@article {pmid40662074,
year = {2025},
author = {Jia, J and Wu, YB and Liu, SW and Chen, WJ and Li, RL and Bai, YL and Hu, L},
title = {Effectiveness and safety of non-pharmacological therapies for the treatment of inflammatory bowel disease: a network meta-analysis.},
journal = {Frontiers in medicine},
volume = {12},
number = {},
pages = {1593483},
pmid = {40662074},
issn = {2296-858X},
abstract = {BACKGROUND: Inflammatory bowel disease (IBD), encompassing both Crohn's disease (CD) and ulcerative colitis (UC), is a chronic, inflammatory, and immune-mediated disorder of the gastrointestinal tract. If left inadequately treated, IBD can lead to disease progression, resulting in severe long-term complications, including irreversible structural damage to the intestinal tissues. While clinical symptoms are traditionally used to assess treatment efficacy, they do not always align with the underlying mucosal inflammation, particularly in CD. This limitation underscores the importance of exploring alternative treatment strategies. To address this gap, the present study evaluates the effectiveness of non-pharmacological treatments (NPTs) for IBD through a network meta-analysis (NMA), providing a thorough assessment of the available evidence.

METHODS: We systematically reviewed randomized controlled trials (RCTs) from the following databases: PubMed, Embase, Springer, Cochrane Controlled Register of Trials (CENTRAL), and Web of Science, comparing various NPTs for IBD, including Cognitive Behavioral Therapy (CBT), diet interventions (DI), fecal microbiota transplantation (FMT), physical training (PT), and acupuncture and moxibustion (APMX). Outcomes assessed included clinical remission, disease activity, quality of life (QOL), serum biomarkers (fecal calprotectin [FC] and C-reactive protein [CRP]), and adverse effects. The quality assessment was assessed by Cochrane Handbook and GRADEpro software. The risk ratio (RR) was calculated for dichotomous outcomes while standardized mean difference (SMD) was used for continuous variables with 95% credible intervals (CI). Funnel plot was performed to evaluate publication bias. Surface under the cumulative ranking curve (SUCRA) was conducted to rank the included interventions. Data were analyzed with STATA 15.0 and Review Manager 5.3.

RESULTS: A total of 62 eligible RCTs were identified in this NMA. The results showed that standard medical therapy (SMT) exhibited the highest probability in inducing clinical remission, as expected. Among non-pharmacological interventions, APMX, a traditional Chinese medicine involving acupuncture and moxibustion, showed promising results in both animal models and clinical trials, reducing serum TNF-α levels and improving intestinal health. DI was most effective in maintaining clinical remission and reducing serum FC levels. FMT emerged as the most effective treatment for reducing serum CRP levels and ranked second in terms of clinical remission induction.

CONCLUSION: APMX, DI, and FMT represent promising non-pharmacological options for managing IBD. APMX was the most effective for clinical remission and symptom relief, while DI was best for maintaining remission, and FMT showed promise in reducing inflammation. Further high-quality clinical trials are needed to strengthen the evidence and guide clinical practice in IBD management.

https://www.crd.york.ac.uk/PROSPERO/view/CRD42024596233, CRD42024596233.},
}

@article {pmid40661942,
year = {2025},
author = {Yin, J and Kaakoush, NO and Massey, J and Danta, M},
title = {Understanding the microbiome in autologous haemopoietic stem cell transplant for multiple sclerosis.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1590601},
pmid = {40661942},
issn = {1664-3224},
mesh = {Humans ; *Hematopoietic Stem Cell Transplantation/methods ; Adult ; Female ; *Gastrointestinal Microbiome ; Male ; *Multiple Sclerosis/therapy/microbiology ; Middle Aged ; Transplantation, Autologous ; Natalizumab/therapeutic use ; RNA, Ribosomal, 16S/genetics ; Feces/microbiology ; },
abstract = {BACKGROUND: MS is a chronic inflammatory and degenerative disease of the central nervous system (CNS) resulting in neurological deficits associated with physical and/or cognitive disability. The gut microbiome can interact with the CNS and immune system through various molecular pathways and has been previously implicated in MS. Autologous Haematopoietic Stem Cell Transplant (AHSCT) in MS arrests inflammatory disease and has evidence of long-term therapeutic benefit. To date, no study has explored the effect of AHSCT on the gut microbiome in people with MS.

