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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

@article {pmid40818981,
year = {2025},
author = {Tao, M and Wu, T and Zhou, X and Li, F and Chen, Y and Ling, K and Liang, Z},
title = {Butyrate enhances gut dysbiosis by activating the cAMP/PKA/CREB signaling pathway to inhibit the progression of endometrial carcinoma.},
journal = {BMC microbiology},
volume = {25},
number = {1},
pages = {516},
pmid = {40818981},
issn = {1471-2180},
support = {2019YFC1005202//National Key Technology R&D Program of China/ ; },
}

@article {pmid40818371,
year = {2025},
author = {Zhang, H and Yan, S and Du, R and Ma, Z and Xue, Y and Zhao, Y and Yao, W and Chen, C and Li, X and Bao, S and Song, Y},
title = {Epiberberine alleviates cadmium-induced duodenal inflammation in Hu sheep by inhibiting HIF-1 signaling pathway.},
journal = {Ecotoxicology and environmental safety},
volume = {303},
number = {},
pages = {118861},
doi = {10.1016/j.ecoenv.2025.118861},
pmid = {40818371},
issn = {1090-2414},
abstract = {Environmental cadmium (Cd) exposure not only poses a significant threat to livestock health but also induces intestinal disorders in sheep. As a critical region for digestion and absorption, damage to the duodenum directly impairs systemic health. To elucidate the key mechanisms underlying Cd-induced duodenal injury and identify preventive and therapeutic strategies, this study utilized Cd-exposed Hu sheep as experimental models and applied multi-omics technologies, including non-targeted metabolomics, proteomics, and transcriptomics. The results showed that Cd exposure caused severe damage to the duodenum of Hu sheep, characterized by inflammatory cell infiltration and disruption of the intestinal barrier. Multi-omics analysis revealed that Cd exposure reduced levels of beneficial metabolites (such as vitamin K and riboflavin) while activating the HIF-1 signaling pathway. Through network pharmacology screening and molecular docking validation, epiberberine (EPI) was identified as a promising therapeutic candidate targeting the HIF-1α. Mouse fecal microbiota transplantation (FMT) experiments further confirmed that EPI can restore the intestinal barrier integrity, mitigate inflammatory responses, and effectively alleviate Cd-induced duodenal damage by inhibiting the HIF-1 signaling pathway, providing a novel approach for preventing and treating intestinal diseases under cadmium exposure.},
}

@article {pmid40816629,
year = {2025},
author = {Xu, J and Lao, Y and Zhang, W and Chen, L and Zhang, H and Liu, H and Yan, T and Huang, R and Xu, Y and Ye, L and Zhi, F and Yang, H},
title = {Berberine alleviates metabolic dysfunction-associated steatohepatitis by enhancing the abundance of Akkermansia muciniphila.},
journal = {The Journal of nutritional biochemistry},
volume = {},
number = {},
pages = {110069},
doi = {10.1016/j.jnutbio.2025.110069},
pmid = {40816629},
issn = {1873-4847},
abstract = {Metabolic dysfunction-associated steatohepatitis (MASH) is associated with intestinal barrier defects and gut microbiota dysbiosis. The gut commensal bacterium Akkermansia muciniphila (Akk) maintains intestinal barrier integrity and improves MASH-related metabolic syndromes. Berberine (BBR), a traditional Chinese medicine, shows promise in treating MASH. However, research on drugs that target Akk regulation and its underlying mechanisms remains limited. This study investigates the mechanisms by which BBR regulates Akk in MASH. We fed C57BL/6J male mice a methionine-choline-deficient (MCD) diet for 6 weeks to establish the MASH mouse models. The gut microbiota was analyzed using 16S rRNA sequencing and bacterial quantification measured by qPCR analysis. An antibiotic cocktail (Abx) and fecal microbiota transplantation (FMT) were applied to modulate gut microbiota. Results showed that BBR reduced hepatic and colonic inflammation, preserved intestinal barrier integrity and prevented microbiota translocation into the liver. The 16S rRNA sequencing and qPCR analysis revealed a significant increase in Akk abundance in fecal samples following BBR treatment. Mechanistically, BBR did not promote Akk growth directly, but it reduced the bacterial load and enhanced MUC2 expression, thereby facilitating Akk colonization indirectly. While disruption of the gut microbiota by antibiotics treatment weakened the therapeutic effect of berberine on MASH, transplanting of the fecal microbiota from BBR-treated mice could mitigate MASH in antibiotic-treated mice. Finally, BBR and Akk exhibited synergistic therapeutic effects against MASH. Our study illustrated that BBR alleviates MASH mice by enhancing Akk abundance and restoring intestinal barrier integrity. BBR and Akk combination therapy would be a promising strategy for MASH prevention.},
}

@article {pmid40816342,
year = {2025},
author = {Wellens, J and Vanderstappen, J and Hoekx, S and Vissers, E and Luppens, M and Van Elst, L and Lenfant, M and Raes, J and Derrien, M and Verstockt, B and Ferrante, M and Verbeke, K and Matthys, C and Vermeire, S and Sabino, J},
title = {Effect of five dietary emulsifiers on inflammation, permeability, and the gut microbiome: a placebo-controlled randomized trial.},
journal = {Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.cgh.2025.08.005},
pmid = {40816342},
issn = {1542-7714},
abstract = {BACKGROUND AND AIMS: Dietary emulsifier consumption might promote intestinal inflammation, eventually leading to inflammatory bowel diseases. However human data are scarce and involve a limited number of emulsifiers. We studied the effects of an emulsifier-free diet (EFD) and specific emulsifier supplementation.

METHODS: Sixty healthy participants followed an EFD for two weeks. Then, using a randomized placebo-controlled trial design, participants continued an EFD for four weeks with the addition of either carboxymethyl cellulose (CMC), polysorbate-80, carrageenan, soy lecithin, native rice starch (NRS), or no additives administered through brownies. Effects on cardiometabolic markers, gut microbiota, intestinal inflammation and permeability were explored.

RESULTS: After two weeks of EFD, cholesterol levels decreased (p=0.00006). Under emulsifier-supplementation, alpha diversity remained stable, yet microbial composition was affected by treatment and visit. Compared to placebo, concentrations of all short chain fatty acids (SCFAs) were lower in those consuming CMC, which was mirrored by other emulsifiers although not all reaching significance. No differences in faecal calprotectin, CRP, LBP, cholesterol levels or other metabolic markers were observed between placebo and emulsifiers at the end of the intervention. Serum inflammatory and cardiometabolic proteins remained unchanged. In individuals consuming carrageenan, transcellular intestinal permeability increased (p=0.04) compared to baseline.

CONCLUSION: In this double-blind placebo-controlled exploratory trial, emulsifier supplementation lowered SCFA concentration compared to placebo. Emulsifier supplementation did not impact intestinal or systemic inflammation, or metabolic endpoints. Cholesterol levels decreased after two weeks of EFD. These results point towards potential intestinal benefits of limiting dietary emulsifiers in the diet, requiring further investigation.},
}

@article {pmid40816329,
year = {2025},
author = {Smith, B},
title = {The heroes within: utilizing the gut microbiome, microbiome therapeutics, and fecal microbiota transplant in managing companion animal health and disease.},
journal = {Journal of the American Veterinary Medical Association},
volume = {},
number = {},
pages = {1-8},
doi = {10.2460/javma.25.03.0218},
pmid = {40816329},
issn = {1943-569X},
abstract = {Microbiome therapeutics are gaining recognition for their role in the management of companion animal health and disease. This narrative review provides the current definition of the gut microbiome, the organisms comprising the theater, and their contributions to host homeostasis. Several testing modalities to determine the composition and distribution of bacterial groups within the gut microbiome are available. Sensitivity, specificity, and depth of analysis differ among these testing platforms and, while further research is needed to build on their interpretation, provides the veterinary practitioner a way to identify dysbiosis occurrence in their patients. Integrating microbiome therapeutics into clinical practice can be achieved through a multimodal approach that utilizes diet, prebiotics, probiotics, postbiotics, bacteriophages, and fecal microbiota transplant to modulate the microbiome balance and restore eubiosis to patients in dysbiotic states. Available literature is revealing the potential broad applications of microbiome modulation, but further study is needed to determine more precise mechanisms of action of these therapies in order to fully explore their potential.},
}

@article {pmid40815946,
year = {2025},
author = {Li, ZX and Kang, KW and Zheng, H and Li, DL and Xu, JC and Lv, HQ and Wu, RH and Gan, LS},
title = {Puerarin-rich compound Puerariae lobatae formulas alleviate hyperuricemia in mice by enhancing renal and intestinal function through regulating gut microbiota.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {146},
number = {},
pages = {157115},
doi = {10.1016/j.phymed.2025.157115},
pmid = {40815946},
issn = {1618-095X},
abstract = {BACKGROUND: Hyperuricemia, a metabolic disorder strongly associated with gout and cardiorenal diseases, has become a global health threat affecting over 15% of the worldwide population. Current pharmacotherapies face limitations due to adverse effects during prolonged use. Natural medicines like Radix Puerariae Lobatae have demonstrated therapeutic potential with superior safety profiles.

