota containing 7α-dehydroxylase, including Lachnospiraceae bacterium, Dorea sp. Clostridium sp. and elevated levels of deoxycholic acid (DCA) in the hippocampus. Upon dietary cholesterol intake, the activity of gut microbiota in mice to produce DCA is increased. Fecal microbiota transplantation confirmed that the cognitive impairment-promoting process was driven by gut microbiota. Reducing circulating bile acid levels with cholestyramine improved cognitive decline in mice, whereas hippocampal administration of DCA worsened cognitive function. Pharmacological inhibition of hippocampal apical sodium bile acid transporter reduces neuronal DCA accumulation and improves neuronal apoptosis as well as cognitive impairments in mice. Overall, this study revealed that dietary cholesterol promotes HFD-induced cognitive impairment by inducing the production of DCA through gut microbiota metabolism.},
}

@article {pmid40714355,
year = {2025},
author = {Nóbrega, R and Costa, CFFA and Cerqueira, Ó and Inês, A and Carrola, JS and Gonçalves, C},
title = {Association between gut microbiota and pediatric obesity: A systematic review.},
journal = {Nutrition (Burbank, Los Angeles County, Calif.)},
volume = {140},
number = {},
pages = {112875},
doi = {10.1016/j.nut.2025.112875},
pmid = {40714355},
issn = {1873-1244},
abstract = {OBJECTIVES: Pediatric obesity is a multifactorial public health problem with increasing prevalence. Among the many contributing factors, the intestinal microbiota has emerged as a key area of investigation due to its potential role in metabolism, immunity, and energy regulation. Understanding and modulating the gut microbiota may offer novel therapeutic strategies. This systematic review aims to explore the relationship between the intestinal microbiota composition and obesity in pediatric age.

METHODS: The review followed PRISMA recommendations. Two databases (PubMed and Scopus) were consulted in May 2024 for research and two independent reviewers screened abstracts, following extraction of relevant data. Risk of bias was assessed using the Cochrane Collaboration's RoB 2 and ROBIN-I tools.

RESULTS: This review included a set of 70 studies, of which 23 were clinical trials and 47 were cross-sectional studies. They all analyzed the intestinal microbiota using fecal DNA sequencing, comparing microbial and metabolomic profiles between normal-weight children and overweight children. The effects of current interventions, such as the use of probiotics, supplementation, physical activity, and fecal microbiota transplantation, are also explored. Despite variability in findings, certain genera-such as Akkermansia, Bifidobacterium, Blautia, and Faecalibacterium-emerged as frequently associated with obesity-related traits. The Firmicutes/Bacteroidetes ratio showed inconsistent associations.

CONCLUSIONS: Pediatric obesity is associated with distinct changes in gut microbiota composition and function. While promising, the current evidence is heterogeneous. Future research should focus on longitudinal designs and standardized methodologies to clarify the role of diet, physical activity, and microbiota-based therapies in obesity prevention and management.},
}

@article {pmid40713811,
year = {2025},
author = {Sun, B and Yuan, J and Zhang, X and Ma, X and Hao, Z and Wang, L and Li, Y and Zhang, L and Li, L},
title = {Metaproteomics Reveals Community Coalescence Outcomes in Co-Cultured Human Gut Microbiota.},
journal = {Proteomics},
volume = {},
number = {},
pages = {e70009},
doi = {10.1002/pmic.70009},
pmid = {40713811},
issn = {1615-9861},
support = {32370050//National Natural Science Foundation of China/ ; 82371559//National Natural Science Foundation of China/ ; },
abstract = {The human gut microbiome exhibits characteristics of complex ecosystems, including the ability to resist and compete with exogenous species or communities. Understanding the microbiome response that emerges from such competitive interactions is crucial, particularly for applications like fecal microbiota transplantation (FMT), where the success of treatment largely depends on the outcome of these microbial competitions. During these processes, microbial communities undergo coalescence, a phenomenon where distinct microbial communities combine and interact, leading to complex ecological outcomes that are still being uncovered. In this study, we examined the coalescent dynamics of 10 different pairs of human gut microbiota by co-culturing the plateau-phase communities of individual samples in vitro, and highlighted the critical role of metaproteomics in elucidating the competitive dynamics of co-cultured human fecal samples. Results showed that microbiome changes observed after coalescent co-culture were not straightforwardly an approximate average of the initial taxonomic or functional compositions of the two samples. Instead, both coalescent microbiotas behaved as cohesive structures, influencing the competitive outcome toward one of them. Although co-cultured communities usually exhibited high degrees of taxonomic similarities to one of its parental samples, we found that 23% of the observed proteins still showed differential expression or abundance at the metaproteomic level. Interestingly, and somewhat counterintuitively, no specific microbial ecological characteristic could linearly determine which of the two initial microbiotas would act as the driving microbiota. Instead, we observed that the outcomes of the microbial co-cultures resembled a "rock-paper-scissors"-like dynamic. Through an analysis of co-colonizing species in such "rock-paper-scissors"-like triangle, we discovered that co-colonizing species that contributed to winning each between-community competition differed from one community pair to another. This suggests that no single species or function consistently dominates across all situations; instead, this involves more complex mechanisms, which require further in-depth investigation in future studies. Our findings demonstrate that the complex competitive interactions between microbial communities make predicting success through a single parameter challenging, whereas pre-co-culturing shows promise as an effective method for predicting outcomes in ecological therapies such as FMT. SUMMARY: This study underscores the critical importance of integrating metaproteomics with microbial systems ecology to gain a functional understanding of microbial coalescence. By addressing the ecological question of how two communities compete when they are brought into contact, we investigated the metaproteomic responses of pairs of coalescent co-cultured human gut microbiotas. Our results revealed significant insights: post-co-culture microbiota changes were not merely a simple average of the initial compositions but instead exhibited distinct shifts toward one of the original samples. Notably, due to the observed rock-paper-scissors-like cycle of winning, we argue that no single microbial ecological characteristic could straightforwardly predict which of the two samples would dominate as the driving microbiota. Overall, our findings suggest that during coalescence, microbial communities behave as cohesive structures both taxonomically and functionally, influencing competitive dynamics and ecosystem complexity, indicating that an in vitro coalescence pretest may help predict the success of therapies like FMT.},
}