METHOD: The microbiome of people with MS (pwMS) undergoing AHSCT was compared with pwMS on Natalizumab (NTZ). Longitudinal microbiome analysis was also conducted within the AHSCT cohort at two timepoints. Amplicon sequencing of the 16S ribosomal RNA V3-4 region (Illumina MiSeq) was used to evaluate alpha and beta diversity, oral-stool microbiota distances, and relative taxa abundances on both oral and stool microbiota.

RESULTS: The pre-transplant, baseline samples from the AHSCT cohort (n=8) was compared to the Natalizumab group (n=22). The AHSCT cohort had lower oral species richness compared to the NTZ cohort (p=0.026). There was a significant difference in oral beta diversity between the two cohorts (p=0.043). The oral taxa analysis of AHSCT subjects showed increased relative abundances of Porphyromonas and decreased Veillonella.

CONCLUSION: This pilot study identified specific microbiome changes, particularly in the oral alpha diversity and abundance of specific bacteria which may reflect treatment status or disease activity in MS.},
}

Humans
*Hematopoietic Stem Cell Transplantation/methods
Adult
Female
*Gastrointestinal Microbiome
Male
*Multiple Sclerosis/therapy/microbiology
Middle Aged
Transplantation, Autologous
Natalizumab/therapeutic use
RNA, Ribosomal, 16S/genetics
Feces/microbiology

@article {pmid40661744,
year = {2025},
author = {Wang, X and Liu, X and Gong, F and Jiang, Y and Zhang, C and Zhou, W and Zhang, W},
title = {Targeting gut microbiota for diabetic nephropathy treatment: probiotics, dietary interventions, and fecal microbiota transplantation.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1621968},
pmid = {40661744},
issn = {1664-2392},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Probiotics/therapeutic use ; *Gastrointestinal Microbiome/physiology ; *Diabetic Nephropathies/therapy/microbiology ; Animals ; Dysbiosis/therapy ; },
abstract = {Diabetic nephropathy (DN) stands as a prominent microvascular complication of diabetes mellitus and presents a significant global health challenge. Despite advancements in glycemic control and renin-angiotensin system inhibition, current treatments merely delay disease progression without targeting fundamental pathological processes. This review explores gut microbiota modulation as a promising treatment strategy for DN through probiotic supplementation, dietary interventions, and fecal microbiota transplantation(FMT) protocols. The gut microbiota, integral to the "gut-kidney axis," is critically implicated in DN pathogenesis. DN is associated with gut dysbiosis-characterized by reduced microbial diversity, depletion of beneficial short-chain fatty acid (SCFA)-producing bacteria, and proliferation of opportunistic pathogens. This dysbiosis impairs gut barrier integrity, fostering systemic inflammation and the accumulation of uremic toxins like indoxyl sulfate. Furthermore, translocated bacterial lipopolysaccharides activate Toll-like receptors and the NLRP3 inflammasome, exacerbating kidney damage and fibrosis. Interventions targeting the microbiota, including dietary strategies (e.g., enhancing fermentable fibers, low-protein diets) and FMT, show promise in preclinical and early clinical studies, though FMT requires stringent safety and donor screening protocols. Significant challenges persist, such as managing inter-individual microbiota variability for personalized therapies, fully elucidating molecular mechanisms like SCFA-GPR43 signaling, and leveraging multiomics for biomarker discovery. Advancing microbiota-focused interventions for DN towards microbiome-centered precision medicine necessitates addressing standardization, deepening mechanistic understanding, and validating combination therapies, heralding a potential shift from traditional nephroprotective approaches.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Probiotics/therapeutic use
*Gastrointestinal Microbiome/physiology
*Diabetic Nephropathies/therapy/microbiology
Animals
Dysbiosis/therapy

@article {pmid40660288,
year = {2025},
author = {Qin, W and Yin, N and Xu, B and Mei, Q and Fu, Y and Fan, J and Lu, Y and Wang, G and Ai, L and Lu, Z and Zeng, Y and Huang, C},
title = {Faecalibacterium prausnitzii enhances intestinal IgA response by host-microbe derived inecalcitol in colitis.},
journal = {BMC medicine},
volume = {23},
number = {1},
pages = {425},
pmid = {40660288},
issn = {1741-7015},
support = {No. 81970555//National Natural Science Foundation of China/ ; No.CCTR-2022B02//Shanghai General Hospital/ ; 202440170//Shanghai Municipal Health Commission/ ; No.22SJKGGG28//Science and Technology Commission of Songjiang District/ ; No.KY-2023-03-02//Shanghai Jiao Tong University School of Medicine, Digestive Institute/ ; },
mesh = {Animals ; Mice ; *Gastrointestinal Microbiome/immunology ; Humans ; *Faecalibacterium prausnitzii/immunology ; Mice, Knockout ; Mice, Inbred C57BL ; *Colitis, Ulcerative/microbiology/immunology ; Male ; *Immunoglobulin A/metabolism/immunology ; Dextran Sulfate ; Disease Models, Animal ; *Colitis/microbiology/immunology ; *Immunoglobulin A, Secretory ; Female ; Feces/microbiology ; },
abstract = {BACKGROUND: Faecalibacterium prausnitzii plays a crucial role in ulcerative colitis (UC) remission, but its action mechanism is unknown. Here, we aimed to explore the potential mechanisms focusing on the interaction of F. prausnitzii with host immune response and its potential modulation on gut microbiome.