PURPOSE: This study investigated the anti-hyperuricemic efficacy of compound Puerariae lobatae formulas (PLF1 and PLF2) and their bioactive component puerarin, focusing on their mechanisms for enhancing renal/intestinal uric acid excretion, alleviating pathological damage, and modulating gut microbiota composition.

METHODS: A hyperuricemic mouse model was established using an adenine/potassium oxonate diet. Mice were treated with PLF1 (250/500 mg/kg), PLF2 (300/600 mg/kg), puerarin (100 mg/kg), or benzbromarone (40 mg/kg, positive control). Plasma and tissue uric acid levels, XOD and ADA activities, and renal/intestinal transporter expression (ABCG2, OAT1) were analyzed. Histopathological examinations were performed using HE staining to assess kidney, liver, and intestinal integrity. Gut microbiota composition was evaluated via PacBio Sequel II 16S rRNA sequencing. Antibiotic-induced microbiota depletion and fecal microbiota transplantation (FMT) approaches were employed to validate microbiota-dependent effects.

RESULTS: PLF1, PLF2, and puerarin significantly reduced plasma uric acid levels and suppressed XOD/ADA activities. Histopathological analysis demonstrated marked improvements in renal tubular injury, hepatic steatosis, and intestinal structural integrity, including restoration of villus architecture and crypt morphology. The expression of renal ABCG2 and OAT1, as well as intestinal ABCG2, was significantly upregulated, accompanied by enhanced expression of colonic tight junction proteins (ZO-1 and occludin). Antibiotic-induced microbiota depletion abolished the hypouricemic effect of puerarin, while FMT from puerarin-treated donors significantly alleviated hyperuricemia in recipient mice. Gut microbiota analysis revealed that both PLF2 and puerarin selectively enriched the beneficial bacterium Akkermansia muciniphila while simultaneously reducing pathogenic taxa.

CONCLUSION: This study establishes Puerariae lobatae formulas and puerarin as multi-target therapeutics for hyperuricemia, offering dual advantages over conventional drugs by enhancing renal/intestinal uric acid excretion while also repairing organ damage, and remodeling gut microbiota to enrich probiotics like A. muciniphila. The microbiota-dependent efficacy of puerarin not only underscores its potential as a novel natural therapeutic agent but also provides critical pharmacological evidence for advancing puerarin and Radix Puerariae Lobatae-based formulas in hyperuricemia treatment, bridging traditional herbal medicine with modern microbiota-targeting strategies.},
}

@article {pmid40815137,
year = {2025},
author = {Skryabin, V},
title = {Gut microbiota and alcohol use disorder: a new frontier in treatment and recovery.},
journal = {BJPsych bulletin},
volume = {},
number = {},
pages = {1-8},
doi = {10.1192/bjb.2025.10129},
pmid = {40815137},
issn = {2056-4694},
abstract = {AIMS AND METHOD: Alcohol use disorder (AUD) is a major global health concern associated with limited treatment efficacy and high relapse rates. Recent research highlights the gut microbiota as a critical modulator of AUD pathophysiology through its influence on the gut-brain axis. Chronic alcohol consumption induces gut dysbiosis, characterised by reduced microbial diversity, impaired gut barrier function and systemic inflammation, which perpetuate neuroinflammation, stress dysregulation and neurotransmitter imbalances. These disruptions exacerbate addiction-related behaviours, contributing to the cycle of dependence and relapse. This critical review synthesises current evidence on the role of gut microbiota in AUD, examining the mechanisms linking dysbiosis to addiction and evaluating therapeutic interventions such as probiotics, prebiotics, faecal microbiota transplantation (FMT), psychobiotics and dietary modifications.

RESULTS: The strategies evaluated show significant potential in restoring microbial homeostasis and improving AUD outcomes, but challenges remain, including gaps in mechanistic understanding, variability in methodologies, and barriers to clinical translation.

CLINICAL IMPLICATIONS: There is a need for multi-omics research, personalised medicine approaches and integrated treatment models to advance microbiota-based therapies. Gut microbiota-targeted strategies might then transform AUD management, offering innovative and personalised solutions for addiction recovery.},
}

@article {pmid40814761,
year = {2025},
author = {Qin, P and Kragsnaes, MS and Holm, DK and Horn, HC and Nilsson, AC and Kjeldsen, J and Kristiansen, K and Ellingsen, T},
title = {Clinical Significance of Gut Microbiota Community Types for Long-term Response to Fecal Microbiota Transplantation in Patients with Psoriatic Arthritis.},
journal = {Arthritis & rheumatology (Hoboken, N.J.)},
volume = {},
number = {},
pages = {},
doi = {10.1002/art.43359},
pmid = {40814761},
issn = {2326-5205},
abstract = {OBJECTIVE: Fecal microbiota transplantation (FMT) holds promises as a beneficial supplement to methotrexate in patients with psoriatic arthritis (PsA). We therefore investigated how gut bacterial signatures in patients and donor strain engraftment associated with long-term response to FMT.

METHODS: This exploratory study is based on the FLORA trial cohort encompassing 31 patients with moderate-to-high PsA disease activity and four FMT donors. Out of fifteen patients receiving one single-donor FMT, thirteen were included in the per-protocol (PP) population. Stool samples were collected before and after FMT (week 4, 12, and 26). We performed shotgun metagenomics to characterize gut microbiota features.

RESULTS: At baseline, 17 patients (55%) had a gut microbiota community type dominated by the Bacteroides genus (B-type) while 14 (45%) had a Prevotella-driven community type (P-type). The B- and P-type patients did not differ in disease activity nor demographics, but the B-type had a significantly higher species diversity compared to the P-type (P=0.005). In the PP population, five out of seven B-type patients vs none out of six P-type patients (P=0.021) achieved a long-term clinical beneficial response at week 26. Bacterial strain richness increased significantly from baseline to week 4 and 26 in B-type (P=0.016), but not in P-type, patients. Eighteen engrafted strains persisted only in B-type recipients by week 26, including a Bacteroides clarus strain, which demonstrated a negative effect size regarding arthritis pain and the patients' global assessment of disease.

CONCLUSION: Recipients with a Bacteroides-dominated community structure were more likely to achieve long-term beneficial response following one FMT.},
}

@article {pmid40812693,
year = {2025},
author = {Pan, Y and Deng, Y and Yang, H and Yu, M},
title = {The aryl hydrocarbon receptor: A promising target for intestinal fibrosis therapy.},
journal = {Pharmacological research},
volume = {219},
number = {},
pages = {107909},
doi = {10.1016/j.phrs.2025.107909},
pmid = {40812693},
issn = {1096-1186},
abstract = {Intestinal fibrosis, a severe complication of inflammatory bowel disease, leads to intestinal stenosis. Effective therapies for this condition are lacking. The aryl hydrocarbon receptor (AhR), a highly conserved nuclear transcription factor activated by diverse ligands, plays dual roles in fibrogenesis, but its relationship to intestinal fibrosis has not been comprehensively reviewed. This review explores the pathogenesis of intestinal fibrosis, and places particular focus on the mechanistic role of AhR signaling pathways, which may be mediated by dietary, microbial, and environmental ligands. We propose a new strategy for the targeting of AhR-related dietary ligands to prevent intestinal fibrosis. Dietary AhR ligands, such as glucobrassicin, flavonoids, and curcumin, exert anti-fibrotic effects by modulating the gut microbiota, suppressing collagen deposition, and inhibiting transforming growth factor-β pathways. Conversely, environmental pollutants (e.g., polycyclic aromatic hydrocarbons, microplastics, and propiconazole) exacerbate fibrosis via AhR activation. In multiple disease models, 16S rRNA sequencing has revealed positive and negative linear relationships between the gut microbiota and fibrosis. Intestinal microbiota-derived metabolites also affect fibrosis, including via immune cell regulation to indirectly reduce collagen deposition and direct action on extracellular matrix-related proteins to relieve intestinal fibrosis. The interaction among the AhR, microbiota, and diet suggests new therapeutic strategies, such as dietary interventions and fecal microbiota transplantation, to restore the microbial balance and inhibit fibrosis. The promotion of intestinal fibrosis by AhR agonists in environmental pollutants further emphasizes the need to reduce exposure to environmental toxins while following a plant-based diet rich in AhR agonists.},
}

@article {pmid40812589,
year = {2025},
author = {Liu, L and Liang, L and Liang, H and Wang, M and Zhou, W and Mai, G and Yang, C and Chen, Y},
title = {Microbiome-metabolome generated bile acids gatekeep infliximab efficacy in Crohn's disease by licensing M1 suppression and Treg dominance.},
journal = {Journal of advanced research},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jare.2025.08.017},
pmid = {40812589},
issn = {2090-1224},
abstract = {INTRODUCTION: Despite the effectiveness of infliximab in treating Crohn's disease (CD), up to 40 % of patients fail to respond adequately.