@article {pmid40713799,
year = {2025},
author = {Soleimani Samarkhazan, H and Nouri, S and Maleknia, M and Aghaei, M},
title = {"The microbiome in graft-versus-host disease: a tale of two ecosystems".},
journal = {Journal of translational medicine},
volume = {23},
number = {1},
pages = {832},
pmid = {40713799},
issn = {1479-5876},
mesh = {*Graft vs Host Disease/microbiology/therapy ; Humans ; *Microbiota ; Hematopoietic Stem Cell Transplantation ; Animals ; *Ecosystem ; Fecal Microbiota Transplantation ; Dysbiosis ; },
abstract = {Graft-versus-host disease (GVHD), a life-threatening complication of allogeneic hematopoietic stem cell transplantation (HSCT), is shaped by a dynamic interplay between two microbial ecosystems: the recipient's disrupted microbiome and the donor's transplanted microbiota. This narrative review unravels the "tale of two ecosystems," exploring how pre-transplant chemotherapy, radiation, and antibiotics induce recipient dysbiosis-marked by loss of beneficial taxa (Clostridia, Faecalibacterium) and dominance of pathobionts (Enterococcus). These shifts impair barrier integrity, fuel systemic inflammation, and skew immune responses toward pro-inflammatory T-cell subsets, exacerbating GVHD. Conversely, emerging evidence implicates donor microbiota in modulating post-transplant immune reconstitution, though its role remains underexplored. Therapeutic strategies, including probiotics, prebiotics, and fecal microbiota transplantation (FMT), demonstrate promise in restoring microbial balance, enhancing short-chain fatty acid (SCFA)-driven immune regulation, and reducing GVHD severity. However, challenges such as strain-specific efficacy, safety in immunocompromised hosts, and protocol standardization persist. By bridging microbial ecology and immunology, this review underscores the microbiome's transformative potential in redefining GVHD management and advocates for personalized, microbiome-targeted interventions to improve HSCT outcomes.},
}

*Graft vs Host Disease/microbiology/therapy
Humans
*Microbiota
Hematopoietic Stem Cell Transplantation
Animals
*Ecosystem
Fecal Microbiota Transplantation
Dysbiosis

@article {pmid40713743,
year = {2025},
author = {Wang, L and Li, M and Dong, Y and Wang, J and Qin, S and Li, L and Li, B and Wang, B and Cao, H},
title = {Magnoflorine alleviates colitis-induced anxiety-like behaviors by regulating gut microbiota and microglia-mediated neuroinflammation.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {172},
doi = {10.1186/s40168-025-02158-y},
pmid = {40713743},
issn = {2049-2618},
support = {82270574, 82070545 and 81970477//National Natural Science Foundation of China/ ; 82270574, 82070545 and 81970477//National Natural Science Foundation of China/ ; 22ZYYJQ02//Tianjin Medical University General Hospital Fund for Distinguished Young Scholars/ ; 21JCYBJC00810//Diversified Fund Project of the Natural Science Foundation of Tianjin, China/ ; TJYXZDXK-002A//Tianjin Key Medical Discipline (Specialty) Construction Project/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Anxiety/drug therapy/etiology/microbiology ; *Microglia/drug effects/metabolism ; *Aporphines/pharmacology/therapeutic use ; *Colitis, Ulcerative/drug therapy/microbiology/complications ; Ziziphus/chemistry ; Male ; *Colitis/complications/drug therapy/microbiology ; Disease Models, Animal ; Mice, Inbred C57BL ; *Neuroinflammatory Diseases/drug therapy ; Humans ; },
abstract = {BACKGROUND: Inflammatory bowel disease (IBD) and anxiety are often comorbid and are interconnected through the microbiota-gut-brain axis. Therapeutic medications for anxiety are often constrained by adverse effects that limit their long-term use. Therefore, recent research has focused on identifying natural, safe drugs for anxiety, and elucidating the precise mechanisms underlying the interplay between drugs and the gut-brain axis in modulating mood.