METHODS: RNA-seq analysis together with 16S rRNA sequencing and metabolomics were performed in a dextran sodium sulfate (DSS)-induced colitis mouse model followed by F. prausnitzii gavage. To present evidence of sIgA involved in the anti-inflammatory effects of F. prausnitzii, we further applied immunoglobulin A (IgA) knockout mice and secretory IgA (sIgA) depletion mouse models using polymeric immunoglobulin receptor (pIgR) neutralizing antibody. Colonic immune cells were characterized by flow cytometry. The fecal relative abundance of F. prausnitzii, inecalcitol, and colonic IgA expression were assessed in UC patients.

RESULTS: F. prausnitzii markedly ameliorated colitis by alleviating intestinal inflammation and barrier dysfunction, with significantly decreased abundance of pro-inflammatory taxa (Enterococcus, Desulfovibrio, Escherichia-Shigella, and Enterorhabdus) and increased abundance of Lachnospiraceae NK4A136_group. Functions related to intestinal immune network for IgA production pathway were up-regulated shown by transcriptomics and KEGG pathway analysis. Increased expression of IgA production associated genes including MHCII-related genes, Aicda, and Tnfrsfl3c were verified, accompanied by up-regulated colonic IgA and pIgR. The IgA knockout mice and sIgA depletion model weakened the anti-inflammation and microbiota-modulation effects of F. prausnitzii, which was further proved by fecal microbiota transplantation (FMT). The shift profile of fecal metabolites after F. prausnitzii supplement was characterized by increased production of inecalcitol, which may account for the enhanced IgA response. In a cohort of UC patients, the relative abundance of F. prausnitzii was decreased and positively correlated with colonic IgA expression and negatively correlated with disease severity.

CONCLUSIONS: F. prausnitzii effectively alleviated colonic inflammation and modulated dysbiosis via enhancing colonic IgA response, thus showing promise as a UC treatment.},
}

Animals
Mice
*Gastrointestinal Microbiome/immunology
Humans
*Faecalibacterium prausnitzii/immunology
Mice, Knockout
Mice, Inbred C57BL
*Colitis, Ulcerative/microbiology/immunology
Male
*Immunoglobulin A/metabolism/immunology
Dextran Sulfate
Disease Models, Animal
*Colitis/microbiology/immunology
*Immunoglobulin A, Secretory
Female
Feces/microbiology

@article {pmid40659786,
year = {2025},
author = {Lin, NY and Fukuoka, S and Koyama, S and Motooka, D and Tourlousse, DM and Shigeno, Y and Matsumoto, Y and Yamano, H and Murotomi, K and Tamaki, H and Irie, T and Sugiyama, E and Kumagai, S and Itahashi, K and Tanegashima, T and Fujimaki, K and Ito, S and Shindo, M and Tsuji, T and Wake, H and Watanabe, K and Maeda, Y and Enokida, T and Tahara, M and Yamashita, R and Fujisawa, T and Nomura, M and Kawazoe, A and Goto, K and Doi, T and Shitara, K and Mano, H and Sekiguchi, Y and Nakamura, S and Benno, Y and Nishikawa, H},
title = {Microbiota-driven antitumour immunity mediated by dendritic cell migration.},
journal = {Nature},
volume = {},
number = {},
pages = {},
pmid = {40659786},
issn = {1476-4687},
abstract = {Gut microbiota influence the antitumour efficacy of immune checkpoint blockade[1-6], but the mechanisms of action have not been fully elucidated. Here, we show that a new strain of the bacterial genus Hominenteromicrobium (designated YB328) isolated from the faeces of patients who responded to programmed cell death 1 (PD-1) blockade augmented antitumour responses in mice. YB328 activated tumour-specific CD8[+] T cells through the stimulation of CD103[+]CD11b[-] conventional dendritic cells (cDCs), which, following exposure in the gut, migrated to the tumour microenvironment. Mice showed improved antitumour efficacy of PD-1 blockade when treated with faecal transplants from non-responder patients supplemented with YB238. This result suggests that YB328 could function in a dominant manner. YB328-activated CD103[+]CD11b[-] cDCs showed prolonged engagement with tumour-specific CD8[+] T cells and promoted PD-1 expression in these cells. Moreover, YB238-augmented antitumour efficacy of PD-1 blockade treatment was observed in multiple mouse models of cancer. Patients with elevated YB328 abundance had increased infiltration of CD103[+]CD11b[-] cDCs in tumours and had a favourable response to PD-1 blockade therapy in various cancer types. We propose that gut microbiota enhance antitumour immunity by accelerating the maturation and migration of CD103[+]CD11b[-] cDCs to increase the number of CD8[+] T cells that respond to diverse tumour antigens.},
}