OBJECTIVES: This study aimed to identify predictive biomarkers of primary non-response to infliximab in treatment-naïve CD patients by characterizing baseline gut microbiome-metabolome interactions and to validate their mechanistic role in driving therapeutic resistance.

METHODS: In a prospective cohort of 100CD patients initiating infliximab therapy and 49 healthy controls, we performed longitudinal 16S rRNA sequencing and untargeted metabolomics on pre-/post-treatment fecal samples. Machine learning (twelve algorithms including K-Nearest Neighbors, Linear Discriminant Analysis, Naive Bayes, and LightGBM) identified predictive microbial and metabolic features, with findings experimentally validated through fecal microbiota transplantation (FMT) in a murine TNBS-induced colitis model.

RESULTS: Non-responders demonstrated significant microbial dysbiosis marked by reduced α-diversity, depletion of Bifidobacterium, Blautia, and Lachnospiraceae, and enrichment of Escherichia/Shigella. Metabolomic profiling identified 179 differentially abundant metabolites, including deficiencies in taurochenodeoxycholic acid (TCDCA) and perturbations in glycerophospholipid metabolism and primary bile acid biosynthesis pathways. Among single-omics models, the microbiome-based Linear Discriminant Analysis achieved optimal performance (test AUC = 0.805), surpassing metabolomics-only (best AUC = 0.634) and integrated multi-omics approaches (best AUC = 0.779). SHAP analysis revealed Bifidobacterium as the dominant protective predictor, with its depletion strongly associated with non-response. Mechanistically, MIMOSA2 analysis linked Bifidobacterium catenulatum to TCDCA production, while FMT from non-responders exacerbated murine colitis through Treg depletion and M1 macrophage polarization, confirming microbiome-driven immune dysregulation.

CONCLUSIONS: These findings establish gut microbiome composition, particularly Bifidobacterium abundance, as a critical determinant of anti-TNF response in CD, mediated through bile acid-dependent regulation of Treg/M1 macrophage homeostasis. While multi-omics integration did not enhance predictive performance, microbiome-based machine learning models offer clinically actionable biomarkers for treatment stratification, providing a roadmap for precision therapy to overcome biological resistance in inflammatory bowel disease.},
}

@article {pmid40812483,
year = {2025},
author = {Han, Q and Xia, S and Huang, X and He, J and Yin, Y and Yin, J},
title = {Age-related differences in the gut microbiota of pigs influence fat deposition in the mouse.},
journal = {The Journal of nutrition},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.tjnut.2025.07.022},
pmid = {40812483},
issn = {1541-6100},
abstract = {BACKGROUND: The gut microbiota significantly influences lipid metabolism, but the impact of its developmental patterns at different growth stages on fat deposition remains unclear.

OBJECTIVES: This study aimed to explore the dynamic changes in microbial diversity and composition during the growth of pig models and assess their involvement in fat deposition.

METHODS: Forty-five Duroc-Landrace-Yorkshire (DLY) crossbred pigs were euthanized at five ages: 90, 120, 150, 180, and 210 days of age (n=9). Fecal samples were collected 1 day and 15 days before each euthanasia, and the fecal microbiota were detected by 16S rRNA sequencing. The backfat thickness, serum lipid levels, intramuscular fat, and fatty acid content in the longissimus dorsi muscle of pigs were measured to assess lipid metabolism. Fecal microbiota transplantation (FMT) from DLY pigs of different ages to antibiotics-challenged mice (n=8) was used to confirm the effects of microbial development on fat deposition. Metagenomic sequencing was conducted on feces from pigs aged 150 and 180 days and their corresponding transplanted mice to identify key strains involved in fat deposition.

RESULTS: We observed marked alterations and an increase in intestinal microbial α-diversity with age, peaking at 150 days of age in DLY pigs (P<0.05). Spearman correlation analyses indicated that 20 genera significantly correlated with the muscle fatty acid contents (P<0.05). FMT further confirmed that the developmental patterns of the gut microbiota affected host fat deposition, with notable differences observed between the fecal microbiota at day 150 and 180 of age in pigs. Schaalia canis was identified as a potential key microbial strain involved in the developmental patterns of the gut microbiota-governed fat deposition, and its colonization in mice reduced fat deposition by downregulating of LXRα/β gene expressions (P<0.05).

CONCLUSIONS: This study indicated that gut microbiota development impacted fat deposition in pigs, with Schaalia canis capable of inhibiting fat deposition.},
}

@article {pmid40811474,
year = {2025},
author = {Hosari, S and Ramser, M and Turina, M},
title = {Faecal incontinence in the era of sacral neuromodulation.},
journal = {Swiss medical weekly},
volume = {155},
number = {},
pages = {4298},
doi = {10.57187/s.4298},
pmid = {40811474},
issn = {1424-3997},
abstract = {Faecal incontinence is a debilitating condition that significantly affects an individual's quality of life. Accurate assessment and a thorough understanding of the underlying aetiology are crucial in determining the appropriate management approach. Conservative management strategies, including dietary modifications, pelvic floor exercises and biofeedback therapy are the first therapeutic steps. If these measures are not effective, patients should be referred to a specialised pelvic floor centre for further treatment evaluations. With the latest updates on national and international guidelines, this review aims to provide a comprehensive overview of current best practices in the management of faecal incontinence, with a particular focus on the role of sacral neuromodulation.},
}

@article {pmid40810777,
year = {2025},
author = {Li, S and Lian, S and Chen, Z and Luo, Y and Xia, P},
title = {The Application and Limitations of Promising Biological Therapies in Livestock Production under the Context of Antibiotic Restrictions.},
journal = {Probiotics and antimicrobial proteins},
volume = {},
number = {},
pages = {},
pmid = {40810777},
issn = {1867-1314},
support = {No. 32072820//The Chinese National Science Foundation/ ; 2021YFD1800404//the National Key Research and Development Program of China/ ; },
abstract = {The inappropriate use of antibiotics in livestock production has raised significant public health concerns, including the emergence of bacterial resistance and the presence of drug residues. In an era characterized by "antibiotic reduction and restriction", scientific inquiry has increasingly focused on developing alternatives to antibiotics, particularly through biocontrol strategies that utilize beneficial microorganisms to counteract pathogenic ones. Common biological therapies include probiotic therapy, phage therapy, and fecal microbiota transplantation (FMT). These innovative approaches can effectively eliminate or suppress pathogenic microorganisms with fewer side effects, thereby enhancing the safety of food animals and their products. This review systematically examines these three biological interventions, elucidating their molecular mechanisms, veterinary applications, and current limitations. This paper aims to critically evaluate the translational potential and practical implementation of these novel therapies while providing evidence-based perspectives on their future optimization and advancement.},
}

@article {pmid40810221,
year = {2025},
author = {Raoqiong, W and Linyao, H and Ye, LU and Lingxue, W and Jianrong, LI and Yan, P and Hongmei, T and Shuangyang, LI and Xue, B},
title = {Mechanism analysis of Tongqiao Yizhi decoction in treating vascular dementia rats by brain tissue untargeted metabonomics and fecal 16S rRNA gene sequencing.},
journal = {Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan},
volume = {45},
number = {4},
pages = {759-769},
pmid = {40810221},
issn = {2589-451X},
support = {southwest Medical University [2021] No. 1//Southwest Medical University Project: Exploring the Neuroprotective Mechanism of Tongqiao Yizhi Decoction on Vascular Dementia Rats Based on the Brain Gut Axis/ ; },
abstract = {OBJECTIVE: To analyze the mechanism of Tongqiao Yizhi decoction (TQYZD,) in treating vascular dementia (VaD) rats using brain tissue untargeted metabonomics and fecal 16S rRNA gene sequencing.