RESULTS: We revealed a significant association between active ulcerative colitis (UC) and anxiety. The results of Mendelian randomization analysis suggested that UC has a causal relationship with anxiety, but not depression. We identified Ziziphus jujuba, a natural plant, as a dual therapeutic agent for both UC and anxiety using the Batman database. Magnoflorine, the predominant compound found in Ziziphus jujuba, exhibits promising therapeutic properties for the treatment of UC and anxiety disorders. We found that magnoflorine not only alleviated colitis but also reduced colitis-induced anxiety behaviors through the gut microbiota. Mechanistically, magnoflorine increased the abundance of Odoribacteraceae and Ruminococcus and regulated bile acid metabolism, especially hyodeoxycholic acid (HDCA) in mice with colitis. HDCA supplementation alleviated both colitis and colitis-induced anxiety. HDCA inhibited the binding of lipopolysaccharide to the TLR4/MD2 complex, thereby inhibiting microglial activation and alleviating neuroinflammation.

CONCLUSION: Our study revealed that magnoflorine alleviated colitis-induced anxiety-like behaviors by regulating the gut microbiota and microglia-mediated neuroinflammation, which has the potential to treat patients with IBD and anxiety disorders. Video Abstract.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
*Anxiety/drug therapy/etiology/microbiology
*Microglia/drug effects/metabolism
*Aporphines/pharmacology/therapeutic use
*Colitis, Ulcerative/drug therapy/microbiology/complications
Ziziphus/chemistry
Male
*Colitis/complications/drug therapy/microbiology
Disease Models, Animal
Mice, Inbred C57BL
*Neuroinflammatory Diseases/drug therapy
Humans

@article {pmid40713718,
year = {2025},
author = {Pisani, A and Petito, V and Paciello, F and Emoli, V and Masi, L and Hizam, VM and Puca, P and Montuoro, R and Chierico, FD and Putignani, L and Grassi, C and Galli, J and Taglialatela, M and Caristo, ME and Ianiro, G and Lopetuso, LR and Cammarota, G and Gasbarrini, A and Fetoni, AR and Scaldaferri, F},
title = {Intestinal inflammation and microbiota modulation impact cochlear function: emerging insights in gut-ear axis.},
journal = {Cell communication and signaling : CCS},
volume = {23},
number = {1},
pages = {357},
doi = {10.1186/s12964-025-02338-1},
pmid = {40713718},
issn = {1478-811X},
mesh = {Animals ; *Gastrointestinal Microbiome ; *Cochlea/physiopathology/pathology ; Female ; Mice, Inbred C57BL ; Mice ; *Inflammation/pathology ; Humans ; Dysbiosis ; Fecal Microbiota Transplantation ; Colitis, Ulcerative/microbiology ; Myeloid Differentiation Factor 88/metabolism ; *Intestines/microbiology/pathology ; },
abstract = {BACKGROUND: Although several evidence demonstrates a "gut-microbiota-brain axis", suggesting a bidirectional communication between gut microbiota and the central nervous system, less is known about a possible link between the gut and the peripheral nervous system, including the inner ear.

METHODS: Here, we investigated the impact of intestinal inflammation and the modulation of gut microbiota through fecal microbiota transplantation on hearing sensitivity. Female C57BL/6 mice were assigned to four groups: control (Ctrl), DSS-induced colitis (DSS), FMT from patients with active ulcerative colitis (FMT aUC), and FMT from patients with ulcerative colitis in remission (FMT rUC). Auditory function was evaluated by auditory brainstem responses (ABR). Morphological and molecular analyses on cochlear tissues were performed using immunofluorescence, histological staining, and Western blot to assess inflammation, oxidative stress, and blood-labyrinth barrier integrity. Donor microbiota composition was characterized by 16S rRNA sequencing, and systemic inflammation was evaluated by measuring serum lipopolysaccharide (LPS) levels.

RESULTS: We found that intestinal dysbiosis is associated with functional, morphological, and molecular alterations in the cochlea, such as increased oxidative stress, inflammation, and altered blood-labyrinth barrier permeability. This leads to macrophage infiltration and immune response activation through the MyD88/NF-κB pathway. Notably, these effects were exacerbated by FMT from subjects with aUC, while FMT from patients with rUC provided a protective effect on cochlear functions.

CONCLUSIONS: Overall, our findings suggest that gut inflammation, microbiota alteration, or its therapeutic modulation can impact inner ear pathology: worsening gut inflammatory status negatively affects hearing sensitivity, while the restoration of gut microbiota positively impacts auditory function.},
}

Animals
*Gastrointestinal Microbiome
*Cochlea/physiopathology/pathology
Female
Mice, Inbred C57BL
Mice
*Inflammation/pathology
Humans
Dysbiosis
Fecal Microbiota Transplantation
Colitis, Ulcerative/microbiology
Myeloid Differentiation Factor 88/metabolism
*Intestines/microbiology/pathology