@article {pmid40659623,
year = {2025},
author = {Wang, Z and Wang, S and Liu, S and Wang, Z and Li, F and Bu, Q and An, X},
title = {Polystyrene microplastics induce potential toxicity through the gut-mammary axis.},
journal = {NPJ science of food},
volume = {9},
number = {1},
pages = {139},
pmid = {40659623},
issn = {2396-8370},
support = {2024NC-YBXM-082//Key Research and Development Projects of Shaanxi Province/ ; K4050422535//Experimental Demonstration Base of Dairy Goat in Heshui, Northwest Agriculture and Forestry University, China/ ; },
abstract = {Microplastics (MPs), as an emerging environmental pollutant, pose a grave threat to food safety and public health. However, studies on MP toxicity to organs other than the intestine remain limited, especially its link to the intestinal microbiota. To address this gap, we evaluated the potential toxicity of polystyrene (PS)-MPs to the gut and mammary glands during lactation exposure in mice. PS-MPs (~1 μm) can disrupt the intestinal barrier and cause colonic inflammation and gut microbiota dysbiosis. Moreover, they can accumulate in mammary tissue and cause inflammatory damage. Transcriptome data suggested that PS-MPs cause maternal mammary lipid metabolism disorders and ferroptosis. Fecal microbial transplant (FMT) was then performed, and it reproduced the observed leakage of the blood-milk barrier and inflammation of the mammary gland. This study demonstrated that MPs induced gut and mammary inflammation and exacerbated inflammatory damage through the gut-mammary axis. In addition, MPs caused mammary lipid disorders and ferroptosis. The findings confirmed that PS-MPs may be transported to mammalian organs other than the intestine (e.g., mammary gland) and revealed the critical role of the intestinal microbiota. These findings will provide guidance for further studies on the potential foodborne risks of MPs.},
}

@article {pmid40659561,
year = {2025},
author = {Yang, L and Hua, M and Li, D and Li, F and He, Y and Miao, X and Sun, M and Niu, H and An, F and Wang, J and Yang, M and Lu, J and Xu, H and Wang, J},
title = {Protective Effects of Ginseng Soluble Dietary Fiber and Its Fecal Microbiota Extract on Antibiotic-Induced Gut Dysbiosis Obese Mice.},
journal = {Journal of microbiology and biotechnology},
volume = {35},
number = {},
pages = {e2502013},
doi = {10.4014/jmb.2502.02013},
pmid = {40659561},
issn = {1738-8872},
mesh = {Animals ; *Dysbiosis/chemically induced/drug therapy/prevention & control/microbiology ; *Gastrointestinal Microbiome/drug effects ; Mice ; *Anti-Bacterial Agents/adverse effects ; *Panax/chemistry ; Mice, Obese ; Male ; *Dietary Fiber/pharmacology ; *Obesity/chemically induced ; *Plant Extracts/pharmacology ; Toll-Like Receptor 4/metabolism ; Feces/microbiology ; Mice, Inbred C57BL ; Bacteria/classification/drug effects ; Signal Transduction/drug effects ; Myeloid Differentiation Factor 88/metabolism ; NF-kappa B/metabolism ; Insulin Resistance ; Body Weight/drug effects ; Disease Models, Animal ; Oxidative Stress/drug effects ; },
abstract = {Prolonged or improper antibiotic use may increase the risk of obesity. Ginseng soluble dietary fiber (G-SDF) has been shown to inhibit obesity and promote the growth of intestinal probiotics. However, its role in antibiotic-induced gut dysbiosis obese mice (ADIO) remains unclear, and this study aimed to elucidate this role. The results indicated that G-SDF and its fecal microbiota extract (SDFfbs) significantly reduced body weight, insulin resistance, hepatic fat accumulation, abnormal blood and liver glucose-lipid metabolism, oxidative stress, and immune-inflammatory responses in ADIO mice. G-SDF and SDFfbs also inhibited the LPS/TLR4/MyD88/NF-κB signaling pathway, restored the expression of the gut barrier proteins Occludin and Claudin1, and protected against intestinal damage in ADIO mice. In particular, G-SDF and SDFfbs significantly increased the abundance of Firmicutes and Bacteroidetes and decreased the abundance of harmful Escherichia and Streptococcus. Additionally, they promoted the growth of beneficial bacteria, such as Enterococcus, Lactobacillus, Bifidobacterium, Parabacteroides, and Akkermansia, and these microbial shifts correlated with significant improvements in metabolic indicators in ADIO mice. Notably, SDFfbs can replicate the efficacy of SDF and has even shown stronger effects than the latter. In summary, this study demonstrated that G-SDF and SDFfbs effectively mitigate the double damage caused by obesity and antibiotic exposure by modulating the LPS/TLR4/MyD88/NF-κB pathway, protecting the intestinal barrier, and restoring the gut microbiota balance. These findings provide an important theoretical basis for the use of G-SDF and SDFfbs as fat-reducing and antibiotic-resistant ingredients in health foods.},
}