METHODS: The chemical composition of TQYZD was analyzed by ultra-high performance liquid chromatography-high resolution mass spectrometry. The effects of TQYZD on VaD rats were evaluated by water maze test, hematoxylin-eosin staining, enzyme-linked immunosorbent assay and Western blot. Untargeted metabolomics and 16S rRNA sequencing were utilized to explore the relationship between metabolic profiles and the structure and function of intestinal flora. Fecal microbiota transplantation (FMT) was used to validate the role of gut microbiota in VaD. Spearman correlation analysis of differential metabolites and gut microbiota was performed.

RESULTS: The results showed that TQYZD improved cognitive function and neuronal damage in VaD rats, and reduced inflammatory response and repaired the intestinal barrier. In addition, TQYZD had the effect of modulating gut microbes in VaD rats, and FMT further confirmed that gut flora plays an important role in TQYZD treatment of VaD. Untargeted metabolomics revealed that VaD could lead to metabolic disorders in brain tissues, and TQYZD significantly altered the metabolites of brain tissues in Middle Cerebral Artery Occlusion rats. The results of spearman correlation analysis showed that there was a significant correlation between intestinal flora and the metabolites of brain tissues.

CONCLUSION: In this study, we demonstrated that TQYZD can improve metabolic disorders in vascular dementia rats by acting on intestinal flora.},
}

@article {pmid40809053,
year = {2025},
author = {Huo, S and Lv, K and Han, L and Zhao, Y and Jiang, J},
title = {Gut microbiota in gastric cancer: from pathogenesis to precision medicine.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1606924},
pmid = {40809053},
issn = {1664-302X},
abstract = {Gastric cancer (GC) remains a significant global health burden, driven by a complex interplay of genetic, environmental, and microbial factors. Emerging evidence highlights the critical role of gut microbiota in gastric carcinogenesis, as microbial dysbiosis disrupts gastrointestinal homeostasis, fuels chronic inflammation, and promotes immunomodulation and metabolic reprogramming. Helicobacter pylori, a key microbial player, initiates tumorigenic pathways through reactive oxygen species production and the manipulation of dietary and microbial metabolites, leading to epigenetic and genetic alterations. Targeting gut microbiota has emerged as a promising therapeutic strategy, with interventions such as probiotics, prebiotics, dietary modifications, antibiotics, and fecal microbiota transplantation (FMT) showing potential in restoring microbial balance and attenuating tumor progression. Furthermore, advances in microbiota research have identified microbial biomarkers as valuable tools for early diagnosis, prognosis, and personalized treatment of GC. This review evaluates therapeutic strategies for microbiota modulation, assesses its diagnostic and prognostic potential, and highlights current gaps in the field. It also advocates for the integration of microbiota-targeted therapies into clinical practice, emphasizing their transformative potential in the prevention and management of GC. By addressing these aspects, this review aims to provide a comprehensive understanding of the role of gut microbiota in GC and to guide future research and clinical applications.},
}

@article {pmid40809043,
year = {2025},
author = {Yan, J and Pan, Y and Liu, H and Yuan, J and Chen, J and Gao, Y and Lin, C and Lin, F and Wang, R and He, Y and Wang, C and Xu, C and Li, T and Zhang, P and Lan, Y and Shao, W and Pang, X and Yin, D and Sun, X and Luo, W},
title = {Bisphenol F exposure induced vascular toxicity through intestinal microbiota imbalance.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1622488},
pmid = {40809043},
issn = {1664-302X},
abstract = {INTRODUCTION: Bisphenol F (BPF), a common substitute for bisphenol A (BPA), has documented toxicity in multiple organs, but its vascular effects remain unclear. This study investigated BPF's role in vascular calcification (VC) and underlying mechanisms.

METHODS: Differences in the intestinal microbiota were analyzed by 16S ribosomal RNA gene sequencing. Metabolites were analyzed using liquid chromatography-mass spectrometry. Faecal microbiota transplantation and antibiotic treatment experiments were performed to evaluate the functions of the intestinal microbiota in VC.

RESULTS: We enrolled consecutively 57 patients. Patients were assigned to a calcification group (30 patients) and a non-calcification group (27 patients) based on the presence or absence of calcification in the thoracic aorta wall. The results showed that patients with vascular calcification (VC) had higher levels of bisphenol F (BPF), bisphenol S (BPS) and bisphenol A (BPA) in the fecal samples than patients without VC. The thoracic aortic calcification score was significantly positively correlated with the BPF (Spearman r = 0.4935, p < 0.001), BPA (Spearman r = 0.2860, p < 0.05) and BPS (Spearman r = 0.2650, p < 0.05). We then explored the effects of BPF exposure on normal and vitamin D3 + nicotine (VDN)-treated rats. BPF exposure induced mild VC in normal rats and aggravated VC in VDN-treated rats. BPF exposure disturbed the gut microbiota and promoted inflammatory responses.

CONCLUSION: The results here elucidate the mechanism underlying BPF-triggered or BPF-aggravated VC through the gut-vascular axis and provide a theoretical basis for cardiovascular disease risk assessment in humans.},
}

@article {pmid40808958,
year = {2025},
author = {Wang, Y and Li, X and Gao, F},
title = {Chronic obstructive pulmonary disease: in-depth analysis of microbiota association and innovative prevention and treatment approaches from the gut-lung axis perspective.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1549865},
pmid = {40808958},
issn = {1664-3224},
abstract = {The pathogenesis of chronic obstructive pulmonary disease (COPD) is complex and affects multiple systems. This article focuses on COPD and elaborates on the roles of the lung and gut microbiota as well as preventive and therapeutic strategies. Innovatively, this article reveals the impact of the connection between the lung and gut microbiota via the gut-lung axis on COPD, clarifies the association between changes in the lung microbiota and clinical features, enriches the understanding of the correlation between gut dysbiosis and COPD, breaks through the limitations of single-organ research, and opens up a completely new path for uncovering the underlying pathogenesis of COPD. In terms of prevention and treatment, gut microbiota-targeted therapies (fecal microbiota transplantation, probiotics and prebiotics) provide new ideas and evidence. Research on dietary factors (vitamins, dietary fiber) helps with precise nutritional interventions and highlights the significance of dietary adjustments. The multi-target actions of natural compounds integrate traditional and modern medicine and lay the foundation for the development of new approaches, which is of great significance and value for COPD research, clinical translation, and the improvement of patient health.},
}

@article {pmid40808658,
year = {2025},
author = {Emile, SH and Oslin, RL and Wignakumar, A and Horesh, N and Garoufalia, Z and Wexner, SD and Boutros, M},
title = {Association between anastomotic leak after rectal resection and bowel dysfunction, a systematic review, meta-analysis and meta-regression.},
journal = {Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland},
volume = {27},
number = {8},
pages = {e70186},
pmid = {40808658},
issn = {1463-1318},
abstract = {BACKGROUND: Anastomotic leak (AL) after colorectal anastomosis can be a risk factor for bowel dysfunction, namely low anterior resection syndrome (LARS). The present study aimed to assess bowel dysfunction in patients who developed AL after anterior resection compared to patients without AL.

METHODS: We conducted a PRISMA-compliant systematic review of PubMed, Scopus and Cochrane Library for randomized and observational studies investigating the association between AL after anterior resection and bowel dysfunction. The main outcomes were LARS, faecal incontinence and urgency. Pairwise meta-analyses were conducted to calculate the relative risk (RR) of the study outcomes and their 95% confidence intervals (CI).

RESULTS: This review included 20 retrospective studies comprising 4764 patients (61.6% male, median age 63 years). AL was detected in 14% of patients and those who experienced AL had a higher risk of LARS (six studies; 1329 patients, RR: 1.27 95%CI: 1.02, 1.58, p = 0.035), major LARS (seven studies; 1395 patients, RR: 1.38, 95%CI: 1.07, 1.79, p = 0.012), urgency (five studies; 955 patients, RR: 1.15, 95%CI: 1.04, 1.27, p = 0.005) and had higher LARS scores (seven studies; 1450 patients, WMD: 6.64, 95%CI: 3.76, 9.52, p < 0.001) and Wexner incontinence scores (seven studies; 1045 patients, WMD: 1.72, 95%CI: 0.16, 3.28, p = 0.031).