@article {pmid40712381,
year = {2025},
author = {Li, Q and Wang, G and Zhao, J and Chen, W and Tian, P},
title = {Gut microbiota and myelination: Crosstalk across the lifespan and microbiota-based modulation strategies.},
journal = {Microbiological research},
volume = {300},
number = {},
pages = {128286},
doi = {10.1016/j.micres.2025.128286},
pmid = {40712381},
issn = {1618-0623},
abstract = {Myelin, a lipid-rich sheath that insulates axons, is essential for efficient neural signal transmission and the modulation of neural circuits. Its formation, maintenance, and regeneration are tightly regulated processes that shape neurodevelopment, cognition, and emotional stability. Recent evidence positions the gut microbiota as a critical modulator of myelination, orchestrating metabolic signaling, immune homeostasis, and neuroinflammatory responses. Notably, the synchronized development and remodeling of gut microbiota and myelin across key life stages suggest a dynamic and bidirectional interplay essential for sustaining neurological health. Disruptions in this axis are increasingly recognized as contributing factors in dysmyelination-related disorders, including autism spectrum disorder, Alzheimer's disease, and multiple sclerosis. Harnessing microbiota-targeted interventions-such as fecal microbiota transplantation, dietary modulation, and probiotic therapies-holds promise for restoring myelin integrity and mitigating disease pathology. This review provides a comprehensive synthesis of the gut microbiota-myelin interface, delineating mechanistic insights and translational opportunities for microbiome-based therapeutic strategies in neuroprotection.},
}

@article {pmid40711721,
year = {2025},
author = {Shoukry, AEA and Rahhal, A and Constantinou, C},
title = {The role of the gut microbiota and metabolites in heart failure and possible implications for treatment.},
journal = {Heart failure reviews},
volume = {},
number = {},
pages = {},
pmid = {40711721},
issn = {1573-7322},
abstract = {The prevalence of heart failure has increased significantly in recent years, prompting investigations into novel contributory factors. Among these, alterations in the gut microbiota composition have garnered attention due to their potential association with heart failure. Disruption in the bacterial environment associated with heart failure is characterized by heightened levels of Proteobacteria and Firmicutes and decreased levels of Bifidobacteria and Bacteroides. Reduced blood supply weakens the gut barrier, facilitating the transportation of bacteria and metabolites into the bloodstream. This breach can trigger an immune response and inflammation, subsequently contributing to the pathogenesis of heart failure through the generation of harmful organic compounds in the gastrointestinal tract and bloodstream. Specific metabolites, including short-chain fatty acids, trimethylamine, and trimethylamine N-oxide also contribute to the development of heart failure. Management of heart failure includes pharmacological management, surgery, and lifestyle modifications including recommendations for the consumption of a diet high in fruits and low in animal products. Heart failure can be managed by modulating the gut microbiota. Clinical interventions include antibiotics, prebiotics, and dietary changes. However, other approaches including fecal microbial transplantation, probiotics, and natural phytochemicals are still under study in animal models. This review highlights the significant yet underexplored link between gut microbiota and heart failure, suggesting that further research could lead to new therapeutic strategies and dietary recommendations to mitigate heart failure progression.},
}

@article {pmid40709504,
year = {2025},
author = {Sheng, H and Xu, W and He, Y and Cai, Y and Wang, Z and Tao, X and Qiu, L and Wei, H},
title = {Amelioration of hypercholesterolemia by Lactiplantibacillus plantarum GLPL02 via regulating intestinal flora and cholesterol metabolism.},
journal = {Journal of the science of food and agriculture},
volume = {},
number = {},
pages = {},
doi = {10.1002/jsfa.70078},
pmid = {40709504},
issn = {1097-0010},
support = {82360114//National Natural Science Foundation of China/ ; 82160791//National Natural Science Foundation of China/ ; },
abstract = {BACKGROUND: In recent years, hypercholesterolemia has become one of the important risk factors for death around the world. Lactic acid bacteria (LAB), especially Lactiplantibacillus plantarum, exhibit strain-specific property of cholesterol-lowering activity. However, the metabolic mechanism involved in lipid-lowering capacity and regulation of intestinal flora of L. plantarum has not been well elucidated comprehensively.

RESULTS: The present study aimed to screen out cholesterol-lowering lactic acid bacteria from healthy lean individuals, evaluate their cholesterol-lowering effect and disclose its mechanism of amelioration of hypercholesterolemia in mice fed a high-cholesterol diet (HCD). Upon probiotic properties evaluation, the cholesterol removal rate of Lactiplantibacillus plantarum GLPL02 was 53.58%, and cholesterol degradation rate was 39.39%. In the systematic exploration of a model of HCD-induced mice and fecal microbiota transplantation, L. plantarum GLPL02 was found to reduce plasma lipid profiles (total cholesterol, triglycerides and low-density lipoprotein-cholesterol) and glucose tolerance, alleviate liver damage and steatosis, positively regulate intestinal flora related to cholesterol metabolism, upregulate genes relevant to decomposition (CYP7A1) and transportation (LDLR, ABCG5/8 and NPC1L1) of cholesterol, and downregulate genes relevant to synthesis (SREBP-2 and HMGCR), thereby improving hypercholesterolemia. Meanwhile, acetate and butyrate affected cholesterol metabolism in HepG2 cell through regulating cholesterol metabolism. Therefore, L. plantarum GLPL02 ameliorated hypercholesterolemia by regulating intestinal flora and genes related to cholesterol metabolism.