Animals
*Dysbiosis/chemically induced/drug therapy/prevention & control/microbiology
*Gastrointestinal Microbiome/drug effects
Mice
*Anti-Bacterial Agents/adverse effects
*Panax/chemistry
Mice, Obese
Male
*Dietary Fiber/pharmacology
*Obesity/chemically induced
*Plant Extracts/pharmacology
Toll-Like Receptor 4/metabolism
Feces/microbiology
Mice, Inbred C57BL
Bacteria/classification/drug effects
Signal Transduction/drug effects
Myeloid Differentiation Factor 88/metabolism
NF-kappa B/metabolism
Insulin Resistance
Body Weight/drug effects
Disease Models, Animal
Oxidative Stress/drug effects

@article {pmid40655582,
year = {2025},
author = {Patel, SP and Bhoraniya, SJ and Kalola, SD and Rukadikar, A and Ravi, R and Farooqui, S and Rukadikar, C},
title = {Gut Microbiota and its Impact on Chronic Diseases: A Comprehensive Review.},
journal = {Journal of pharmacy & bioallied sciences},
volume = {17},
number = {Suppl 2},
pages = {S1080-S1082},
pmid = {40655582},
issn = {0976-4879},
abstract = {The intricate community of bacteria that live in the gastrointestinal system, known as the gut microbiota, is essential to preserving human health and equilibrium. The pathophysiology of several chronic illnesses, including as neurological, cardiovascular, immunological, and metabolic disorders, has been progressively associated with its dysbiosis. This thorough analysis looks at the complex relationships that exist between gut microbiota and host physiology, examining processes including metabolic signaling, immunological regulation, and gut-brain axis communication. We discuss current developments in the study of the microbiome, with an emphasis on the role that the variety and makeup of gut microbes play in the development of chronic diseases. In order to restore microbial balance and lessen the severity of the condition, the study also covers new treatment approaches such as dietary changes, probiotics, prebiotics, and fecal microbiota transplantation. The development of novel, microbiome-based diagnostic and therapeutic strategies is made possible by an understanding of the complex link between the gut microbiota and chronic illnesses, highlighting the vital role that personalized medicine plays in enhancing health outcomes.},
}