CONCLUSION: Based on low to moderate certainty evidence, AL after colorectal and coloanal anastomoses was significantly associated with an increased risk of LARS, particularly major LARS, urgency and higher LARS and Wexner/Cleveland Clinic Florida-Fecal Incontinence Scores.},
}

@article {pmid40806882,
year = {2025},
author = {Lahoud, C and Habib, T and Kalta, D and Dimachkie, R and El Sayegh, S and Deeb, L},
title = {Intestinal Microbiota and Fecal Transplantation in Patients with Inflammatory Bowel Disease and Clostridioides difficile: An Updated Literature Review.},
journal = {Journal of clinical medicine},
volume = {14},
number = {15},
pages = {},
pmid = {40806882},
issn = {2077-0383},
abstract = {Background/Objectives: Inflammatory bowel disease (IBD) is characterized by chronic relapsing and remitting inflammation of the gastrointestinal tract. Fecal microbiota transplantation (FMT) has emerged as an FDA-approved treatment for recurrent Clostridioides difficile infections (CDIs), with promising potential in patients with IBD. This manuscript aimed to provide a comprehensive and updated review of the available literature on fecal microbiota transplantation, its clinical use in IBD in general, as well as in patients with IBD and CDI. Methods: An extensive literature search was performed from October 2024 to March 2025. All publications available within PubMed, Medline, Embase, Google Scholar, and Cochrane databases were reviewed. All original articles, case reports, review articles, systematic reviews, and meta-analyses were included. Qualitative and quantitative data were both extracted. Discussion: Intestinal microbiota is an integral part of the human body, and dysbiosis (an imbalance in the gut's microbial community) has been linked with several pathologies. Dysbiosis in IBD is marked by reduced beneficial bacteria and increased pro-inflammatory pathogens, contributing to mucosal damage and immune dysregulation. FMT has emerged as a solution to dysbiosis, with the first case recorded in 1917. FMT has been successful in treating patients with CDI. The diagnostic value of the gut microbiome is currently being explored as a possible therapeutic approach to IBD. Several studies have assessed FMT in patients with IBD and CDI with promising results in both ulcerative colitis (UC) and Crohn's disease (CD) but varying efficacy based on administration routes, donor selection, and processing methods. In the context of recurrent CDI in patients with IBD, FMT demonstrates a high cure rate and potential benefit in concurrently improving IBD activity. However, risks such as IBD flare-ups post-FMT remain a concern. Conclusions: FMT holds promising potential in the management of CDI in patients with IBD. By restoring microbial diversity and correcting dysbiosis, FMT offers a novel, microbiota-targeted alternative to conventional therapies. While data support its efficacy in improving disease remission, variability in outcomes underscores the need for standardized protocols and additional large-scale, controlled studies. Continued research efforts into donor selection, treatment regimens, and long-term safety will be critical to optimizing FMT's role in IBD and CDI care as well as improving patient outcomes.},
}

@article {pmid40806022,
year = {2025},
author = {Yang, H and Er, D and Wang, YH and Zhai, BT and Ge, R},
title = {Camel Milk-Derived Extracellular Vesicles as a Functional Food Component Ameliorate Hypobaric Hypoxia-Induced Colonic Injury Through Microbiota-Metabolite Crosstalk.},
journal = {Nutrients},
volume = {17},
number = {15},
pages = {},
pmid = {40806022},
issn = {2072-6643},
support = {2024-QYY-1//2024 Qinghai University Youth Research Fund Project (Natural Sciences)/ ; Grant No. 2025-ZJ-911Q//2025 Youth Project of Qinghai Provincial Basic Research Program/ ; Grant No. 2025-ZJ-748//2025 Basic Research Program/ ; },
abstract = {Background/Objectives: This study investigates the therapeutic potential of camel milk-derived extracellular vesicles (CM-EVs) for treating colonic damage caused by high-altitude hypoxia, supporting the WHO's "Food as Medicine" initiative. Methods: Using a 5500 m mouse model, researchers induced colonic injury and treated it with oral CM-EVs for 15 days, comparing results to whole camel milk. Results: CM-EVs outperformed whole milk, significantly improving colon health by restoring barrier integrity and reducing disease activity index (DAI) (p < 0.01). They boosted beneficial bacteria like Lactobacillus and Bifidobacterium and decreased Enterobacteriaceae (p < 0.01). Metabolic analysis showed restored bile acid balance and amino acid modulation via the FXR/NF-κB pathway, reducing TLR4/MyD88-mediated inflammation and oxidative stress (p < 0.01). Fecal microbiota transplantation in the CM-EVs group notably decreased DAI and increased colon length (p < 0.05). Conclusions: CM-EVs repair mucosal damage, balance microbiota, and regulate metabolism to combat hypoxia-induced colonic damage, suggesting their potential as nutraceuticals and altitude-adaptive foods. This showcases nanotechnology's role in enhancing traditional dietary benefits via precision nutrition.},
}

@article {pmid40803572,
year = {2025},
author = {Mahajan, S and Navya, M and Banerjee, SK},
title = {Future potential therapeutics to treat MASH.},
journal = {Drug discovery today},
volume = {},
number = {},
pages = {104451},
doi = {10.1016/j.drudis.2025.104451},
pmid = {40803572},
issn = {1878-5832},
abstract = {Metabolic dysfunction-associated steatohepatitis (MASH), a progressive form of Metabolic-associated steatotic liver disease (MASLD), poses a significant global health challenge due to its association with obesity, type 2 diabetes, and cardiovascular complications. Despite its rising prevalence, effective therapies remain limited. This review highlights emerging therapeutic strategies that target key pathways involved in MASH pathogenesis, including THR-β, FXR, PPAR, GLP-1RA, FGF21, and SGLT2. In addition, novel approaches such as gene therapy (siRNA), probiotics, fecal microbiota transplantation, and stem cell therapy show promise for the treatment of MASH. Ongoing clinical trials and mechanistic insights into fibrosis, inflammation, and lipid metabolism provide hope for tailored, multi-targeted treatments. Future efforts must address safety, long-term efficacy, and non-invasive diagnostics to advance the management of MASH.},
}

@article {pmid40803054,
year = {2025},
author = {Moutsoglou, D and Blake, M and Belhasan, DC and Peichel, G and Vang, BM and Weir, EK and Lopez, S and Prins, KW and Kabage, AJ and Prisco, SZ and Kremer, BP and Khoruts, A and Thenappan, T},
title = {Microbiota Transplant Therapy Is Safe and Feasible in Pulmonary Arterial Hypertension.},
journal = {JACC. Basic to translational science},
volume = {10},
number = {9},
pages = {101347},
doi = {10.1016/j.jacbts.2025.101347},
pmid = {40803054},
issn = {2452-302X},
support = {R01 HL158795/HL/NHLBI NIH HHS/United States ; R01 HL162927/HL/NHLBI NIH HHS/United States ; },
abstract = {Pulmonary arterial hypertension (PAH) is a complex inflammatory disease that the gut microbiome likely contributes to and may be a potential therapeutic avenue for nontoxically improving outcomes. Here, we show that microbiota transplant therapy (MTT) is safe and feasible. The MTT regimen achieves only modest levels of donor microbiota engraftment but is accompanied by a transient reduction in circulating pro-inflammatory cytokines. These findings of decreased systemic inflammation with only modest donor engraftment support the potential of MTT as a novel treatment for PAH. (Microbiota Transplant Therapy for Pulmonary Arterial Hypertension: Early Safety and Feasibility Study; NCT04884971).},
}