CONCLUSION: The present study indicates that L. plantarum GLPL02 and short-chain fatty acids (propionate, butyrate) ameliorated hypercholesterolemia and offers new insights into the role of L. plantarum in systemic cholesterol reduction from the perspective of microbiota-short-chain fatty acid interactions. © 2025 Society of Chemical Industry.},
}

@article {pmid40709417,
year = {2025},
author = {Lee, SB},
title = {[Expanding Role of Gastroenterologists in Acute Gastrointestinal Graft-versus-Host Disease: From Diagnosis and Management to Microbiome-Based Strategies].},
journal = {The Korean journal of gastroenterology = Taehan Sohwagi Hakhoe chi},
volume = {85},
number = {3},
pages = {268-273},
doi = {10.4166/kjg.2025.049},
pmid = {40709417},
issn = {2233-6869},
mesh = {Humans ; *Graft vs Host Disease/diagnosis/therapy/pathology/drug therapy ; Hematopoietic Stem Cell Transplantation/adverse effects ; *Gastrointestinal Microbiome ; Fecal Microbiota Transplantation ; Pyrimidines ; Acute Disease ; Antibodies, Monoclonal, Humanized/therapeutic use ; Pyrazoles/therapeutic use ; Nitriles ; },
abstract = {Acute graft-versus-host disease (GVHD) is a major complication following allogeneic hematopoietic stem cell transplantation. Steroid-refractory cases have poor outcomes, so an accurate diagnosis, particularly differentiation from cytomegalovirus colitis, is critical. Ruxolitinib is the standard second-line therapy, while Vedolizumab has shown potential in gut-specific modulation. Recent studies have reported that reduced microbiome diversity and the loss of short-chain fatty acid-producing bacteria are linked to acute GVHD severity and mortality. Fecal microbiota transplantation may offer benefit in selected steroid-refractory cases, but the evidence remains limited and variable. Gastroenterologists play an essential role in diagnosis and microbiome-guided care. A personalized approach incorporating microbial biomarkers may improve the future outcomes.},
}

Humans
*Graft vs Host Disease/diagnosis/therapy/pathology/drug therapy
Hematopoietic Stem Cell Transplantation/adverse effects
*Gastrointestinal Microbiome
Fecal Microbiota Transplantation
Pyrimidines
Acute Disease
Antibodies, Monoclonal, Humanized/therapeutic use
Pyrazoles/therapeutic use
Nitriles

@article {pmid40708926,
year = {2025},
author = {Zhang, Y and Dong, Y and Sun, C and Zhang, L and Zhang, Y and Wang, D and Chen, Q and Yao, J and Wu, Y and Wang, T},
title = {Shouhui Tongbian Capsule ameliorates 5-fluorouracil induced constipation in mice by modulating gut microbiota and activating PI3K/AKT/AQP3 signaling pathway.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1596881},
pmid = {40708926},
issn = {1664-302X},
abstract = {OBJECTIVE: Shouhui Tongbian Capsule (SHTC) has been clinically applied to treat various types of constipation, including chemotherapy-induced constipation. However, the pharmacological mechanism by which it regulates intestinal peristalsis and treats constipation is unclear. In this study, we aimed to investigate the underlying mechanism of SHTC on chemotherapy-induced constipation through regulating of gut microbiota and PI3K/AKT/AQP3 signaling pathway.

METHODS: Chemotherapy-induced constipation was induced with 5-Fluorouracil in C57BL/6 mice. SHTC was administrated with different dosages (100, 200, 400 mg/kg) for 12 days. The intestinal tissues were collected for the measurements of intestinal propulsion rate, time of first black stool, and expressions of colonic aquaporin. 16S rRNA sequencing, short-chain fatty acids (SCFAs) profiling, and fecal microbiota transplantation (FMT) were performed to confirm whether gut microbiota is a key target for SHTC. Finally, the expressions of proteins or genes related to PI3K/AKT/AQP3 pathway were detected.

RESULTS: SHTC markedly improved the pathological manifestations associated with constipation and restored the deregulated gut microbiota. The mice that were given fecal supernatant from SHTC-treated mice showed significant improvement in constipation symptoms. Additionally, SHTC increased the level of acetic acid and upregulated the expression of AQP3, with activation of PI3K/AKT. Furthermore, the blockade of PI3K reversed the beneficial effect of acetic acid on the expression of AQP3.

CONCLUSION: Our findings indicated that SHTC effectively relieved 5-FU-induced constipation in mice, mainly by regulating homeostasis of gut microbiota and activating PI3K/AKT/AQP3 pathway, making it a potential protective agent against chemotherapy-induced constipation.},
}

@article {pmid40708753,
year = {2025},
author = {Zheng, YM and Ye, MM and Zhang, HY and Luo, DP and Liu, T and He, XX and Chen, XY and Wu, LH},
title = {Retrospective review: single- and multidonor washed microbiota transplantation have equivalent efficacy in the treatment of autism.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1606417},
pmid = {40708753},
issn = {2235-2988},
mesh = {Humans ; Retrospective Studies ; Male ; *Fecal Microbiota Transplantation/methods ; Female ; Feces/microbiology ; Child ; Treatment Outcome ; *Autism Spectrum Disorder/therapy/microbiology ; Child, Preschool ; Gastrointestinal Microbiome ; Adolescent ; *Autistic Disorder/therapy ; },
abstract = {BACKGROUND: Autism spectrum disorder (ASD) is a serious neurodevelopmental disorder with no effective treatment. This study explored the short-term clinical effects of washed microbiota transplantation (WMT) with different numbers of donors on autism.