@article {pmid40654576,
year = {2025},
author = {Xie, H and Yu, S and Tang, M and Xun, Y and Shen, Q and Wu, G},
title = {Gut microbiota dysbiosis in inflammatory bowel disease: interaction with intestinal barriers and microbiota-targeted treatment options.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1608025},
pmid = {40654576},
issn = {2235-2988},
mesh = {Humans ; *Dysbiosis/therapy/microbiology ; *Inflammatory Bowel Diseases/therapy/microbiology ; *Gastrointestinal Microbiome/drug effects ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Anti-Bacterial Agents/therapeutic use ; *Intestinal Mucosa/microbiology ; Animals ; },
abstract = {Recent studies have deepened our understanding on gut microbiota alterations and the interaction with intestinal barrier impairments, which play a crucial role in the etiology and pathophysiology of Inflammatory bowel disease (IBD). The intestinal microbiota dysbiosis in IBD including the altered microbiota composition, decreased beneficial species and increased harmful species. The disturbed gut microbiota results in the aggravation of intestinal barrier dysfunction through regulation of antimicrobial substances in mucus layer, tight junction protein in mechanical layer and inflammatory response in immune layer. The therapeutic options targeted on the microbiota including antibiotics, probiotics and fecal microbiota transplantation (FMT) exhibit efficacies and limitations in the treatment of IBD. Reasonable single or combined use of these treatments can restore intestinal microecological homeostasis, which further contributes to the treatment of IBD. This review analyzes the underlying mechanisms for the interaction between microbiota alterations and gut barrier dysfunction in IBD; meanwhile, it provides new insights into the microbiota-targeted therapeutic options IBD, including the benefits, risks and limitations of antibiotic and probiotic therapies, unresolved clinical application strategies for FMT, and combination administrations of antibiotics and FMT.},
}

Humans
*Dysbiosis/therapy/microbiology
*Inflammatory Bowel Diseases/therapy/microbiology
*Gastrointestinal Microbiome/drug effects
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Anti-Bacterial Agents/therapeutic use
*Intestinal Mucosa/microbiology
Animals

@article {pmid40653357,
year = {2025},
author = {Meena, AS and Singh, P and Shukla, PK},
title = {Cancer and microbiome-targeted therapies.},
journal = {International review of cell and molecular biology},
volume = {395},
number = {},
pages = {99-132},
doi = {10.1016/bs.ircmb.2024.12.006},
pmid = {40653357},
issn = {1937-6448},
mesh = {Humans ; *Neoplasms/therapy/microbiology ; *Microbiota/drug effects ; Animals ; Probiotics/therapeutic use ; Tumor Microenvironment ; Fecal Microbiota Transplantation ; },
abstract = {Emerging research highlights the profound interplay between the microbiome and cancer, offering novel avenues for therapeutic interventions. This review explores the burgeoning field of microbiome-targeted therapies in oncology, focusing on how microbial communities influence cancer development, progression, and response to treatment. The microbiome's role in modulating immune responses, drug metabolism, and tumor microenvironment is examined, revealing its potential to both inhibit and promote tumorigenesis. We discuss current strategies that leverage microbiome modulation, including probiotics, prebiotics, and fecal microbiota transplantation, to enhance the efficacy of conventional cancer therapies and mitigate side effects. Additionally, the review addresses the challenges and future directions in integrating microbiome-based approaches into clinical practice. By elucidating the mechanisms through which the microbiome affects cancer and therapy outcomes, this work aims to pave the way for innovative, personalized treatment strategies that harness the power of microbial communities to improve cancer care.},
}

Humans
*Neoplasms/therapy/microbiology
*Microbiota/drug effects
Animals
Probiotics/therapeutic use
Tumor Microenvironment
Fecal Microbiota Transplantation

@article {pmid40653356,
year = {2025},
author = {Sarath Krishnan, MP and Goyal, B and Nampui, L and Gupta, SC},
title = {The role of microbiome in gastrointestinal cancer.},
journal = {International review of cell and molecular biology},
volume = {395},
number = {},
pages = {67-98},
doi = {10.1016/bs.ircmb.2024.12.009},
pmid = {40653356},
issn = {1937-6448},
mesh = {Humans ; *Gastrointestinal Neoplasms/microbiology/pathology/therapy ; *Gastrointestinal Microbiome ; Animals ; },
abstract = {The human microbiome consists of the diverse microorganisms with their equally diverse functional abilities that have evolved over millions of years with humans. This microbiome creates a mutually beneficial symbiotic relationship with their host. Through their varied functions, the human gut microbiota is crucial for preserving health and homeostasis. Any imbalance in this microbial population can lead to an array of diseased states, including cancer especially of the gastrointestinal system. The focus of this chapter is to discuss the mechanisms through which the gut microbiome creates a conducive environment for initiation and progression of cancer. In addition, the effect of microbial products such as short chain fatty acids, bile acids and Trimethylamine N-oxide on the formation of gastrointestinal cancer is also discussed. The various experimental methods and new molecular techniques that have facilitated the characterization and study of microorganisms is also discussed. The developments in microbiome research have shed light on the potential role of gut microbiota for novel biomarker discovery and therapeutic interventions in gastrointestinal cancer, like fecal microbiota transplantation. The prospects of these areas for further exploration are discussed.},
}