@article {pmid40801260,
year = {2025},
author = {Yan, B and Zheng, X and Lu, D and Li, T and Chen, X and Shao, Z and Fu, T},
title = {Silibinin-drived microbiota enrich (R)-2,3-dihydroxy-isovalerate and ameliorate colitis via the GAT-3/RARβ/RORγt axis.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wraf175},
pmid = {40801260},
issn = {1751-7370},
abstract = {Microbiota-associated factors are increasingly recognized as significant contributors to the progression of ulcerative colitis, and microbial modulation has emerged as an effective therapy for this condition. The herbal compound silibinin has demonstrated properties that modulate gut microbiota. Herein, we investigated the response of gut microbiota to silibinin in ameliorating colitis, using a mouse model of colitis coupled with antibiotic exposure. Results indicated that antibiotic pretreatment negated the benefits of silibinin in mice with colitis. Furthermore, fecal microbiota transplantation involving silibinin-modulated gut microbiota further substantiated the gut microbiota-dependent effects of silibinin. Within the metabolic profiles of silibinin-regulated microbiota, we identified that Alistipes-associated (R)-2,3-dihydroxy-isovalerate exhibited the most pronounced anti-inflammatory effects in vitro and demonstrated protective effects against colitis. Moreover, (R)-2,3-dihydroxy-isovalerate reinstated the protective effects of silibinin in mice with colitis under antibiotic exposure. These effects were primarily mediated via the targeting of the colonic GABA transporter 3 by (R)-2,3-dihydroxy-isovalerate. We further revealed that the retinoic acid receptor β and the retinoid-related orphan nuclear receptor γt may mediate the impact of silibinin-derived microbiota and (R)-2,3-dihydroxy-isovalerate on colitis. Additionally, the knockdown of colonic GABA transporter 3 diminished the impact of silibinin on the GABA transporter 3/retinoic acid receptor β/retinoid-related orphan nuclear receptor γt axis and colitis. Our findings highlight that (R)-2,3-dihydroxy-isovalerate, enriched from microbiota derived from silibinin, can target the GABA transporter 3/retinoic acid receptor β/retinoid-related orphan nuclear receptor γt axis, which is essential for anti-colitis properties of silibinin-regulated microbiota.},
}

@article {pmid40799652,
year = {2025},
author = {Liu, M and Geng, J and Liu, T and Liu, X},
title = {Gut microbiome dysregulation in noninfectious uveitis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1614304},
pmid = {40799652},
issn = {1664-3224},
abstract = {Noninfectious uveitis (NIU) is a vision-threatening autoimmune disease of the eye, but its pathogenesis is still not fully understood. Recently, accumulating evidence suggests that gut microbiome dysbiosis may affect the development and progression of NIU through potential mechanisms, including translocation, molecular mimicry, and bystander activation. Understanding the mechanisms of gut microbiome-host interactions, especially the gut-eye axis regulation, can offer a theoretical foundation for developing novel therapeutic strategies. We summarized current evidence on the dysregulation of gut microbiome and metabolites in NIU, and explored potential mechanisms involved. Furthermore, possible therapeutic measures are discussed, including probiotics, prebiotics, dietary modifications, antibiotic interventions, as well as fecal microbial transplantation, aiming to exert beneficial effects on NIU progression by reshaping the gut microbial composition.},
}

@article {pmid40797316,
year = {2025},
author = {Tang, A and Jiang, H and Li, J and Chen, Y and Zhang, J and Wang, D and Hu, S and Lai, J},
title = {Gut microbiota links to cognitive impairment in bipolar disorder via modulating synaptic plasticity.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {470},
pmid = {40797316},
issn = {1741-7015},
support = {82201676//National Natural Science Foundation of China/ ; 82471542//National Natural Science Foundation of China/ ; No. JNL-2023001B//Research Project of Jinan Microecological Biomedicine Shandong Laboratory/ ; 2023YFC2506200//National Key Research and Development Program of China/ ; 2021C03107//Zhejiang Provincial Key Research and Development Program/ ; 2023ZFJH01-01//Fundamental Research Funds for the Central Universities/ ; 2024ZFJH01-01//Fundamental Research Funds for the Central Universities/ ; No. 2021R52016//Leading Talent of Scientific and Technological Innovation - "Ten Thousand Talents Program" of Zhejiang Province/ ; 2022KTZ004//Chinese Medical Education Association/ ; },
abstract = {BACKGROUND: Cognitive impairment is an intractable clinical manifestation of bipolar disorder (BD), but its underlying mechanisms remain largely unexplored. Preliminary evidence suggests that gut microbiota can potentially influence cognitive function by modulating synaptic plasticity. Herein, we characterized the gut microbial structure in BD patients with and without cognitive impairment and explored its influence on neuroplasticity in mice.

METHODS: The gut structure of microbiota in BD without cognitive impairment (BD-nCI) patients, BD with cognitive impairment (BD-CI) patients, and healthy controls (HCs) were characterized, and the correlation between specific bacterial genera and clinical parameters was determined. ABX-treated C57 BL/J male mice were transplanted with fecal microbiota from BD-nCI, BD-CI patients or HCs and subjected to behavioral testing. The change of gut microbiota in recipient mice and its influence on the dendritic complexity and synaptic plasticity of prefrontal neurons were examined. Finally, microbiota supplementation from healthy individuals in the BD-CI mice was performed to further determine the role of gut microbiota.

RESULTS: 16S-ribosomal RNA gene sequencing reveals that gut microbial diversity and composition are significantly different among BD-nCI patients, BD-CI patients, and HCs. The Spearman correlation analysis suggested that glucose metabolism-related bacteria, such as Prevotella, Faecalibacterium, and Roseburia, were correlated with cognitive impairment test scores, and inflammation-related bacteria, such as Lachnoclostridium and Bacteroides, were correlated with depressive severity. Fecal microbiota transplantation resulted in depression-like behavior, impaired working memory and object recognition memory in BD-CI recipient mice. Compared with BD-nCI mice, BD-CI mice exhibited more severely impaired object recognition memory, along with greater reductions in dendritic complexity and synaptic plasticity. Supplementation of gut microbiota from healthy individuals partially reversed emotional and cognitive phenotypes and neuronal plasticity in BD-CI mice.

CONCLUSIONS: This study first characterized the gut microbiota in BD-CI patients and highlighted the potential role of gut microbiota in BD-related cognitive deficits by modulating neuronal plasticity in mice model.},
}

@article {pmid40796882,
year = {2025},
author = {He, Y and Li, Q and Sun, Q and Li, H and Yu, T and Chen, M and Zhang, G and Zhang, B and Wang, W and Ju, S},
title = {Gut microbiota contributes to polystyrene nanoplastics-induced fetal growth restriction by disturbing placental nicotinamide metabolism.},
journal = {Journal of nanobiotechnology},
volume = {23},
number = {1},
pages = {561},
pmid = {40796882},
issn = {1477-3155},
support = {PAPD//Priority Academic Program Development of Jiangsu Higher Education Institutions/ ; KYCX24_0999//Graduate Research and Innovation Projects of Jiangsu Province/ ; },
abstract = {Polystyrene nanoplastics (PS-NPs) are ubiquitous in the environment, eliciting significant concerns about their possible risks to human health, especially reproductive health. Various reproductive toxicities of PS-NPs have been reported, however, information regarding the effects of PS-NPs exposure during pregnancy on offspring development and the underlying mechanisms remains limited. In this study, pregnant mice were orally administered PS-NPs (approximately 100 nm in diameter) at different concentrations (1, 10, and 100 mg/kg/day) for 17.5 consecutive days, from gestational day (GD) 0.5 to GD 17.5. The relevant samples were collected on GD 18.5 to investigate the intergenerational effects. The results indicated that PS-NPs induced placental injury and metabolic abnormalities, leading to adverse pregnancy outcomes. Specifically, PS-NPs exposure observably reduced the levels of nicotinamide (NAM) and nicotinamide adenine dinucleotide (NAD[+]) in the placenta, resulting in decreased ATP production, increased oxidative stress and ferroptosis. Meanwhile, PS-NPs disrupted the maternal gut microbiome, specifically manifested as a reduction in Lactobacillus levels and abundances of norank_f_Muribaculaceae, Turicibacter, Alloprevotella, Parabacteroides and Ruminococcus. Fecal microbial transplant (FMT) experiments demonstrated that the microbiota from PS-NPs-administered pregnant mice could similarly induce intestinal barrier damages and placental injury. Treatment with NAM effectively mitigated disruptions in placental metabolism and reversed the adverse pregnancy outcomes caused by PS-NPs. These findings highlight the novel role of the gut microbiota in PS-NPs-induced placental injury and adverse pregnancy outcomes, and suggest that NAM could serve as a promising preventative strategy against this intergenerational damage caused by PS-NPs.},
}