METHODS: Consecutive ASD patients treated with two continuous WMT courses from March 2020 to March 2022 at the First Affiliated Hospital of Guangdong Pharmaceutical University were retrospectively assessed. Basic information, aberrant behavior checklist (ABC) scores, childhood autism rating scale (CARS) scores, sleep disturbance scale for children (SDSC) scores, adverse reactions, and feces were collected.

RESULTS: Forty-four patients were included (single-donor group: 17 patients; multidonor group: 27 patients). The CARS, ABC and SDSC scores didn't differ between the two groups before treatment. After two courses, the scores for the 44 patients were lower than those at baseline (P<0.05), with no severe adverse reactions observed. After the first course, the mean ABC (P=0.049) and SDSC (P=0.019) scores were significantly different between the single-donor and multidonor groups, but the difference disappeared after two courses. The alpha-diversity of the faecal flora in the effective-group was greater than that in the ineffective-group (Shannon index P=0.0018). Lactobacillus was the predominant genus in the effective group, whereas Faecalibacterium, Campylobacter, and Sphingomonas were predominant genera in the ineffective group.

CONCLUSION: After two WMT courses, the symptoms of ASD improved, with good short-term treatment efficacy. The ASD symptom improvement did not differ between the single-donor and multidonor groups. Changes in the alpha-diversity and abundance of the faecal microbiota after WMT may be related to treatment efficacy.},
}

Humans
Retrospective Studies
Male
*Fecal Microbiota Transplantation/methods
Female
Feces/microbiology
Child
Treatment Outcome
*Autism Spectrum Disorder/therapy/microbiology
Child, Preschool
Gastrointestinal Microbiome
Adolescent
*Autistic Disorder/therapy

@article {pmid40707990,
year = {2025},
author = {Drevland, OM and de Muinck, EJ and Trosvik, P and Hammerstad, M and Kvitne, KE and Midtvedt, K and Åsberg, A and Robertsen, I},
title = {Microbiome-derived reactivation of mycophenolate explains variations in enterohepatic recirculation in kidney transplant recipients.},
journal = {Microbiome},
volume = {13},
number = {1},
pages = {169},
pmid = {40707990},
issn = {2049-2618},
support = {315792//Norges Forskningsråd/ ; 315792//Norges Forskningsråd/ ; },
mesh = {*Mycophenolic Acid/pharmacokinetics/analogs & derivatives/metabolism ; *Kidney Transplantation ; Humans ; *Gastrointestinal Microbiome/drug effects ; Male ; Female ; *Immunosuppressive Agents/pharmacokinetics/therapeutic use ; Middle Aged ; Feces/microbiology ; Adult ; Transplant Recipients ; Glucuronidase/metabolism/genetics ; Glucuronides/metabolism ; Metagenomics/methods ; *Enterohepatic Circulation ; },
abstract = {BACKGROUND: The pivotal role of microbes in drug metabolism is increasingly recognized, as variation in the gut microbiome composition between individuals has been shown to impact systemic drug exposure, efficacy and toxicity. Mycophenolate mofetil (MMF) is a cornerstone in immunosuppressive therapy following solid organ transplantation. However, dosing and tolerance are challenged by significant pharmacokinetic variability among patients, largely due to variable degrees of enterohepatic recirculation of mycophenolic acid (MPA), the active moiety of MMF. It is hypothesized that the variability in MPA recirculation is driven by gut microbiome-derived β-glucuronidase (β-GUS) mediated cleavage of MPA-glucuronide (MPAG) excreted in the bile. Here, we investigated the bidirectional interaction between MPA and the gut microbiome in kidney transplant recipients, using a combination of in vivo and in vitro data.

RESULTS: We compared the fecal microbiomes of kidney transplant recipients (n = 21) both pre- and post-transplantation to healthy individuals (n = 15) using shotgun metagenomic sequencing. We also determined the individual microbiome-derived reactivation rate of MPAG to MPA and show a strong positive correlation between this reactivation rate and the degree of MPA enterohepatic recirculation in vivo. Through metagenomic analysis, the reactivation rate of MPA was linked to specific gut microbial species. In particular, specific β-GUS gene variants associated with Faecalibacterium prausnitzii showed a strong impact on the conversion of MPAG to MPA. Furthermore, our study confirmed a significant shift in microbial composition post-transplantation and revealed notable fluctuations in species such as F. prausnitzii and Akkermansia muciniphila across different time points after transplantation. Lastly, we provide evidence that the microbiome-derived reactivation rate of MPA is linked to specific beta-glucuronidase alleles.