Humans
*Gastrointestinal Neoplasms/microbiology/pathology/therapy
*Gastrointestinal Microbiome
Animals

@article {pmid40653352,
year = {2025},
author = {Singh, K and Bhadauriya, AS},
title = {Effect of microbial dysbiosis on autoimmune associated inflammation.},
journal = {International review of cell and molecular biology},
volume = {395},
number = {},
pages = {1-22},
doi = {10.1016/bs.ircmb.2024.12.016},
pmid = {40653352},
issn = {1937-6448},
mesh = {Humans ; *Dysbiosis/complications/microbiology/immunology ; *Autoimmune Diseases/microbiology/immunology ; *Inflammation/microbiology/immunology/complications ; Animals ; *Gastrointestinal Microbiome/immunology ; },
abstract = {Trillions of microorganisms inhabit the human body, playing crucial roles in the development of the immune system, maintaining balance within the gut's immune system, and overall well-being. When these microbial communities experience imbalance, known as dysbiosis, it can lead to localized inflammatory conditions such as colitis and inflammatory bowel diseases, as well as systemic autoimmune disorders like type 1 diabetes, rheumatoid arthritis, and multiple sclerosis. Gut microbes engage with the immune system through various means, including influencing host microRNAs to regulate gene expression and generating metabolites that interact with cellular receptors such as TLRs and GPCRs. These interactions impact critical immune processes like the differentiation of lymphocytes, the production of interleukins, and the maintenance of gut barrier function. Looking into, how gut microbes contribute to or defend against systemic autoimmune diseases is crucial for developing strategies to manage or prevent these conditions. These approaches may include dietary or lifestyle modifications, microbiome-targeted therapies such as prebiotics or probiotics, the identification of diagnostic biomarkers for predicting disease risk, and monitoring and intervening in shifts in microbial populations during autoimmune flare-ups. Recognizing the microbiome's significance in systemic autoimmune diseases offers promise for transforming these presently challenging-to-treat conditions into more controllable or preventable ones.},
}

Humans
*Dysbiosis/complications/microbiology/immunology
*Autoimmune Diseases/microbiology/immunology
*Inflammation/microbiology/immunology/complications
Animals
*Gastrointestinal Microbiome/immunology

@article {pmid40651297,
year = {2025},
author = {Chen, LJ and Liu, Y and Liu, JL and Chen, ZJ and Zhao, W and Li, JH and Hsu, C and Chen, L and Zeng, JH and Li, XW and Yang, JZ and Li, JH and Xie, XL and Tao, SH and Wang, Q},
title = {Lycopene ameliorates Di-(2-ethylhexyl) phthalate-induced neurotoxicity in mice via the gut-brain axis.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157057},
doi = {10.1016/j.phymed.2025.157057},
pmid = {40651297},
issn = {1618-095X},
abstract = {BACKGROUND: Di(2-ethylhexyl) phthalate (DEHP), a ubiquitous plasticizer present in numerous consumer products, poses a substantial neurotoxic risk through environmental and dietary exposure. Growing evidence highlights a critical association between DEHP-induced neurotoxicity and gut microbiota dysbiosis. Renowned for its potent antioxidant and anti-inflammatory capabilities, the natural carotenoid lycopene (Lyc) demonstrates therapeutic promise in treating various neurological disorders.

PURPOSE: The potential neuroprotective mechanisms of Lyc against DEHP-induced neurotoxicity in mice were investigated in this study, with a specific focus on its interaction with the gut-brain axis.

METHODS: For 35 consecutive days, mice received daily intragastric administrations of DEHP or Lyc. A comprehensive approach involving integrated transcriptome, microbiome, and molecular biology analyses, in conjunction with bacteriotherapy, was utilized to thoroughly investigate the underlying mechanisms.

RESULTS: Our findings demonstrated that Lyc administration or fecal microbiota transplantation (FMT) from Lyc-treated mice effectively ameliorated DEHP-induced anxiety- and depression-like behaviors. At the molecular level, Lyc mitigated neuroinflammation in the hippocampus, potentially through modulation of the NOD-like receptor signaling pathway. Furthermore, Lyc treatment improved gut microbiota composition by promoting the growth of beneficial bacteria, such as Akkermansiaceae, and enhanced intestinal barrier integrity via increased expression of tight junction proteins. Lyc also regulated the LPS-TLR4/MyD88 signaling pathway in the colon, thereby reducing local inflammation.