@article {pmid40796472,
year = {2025},
author = {Lucky, CW and Kelly, BJ and Kwon, JH and Woodworth, MH and Medernach, RL},
title = {Microbiome Therapeutics for Clostridioides difficile Infection.},
journal = {Infectious disease clinics of North America},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.idc.2025.07.007},
pmid = {40796472},
issn = {1557-9824},
abstract = {Microbiota-based therapies are used increasingly for the treatment and prevention of Clostridioides difficile infection (CDI), particularly in cases of recurrent CDI (rCDI). This review discusses the different types of microbiota-based therapies, including fecal microbiota transplant, fecal microbiota products, and live biotherapeutic products. The authors present efficacy data regarding clinical use in rCDI and highlight the unique aspects of each product.},
}

@article {pmid40796471,
year = {2025},
author = {Sehgal, K and Feuerstadt, P and Wilcox, MH},
title = {Making Sense of Differing Guidelines for Clostridioides difficile Infection.},
journal = {Infectious disease clinics of North America},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.idc.2025.07.010},
pmid = {40796471},
issn = {1557-9824},
abstract = {The Clostridioides difficile infection (CDI) epidemic has been impacting the world for years. Understanding accurate diagnostics is imperative to allow the appropriate patients to be treated and improve outcomes. This article leverages multiple global societal guidelines to focus on the evolving diagnostic tests available summarizing best diagnostic practices including 2-step diagnostic testing. Therapeutically, guideline recommendations more recently have favored fidaxomicin and incorporated immune-based therapies and microbial restoration therapies. As treatment options and guideline recommendations change, it is imperative to understand why these recommendations have evolved and understand current best diagnostic and therapeutic practices in managing CDI.},
}

@article {pmid40796226,
year = {2025},
author = {Skawratananond, S and McCrea, G and Lie, P and Buxton, MB and Daly, SP and Vojtkofsky, NA and Smith, SC and Zhang, C and Hernandez, M and Hindle, A and Logsdon, AF and Lawrence, JJ},
title = {The Synergistic Interplay between Vitamin A, Dietary Fiber, and the Microbiota-Gut-Brain Axis: A Potential Mechanism for Preventing Alzheimer's Disease.},
journal = {American journal of physiology. Gastrointestinal and liver physiology},
volume = {},
number = {},
pages = {},
doi = {10.1152/ajpgi.00097.2025},
pmid = {40796226},
issn = {1522-1547},
support = {AG071859//HHS | NIH | National Institute on Aging (NIA)/ ; MSSRP//Texas Tech University Health Sciences Center (TTUHSC)/ ; MSSRP//Texas Tech University Health Sciences Center (TTUHSC)/ ; AG073826//HHS | NIH | National Institute on Aging (NIA)/ ; },
abstract = {The human gastrointestinal tract harbors a vast and diverse microbial community, with the gut microbiome playing a fundamental role in numerous biological processes that influence overall health and disease progression. Emerging evidence has identified bacterial lipopolysaccharides in the hippocampus of Alzheimer's disease (AD) patients, highlighting the intricate relationship between the gastrointestinal tract, gut microbiome, and the central and enteric nervous systems-commonly referred to as the "microbiota-gut-brain axis." In this review, we explore the mechanisms by which the microbiota-gut-brain axis contributes to AD pathogenesis. We propose that sufficient levels of all-trans retinoic acid (ATRA), the bioactive form of vitamin A, enhance intestinal barrier integrity by upregulating tight junction proteins and modulating immune function through the induction of regulatory T-cell differentiation, thereby mitigating inflammation. Furthermore, dietary fiber complements this process by promoting the production of short-chain fatty acids, such as butyrate, via bacterial fermentation. Butyrate, in turn, acts as a histone deacetylase inhibitor, upregulating ATRA bioavailability by elevating aldehyde dehydrogenase gene expression. Our mechanistic framework is supported by the endotoxin hypothesis of AD, which purports that the movement of infectious pathogens across the blood-brain barrier causes a vicious cycle of neuroinflammation, a key factor of AD pathogenesis, leading to amyloid-beta deposition, microglial activation, and CYP26A1-mediated ATRA degradation. Finally, we discuss microbiome-based therapeutic strategies and dietary interventions, including prebiotic compounds, probiotic bacteria, fecal microbiota transplantation, the MIND diet, and a combined approach consisting of vitamins A/D, and dietary fiber, as potential approaches to mitigate AD progression via the microbiota-gut-brain axis.},
}

@article {pmid40796104,
year = {2025},
author = {Fan, Z and Huang, L and Zheng, M and Lin, Z and Li, Z and Liu, Y and Liu, B and Xiao, L and Chen, Y and Mai, X and Xu, Y and Xie, L},
title = {Fecal Microbiota Transplantation Reveals the Impact of Gut Microbiota Dysbiosis on Osteoporosis Development in Ovariectomized Mice.},
journal = {FEMS microbiology letters},
volume = {},
number = {},
pages = {},
doi = {10.1093/femsle/fnaf081},
pmid = {40796104},
issn = {1574-6968},
abstract = {Osteoporosis is characterized by low bone mineral density and deteriorated bone microarchitecture. The gut microbiota has emerged as a potential regulator of bone metabolism through the gut-bone axis. This study investigates the role of gut microbiota dysbiosis in osteoporosis. Fecal microbiota transplantation (FMT) was employed to assess the transferability of osteoporosis-associated gut microbiota dysbiosis to healthy mice and to explore whether restoration of gut microbial composition could reverse bone loss in OVX mice. It was demonstrated that gut microbiota from OVX mice induced osteoporosis in healthy recipient mice, establishing a causal link between gut microbiota dysbiosis and bone health. Short-term FMT from healthy donors restored microbial diversity; however, a significant improvement in trabecular bone density was not observed in OVX mice. This suggest that longer colonization periods or additional interventions may be required. Correlation analysis revealed significant associations between specific bacterial taxa and bone health parameters. These findings highlight the complexity of the gut-bone axis and underscore the need for further research investigating targeted microbial interventions for the management of osteoporosis. Future therapeutic strategies should be considered for modulation of the gut microbiota, enhancement of gut barrier integrity, and mitigation of systemic inflammation as novel approaches to osteoporosis treatment.},
}

@article {pmid40794475,
year = {2025},
author = {Lin, J and Qi, Z and Wang, G and Wu, C and Mumby, W and Huang, Y and Peng, Y and Sun, Q},
title = {Permethrin Stimulates Fat Accumulation via Regulating Gut Microbiota and Its Metabolites in Mice.},
journal = {Journal of agricultural and food chemistry},
volume = {},
number = {},
pages = {},
doi = {10.1021/acs.jafc.5c05013},
pmid = {40794475},
issn = {1520-5118},
abstract = {Permethrin, a commonly used type I pyrethroid insecticide, has been shown to induce insulin resistance and adipogenesis, however the molecular mechanisms driving these effects remain unclear. This research demonstrated that permethrin disrupts the balance of gut microbiota, particularly altering Firmicutes and Bacteroidetes ratios, leading to increased adipogenesis and metabolic disorders. Antibiotic treatment significantly alleviated the effects of permethrin, highlighting the potential role of gut microbiota in obesity and insulin resistance. Fecal microbiota transplantation further confirmed the causal role of microbiota in fat accumulation. Additionally, microbial metabolites such as butyrate and indole were found to mitigate the fat accumulation induced by permethrin. Overall, our findings reveal that permethrin promotes obesity through the regulation of gut microbiota and their metabolites, providing important new insights into the health risks associated with permethrin exposure.},
}

@article {pmid40791287,
year = {2025},
author = {Jha, M and Waheed, A and Hooti, JA and Nair, S and Najam, A and Mal, M and Tummala, N and Shariq, AS and Hurairah, A and Daniel, M},
title = {Advancements in Immunomodulatory Therapies for IBD and Their Interplay With the Gut-Brain Axis: An Updated Review of Current Literature and Beyond.},
journal = {Health science reports},
volume = {8},
number = {8},
pages = {e71157},
pmid = {40791287},
issn = {2398-8835},
abstract = {BACKGROUND AND AIMS: The incidence of inflammatory bowel disease (IBD), characterized by chronic gastrointestinal inflammation, has significantly increased over the last two decades. Concurrently, advancements in treatment strategies have accelerated, aiming not only to induce but also to maintain remission. Emerging evidence highlights the intricate bidirectional relationship between the gut and brain, forming the gut-brain axis, which is now a major therapeutic target.