CONCLUSIONS: We highlight for the first time that the ex vivo determined reactivation rate of MPA explains the variation of enterohepatic recirculation, emphasizing the important role of F. prausnitzii in this process. More broadly, our findings suggest that the gut microbiome significantly influences the degree of enterohepatic recirculation of MPA, providing valuable insights that could be relevant for optimizing individualized immunosuppressive drug dosing in transplant patients. Video Abstract.},
}

*Mycophenolic Acid/pharmacokinetics/analogs & derivatives/metabolism
*Kidney Transplantation
Humans
*Gastrointestinal Microbiome/drug effects
Male
Female
*Immunosuppressive Agents/pharmacokinetics/therapeutic use
Middle Aged
Feces/microbiology
Adult
Transplant Recipients
Glucuronidase/metabolism/genetics
Glucuronides/metabolism
Metagenomics/methods
*Enterohepatic Circulation

@article {pmid40707965,
year = {2025},
author = {Wang, X and Xiao, ZJ and Xue, CZ and Wu, WT and Yang, JH and Yan, C and Wang, Y and Kui, Y and Luo, WB and Du, X and Zan, RN and Shang, RJ and Li, S and Na, R and Han, S and Li, SZ},
title = {Clinical confirmation of an infection with Echinococcus multilocularis (Mongolian genotype): first case report of human alveolar echinococcosis in Inner Mongolia, China.},
journal = {Infectious diseases of poverty},
volume = {14},
number = {1},
pages = {74},
pmid = {40707965},
issn = {2049-9957},
support = {82404325//National Natural Science Foundation of China/ ; GWVI-11.1-12//Three-Year Initiative Plan for Strengthening Public Health System Construction in Shanghai (2023-2025) Key Discipline Project/ ; },
mesh = {*Echinococcus multilocularis/genetics/isolation & purification/classification ; Humans ; Female ; China ; Middle Aged ; Animals ; Genotype ; *Echinococcosis/parasitology/diagnosis ; Phylogeny ; *Echinococcosis, Hepatic/parasitology/diagnosis/surgery ; Fatal Outcome ; Dogs ; Liver Transplantation ; },
abstract = {BACKGROUND: Alveolar echinococcosis (AE), caused by the larval stage of Echinococcus multilocularis, poses a substantial global health challenge due to its high mortality profile. This study reports the inaugural human infection of echinococcosis caused by the Mongolian genotype of E. multilocularis in China, also the first reported indigenous AE case in Inner Mongolia.

CASE PRESENTATION: A 58-year-old female pastoralist from Inner Mongolia, who had no endemic region exposure history but prolonged occupational contact with dogs, presented with severe AE. Clinical examinations revealed a massive hepatic lesion exceeding 10 cm in diameter, accompanied by elevated eosinophils (0.90 × 10[9]/L) and basophils (0.08 × 10[9]/L). Despite undergoing liver transplantation, the patient succumbed postoperatively. Histopathological confirmation and molecular phylogenetics identified the Mongolian genotype of E. multilocularis infection, distinct from the predominant Asian genotype in China. Potential evidence of zoonotic transmission was discovered through genotype-matched E. multilocularis detection in corsac fox (Vulpes corsac) feces from the grasslands along the shores of Hulun Lake (Hulun Buir City, northeastern Inner Mongolia, China).

CONCLUSIONS: This report provides the primary evidence of a locally acquired human AE infection in China caused by the Mongolian genotype of Echinococcus multilocularis. The discovery of this case challenges historical classifications of echinococcosis endemic areas. The findings call for revised AE-endemic identification criteria, improved AE diagnostic protocols, and enhanced AE surveillance in the Inner Mongolia region to generate further epidemiological evidence and information on disease progression.},
}

*Echinococcus multilocularis/genetics/isolation & purification/classification
Humans
Female
China
Middle Aged
Animals
Genotype
*Echinococcosis/parasitology/diagnosis
Phylogeny
*Echinococcosis, Hepatic/parasitology/diagnosis/surgery
Fatal Outcome
Dogs
Liver Transplantation