METHODS AND RESULTS: This narrative review synthesizes findings from a wide range of research studies to summarize IBD incidence trends, underlying pathophysiological mechanisms, and recent therapeutic advancements. A major focus is placed on dysregulated immunomodulation and its role in disease progression. The review examines conventional treatments such as aminosalicylates and corticosteroids, surgical interventions, and newer therapies targeting the gut-brain microbiota axis, including biological agents, stem cell therapy, probiotics, and fecal microbiota transplantation (FMT).

CONCLUSION: Recent advancements in immunomodulatory therapies have significantly improved patient outcomes. Biological agents such as infliximab and vedolizumab have demonstrated remission rates of 40%-69% in IBD patients, with infliximab reducing colectomy. Rates to 10% at 54 weeks. Meanwhile, fecal microbiota transplantation (FMT) has emerged as a promising therapy for ulcerative colitis, with trials reporting 87.1% clinical remission at 48 weeks compared to 66.7% in the placebo group, along with higher endoscopic and histological remission rates. A trial on multidonor-intensive FMT found a 27% clinical remission rate at week 8, significantly higher than 8% in the placebo group, reinforcing its potential as an adjunct therapy in IBD. By examining their interplay with the gut-brain axis, this review provides insights into the mechanisms and clinical relevance of these therapies, paving the way for more targeted and effective IBD management strategies.},
}

@article {pmid40791147,
year = {2025},
author = {Ji, X and Wang, J and Lan, T and Zhao, D and Xu, P},
title = {Gut microbial metabolites and the brain-gut axis in Alzheimer's disease: A review.},
journal = {Biomolecules & biomedicine},
volume = {},
number = {},
pages = {},
doi = {10.17305/bb.2025.12921},
pmid = {40791147},
issn = {2831-090X},
abstract = {Alzheimer's disease (AD) is increasingly recognised as a disorder that extends beyond the brain, with accumulating evidence implicating gut microbiota-derived metabolites in its onset and progression. This narrative review synthesises 92 peer-reviewed animal, human and meta-analytic studies published between 2010 and 2025 that investigated short-chain fatty acids (SCFAs), tryptophan-derived indoles and kynurenines, trimethylamine N-oxide (TMAO) and secondary bile acids in the context of AD. Collectively, the literature shows that SCFAs support blood-brain-barrier integrity, dampen microglial reactivity and enhance synaptic plasticity, yet can paradoxically amplify β-amyloid (Aβ) deposition under germ-free or supraphysiological conditions, highlighting the importance of host status and dosing. Beneficial indole metabolites such as indole-3-propionic acid counter oxidative stress, strengthen intestinal and cerebral barriers and suppress pro-inflammatory cascades, whereas a shift toward neurotoxic kynurenines correlates with cognitive decline. TMAO emerges as a consistently deleterious metabolite that aggravates endothelial dysfunction, neuroinflammation and Aβ aggregation; dietary precursor restriction and microbial enzyme inhibitors are therefore being explored as mitigation strategies. Secondary bile acids and polyphenol derivatives further modulate mitochondrial bioenergetics and NF-κB signalling, broadening the therapeutic landscape. Multi-omics profiling reveals that AD patients typically exhibit reduced SCFAs and indoles but elevated TMAO, changes that scale with Mini-Mental State Examination scores, brain atrophy and cerebrospinal Aβ42 levels. Early probiotic and faecal-microbiota-transplant trials have begun to normalise these metabolite profiles and yield modest cognitive benefits, underscoring translational potential. Altogether, gut-derived metabolites are not passive by-products but active modulators of neural, immune and metabolic circuits along the microbiota-gut-brain axis; their targeted manipulation and standardised metabolomic assessment could enable earlier diagnosis and precision microbiome-based interventions for AD, a promise that now warrants validation in large, longitudinal and mechanistically informed clinical studies.},
}

@article {pmid40789505,
year = {2025},
author = {Zhou, Y and Yang, T and Zheng, S and Gan, T and Yu, F and Liu, G and Zhou, T},
title = {Genetical TRPV4 deletion-associated gut microbiota alleviates cardiac dysfunction in mice with diabetic cardiomyopathy.},
journal = {Journal of molecular and cellular cardiology},
volume = {207},
number = {},
pages = {37-50},
doi = {10.1016/j.yjmcc.2025.08.001},
pmid = {40789505},
issn = {1095-8584},
abstract = {Diabetic cardiomyopathy (DCM) is a serious complication associated with diabetes that characterized by the cardiac dysfunction and myocardial fibrosis. Recent studies emphasize the significance of the gut-heart axis in the development of DCM. This current study investigates the effect of systematic-genetical TRPV4 knockout on DCM progression and explores the underlying mechanisms involving gut microbiota modulation and intestinal barrier integrity. The removal of TRPV4 in mice with DCM markedly enhances cardiac performance, decreases myocardial fibrosis, and modifies the composition of gut microbiota, resulting in a significant rise in Bacteroides acidifaciens (BA). TRPV4 deletion also upregulates tight junction proteins (Zonula occludens-1 (ZO-1), Occludin, and Claudin-1) and reduces serum lipopolysaccharide levels. Furthermore, fecal microbiota transplantation from the DCM donors with TRPV4 knockout to the DCM receptors replicates these cardioprotective effects in mice, and administration of BA improves cardiac function and relieves the fibrosis. Our study suggests that the cardioprotective effects of the genetic deletion of TRPV4 are related to changes in the gut microbiome, highlighting the importance of the connection between TRPV4, the gut, and the heart in the disease mechanism and potential therapeutic strategies for DCM.},
}

@article {pmid40789485,
year = {2025},
author = {Mullish, BH and Javed, A and Ghani, R and Davies, F and Ghazy, A and Ranganathan, N and Alexander, JL and Roberts, LA and Chrysostomou, D and Thursz, MR and Marchesi, JR and Gilchrist, M and Williams, HRT},
title = {Operational considerations for the running of an NHS faecal microbiota transplant (FMT) service.},
journal = {The Journal of hospital infection},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jhin.2025.07.022},
pmid = {40789485},
issn = {1532-2939},
}

@article {pmid40789381,
year = {2025},
author = {Fan, XQ and Fan, SM and Dong, BY and Zhang, CM and Zuo, J and Zhang, DW and Xiong, X and Luo, D and Fan, XM},
title = {Recent advances in the interaction between acute respiratory distress syndrome and gut microbiota: A narrative review.},
journal = {Infection, genetics and evolution : journal of molecular epidemiology and evolutionary genetics in infectious diseases},
volume = {134},
number = {},
pages = {105810},
doi = {10.1016/j.meegid.2025.105810},
pmid = {40789381},
issn = {1567-7257},
abstract = {Acute respiratory distress syndrome (ARDS) is a sudden, widespread inflammatory damage to the lungs resulting from multiple etiologies. ARDS is characterized by high sickness rates, mortality, and costly treatments and is a significant global health issue that lacks an effective treatment strategy. The microbiota of the gut is an intricate ecology indispensable for the host's health, immunology, and metabolism. Human immunity and intestinal barrier function depend on gut microbes. Several disorders are linked to gut microbiota dysbiosis. Scientists have been concentrating on the role that gut microbes play in the onset of ARDS. This study examines the relationship between ARDS and intestinal microbiota, specifically addressing two facets: how ARDS affects the composition of the gut microbiota and the integrity of the intestinal barrier, alongside the effects of mechanisms such as bacterial translocation and inflammatory activation resulting from gut microbiota dysregulation on ARDS. Additionally, various therapeutic strategies involving gut microbiota and its metabolites, such as selective digestive decontamination (SDD), fecal microbiota transplantation (FMT), microbiological preparations, and metabolites produced from the microbiota, are explored. It is anticipated that this exploration will make a substantial contribution to the prevention and therapy of ARDS.},
}

@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 Di Marco, M 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 = {225},
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 Abd El-Aty, AM},
title = {A selenium-enriched glycosaminoglycan from sturgeon cartilage: characterization and anti-metabolic syndrome potential.},
journal = {International journal of biological macromolecules},
volume = {322},
number = {Pt 1},
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},
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 = {216},
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 100 g 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 {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 = {},
pmid = {40766454},
issn = {2692-8205},
support = {P30 DK034854/DK/NIDDK NIH HHS/United States ; R01 AI179807/AI/NIAID NIH HHS/United States ; },
abstract = {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.},
}

@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 {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},
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 = {353},
number = {Pt A},
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},
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},
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 = {379},
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.},
}