@article {pmid40398302,
year = {2025},
author = {Yu, M and Xu, M and Wang, G and Feng, J and Zhang, M},
title = {Effect of cecal microbiota transplantation on peripheral 5-hydroxytryptamine and breast muscle glucose metabolism in long-photoperiod broilers.},
journal = {Poultry science},
volume = {104},
number = {8},
pages = {105225},
pmid = {40398302},
issn = {1525-3171},
mesh = {Animals ; *Chickens/physiology/metabolism/microbiology ; *Glucose/metabolism ; Male ; *Serotonin/metabolism ; *Photoperiod ; *Gastrointestinal Microbiome ; *Fecal Microbiota Transplantation/veterinary ; *Muscle, Skeletal/metabolism ; Random Allocation ; Cecum/microbiology ; },
abstract = {Prolonged light periods resulted in up-regulation of cecal 5-hydroxytryptamine (5-HT) synthesis and secretion, disorders of breast muscle glucose metabolism and alteration in gut microbiota composition. The present study was conducted to investigate the effects of cecal microbiota on peripheral 5-HT metabolism and breast muscle glucose metabolism in broiler chickens underlying prolonged light periods. A total of 144 5-day-old male Arbor Acres (AA) broiler chickens were randomly divided into four treatment groups i.e., 12 hours light: 12 hours dark (12L:12D) photoperiod group, 18 hours light: 6 hours dark (18L:6D) photoperiod group, 18L:6D photoperiod with phosphate buffered saline (PBS) solution administration group (18L:6D+PBS) and 18L:6D photoperiod with cecal microbiota transplantation (CMT) group (18L:6D+CMT) for 14 days. The results demonstrated that the 18L:6D photoperiod increased breast muscle rate (P < 0.05) but induced the morphological damage of breast muscle, dysregulation of breast muscle glucose metabolism and higher peripheral 5-HT synthesis (P < 0.05). In contrast, CMT significantly improved breast muscle weight and breast muscle ratio while reducing the breast muscle injury. Furthermore, CMT alleviated glucose metabolism dysregulation, as evidenced by significant reductions in serum glucose (P < 0.05), insulin (INS) (P < 0.05), homeostasis model assessment of insulin resistance (HOMA-IR) (P < 0.05), and the lactic acid-to-pyruvate ratio (L/P) (P < 0.05), as well as an increase in muscle glycogen concentrations (P < 0.05). Additionally, the expression of glycogen synthase (GS), pyruvate dehydrogenase (PDH) and glucose transporter-4 (GLUT4) up-regulated, while the expression of glycogen phosphorylase L (PYGL), hexokinase (HK), 6-phosphofructokinase (PFK), pyruvate kinase (PK) and lactate dehydrogenase (LDH) down-regulated (P < 0.05) in breast muscle of CMT-treated broiler chickens. Notably, both peripheral 5-HT concentrations and cecal 5-HT synthesis was significantly reduced (P < 0.05) in the 18L:6D+CMT group. In summary, these findings indicate that CMT promotes breast muscle rate, reduces breast muscle injury, alleviates breast muscle glucose metabolism disorder in broiler chickens exposed to prolonged light periods. Moreover, peripheral 5-HT metabolism may serve as a key pathway through which cecal microbiota regulates skeletal muscle glucose metabolism.},
}

Animals
*Chickens/physiology/metabolism/microbiology
*Glucose/metabolism
Male
*Serotonin/metabolism
*Photoperiod
*Gastrointestinal Microbiome
*Fecal Microbiota Transplantation/veterinary
*Muscle, Skeletal/metabolism
Random Allocation
Cecum/microbiology

@article {pmid39758049,
year = {2025},
author = {Bartha, V and Boutin, S and Schüßler, DL and Felten, A and Fazeli, S and Kosely, F and Luft, T and Wolff, D and Frese, C and Schoilew, K},
title = {Exploring the Influence of Oral and Gut Microbiota on Ulcerative Mucositis: A Pilot Cohort Study.},
journal = {Oral diseases},
volume = {31},
number = {6},
pages = {1776-1788},
doi = {10.1111/odi.15246},
pmid = {39758049},
issn = {1601-0825},
support = {//Deutsche Gesellschaft für Präventivzahnmedizin e. V. and CP GABA/ ; },
mesh = {Humans ; Pilot Projects ; Female ; Male ; Middle Aged ; *Gastrointestinal Microbiome ; Adult ; Feces/microbiology ; *Mouth Mucosa/microbiology ; Saliva/microbiology ; *Stomatitis/microbiology ; Aged ; Cohort Studies ; *Oral Ulcer/microbiology ; *Mucositis/microbiology ; RNA, Ribosomal, 16S/genetics ; Hematopoietic Stem Cell Transplantation/adverse effects ; },
abstract = {AIM: Comparing oral and gut microbiome profiles between patients with and without ulcerative mucositis during allogeneic stem cell transplantation (aSCT).

MATERIALS AND METHODS: Specimens from oral mucosa, saliva, and stool were collected pre-(T0) and post- (T0 +28d ± 14d) aSCT (T1). Microbiome structure differences were analyzed by 16S-rRNA-gene sequencing, and associations to patients' clinical characteristics were investigated.

RESULTS: Ten of 25 included patients developed ulcerations. The α-diversity decreased between T0 and T1, independent of ulcerations. PERMANOVA revealed differences in beta diversity between T1 stool samples from patients with and without ulcerations. At T1, saliva samples of patients with ulcerations showed an increase of Mycoplasma salvarius, while commensals decreased in saliva and mucosal swabs. The gut microbiome of both groups showed an overabundance of Enterococcus spp., associated with inflammatory conditions. Salival α-diversity of older and overweight patients decreased slower, whereas in mucosal swabs mucositis or impaired renal function was associated with a higher decline. Female gender and history of periodontitis were associated with increased stool microbiome changes, while self-reported probiotics intake was related to reduced changes.

CONCLUSIONS: Ulcerations appeared in 40% of the patients. Distinct microbial changes, including increased abundance of Mycoplasma salivarius in saliva and decreased abundance of commensals, marked those with ulcerations.

TRIAL REGISTRATION: The study was registered in the German Register for Clinical Studies (DRKS00032882).},
}

Humans
Pilot Projects
Female
Male
Middle Aged
*Gastrointestinal Microbiome
Adult
Feces/microbiology
*Mouth Mucosa/microbiology
Saliva/microbiology
*Stomatitis/microbiology
Aged
Cohort Studies
*Oral Ulcer/microbiology
*Mucositis/microbiology
RNA, Ribosomal, 16S/genetics
Hematopoietic Stem Cell Transplantation/adverse effects