CONCLUSION: These results provide compelling evidence that Lyc confers protection against DEHP-induced neurotoxicity through a multifaceted strategy involving modulation of gut-brain axis, suppression of neuroinflammation, and restoration of gut homeostasis. We propose a novel therapeutic strategy to alleviate the risks posed by DEHP to both neurological and intestinal health. This approach involves either supplementation with Lyc or the application of bacteriotherapy.},
}

@article {pmid40650758,
year = {2025},
author = {Kearns, R},
title = {Gut modulation to regulate NF-κB in colorectal and gastric cancer therapy and inflammation.},
journal = {Cancer immunology, immunotherapy : CII},
volume = {74},
number = {8},
pages = {264},
pmid = {40650758},
issn = {1432-0851},
mesh = {Humans ; *NF-kappa B/metabolism ; *Gastrointestinal Microbiome/immunology ; *Stomach Neoplasms/therapy/immunology/metabolism/microbiology/pathology ; *Inflammation/metabolism ; *Colorectal Neoplasms/therapy/immunology/metabolism/microbiology/pathology ; Animals ; Dysbiosis ; Fecal Microbiota Transplantation ; Signal Transduction ; },
abstract = {The nuclear factor-kappa B (NF-κB) pathway plays a pivotal role in cancer progression, immune regulation, and inflammation. Aberrant activation of this pathway, often driven by gut microbiota dysbiosis, contributes to tumorigenesis, therapy resistance, and chronic inflammation. Emerging evidence highlights the bidirectional interaction between gut microbiota and NF-κB signalling, suggesting that microbiota modulation may enhance cancer treatment efficacy and reduce treatment-induced inflammation. This review explores the mechanistic underpinnings of gut microbiota-mediated NF-κB regulation, focusing on microbial metabolites such as short-chain fatty acids (SCFAs) and microbial-associated molecular patterns, including lipopolysaccharides (LPS). It examines how conventional cancer treatments, chemotherapy, radiotherapy, and immune checkpoint inhibitors, exacerbate dysbiosis and NF-κB-driven inflammation, further complicating treatment outcomes. Additionally, this review evaluates the therapeutic potential of gut-targeted interventions, including probiotics, prebiotics, faecal microbiota transplantation (FMT), and dietary modifications, in restoring microbial homeostasis and modulating NF-κB signalling. Despite promising findings, challenges remain regarding the clinical translation of microbiota-based therapies, including the need for standardised microbiota profiling, regulatory frameworks, and long-term safety assessments. Advances in metagenomics and metabolomics are proposed as essential tools to personalise gut-targeted interventions and optimise cancer treatment strategies. Integrating gut modulation into oncology represents a paradigm shift, offering a holistic, patient-centric approach to cancer therapy. However, further research is required to validate these strategies and ensure their efficacy in clinical applications.},
}

Humans
*NF-kappa B/metabolism
*Gastrointestinal Microbiome/immunology
*Stomach Neoplasms/therapy/immunology/metabolism/microbiology/pathology
*Inflammation/metabolism
*Colorectal Neoplasms/therapy/immunology/metabolism/microbiology/pathology
Animals
Dysbiosis
Fecal Microbiota Transplantation
Signal Transduction

@article {pmid40649988,
year = {2025},
author = {Kaltsas, A and Giannakodimos, I and Markou, E and Stavropoulos, M and Deligiannis, D and Kratiras, Z and Chrisofos, M},
title = {The Androbactome and the Gut Microbiota-Testis Axis: A Narrative Review of Emerging Insights into Male Fertility.},
journal = {International journal of molecular sciences},
volume = {26},
number = {13},
pages = {},
doi = {10.3390/ijms26136211},
pmid = {40649988},
issn = {1422-0067},
mesh = {Humans ; Male ; *Gastrointestinal Microbiome/physiology ; *Infertility, Male/microbiology/metabolism ; *Testis/metabolism/microbiology ; Animals ; *Fertility ; Spermatogenesis ; Dysbiosis/microbiology ; },
abstract = {Male infertility is an under-recognized global health burden. Accumulating evidence position the intestinal microbiota as a pivotal regulator of testicular function, underpinning the emerging gut microbiota-testis axis. This narrative review introduces the conceptual term "androbactome", referring to gut microorganisms and microbial genes that are hypothesized to influence androgen biosynthesis, spermatogenesis, and broader reproductive endocrinology. The documented worldwide decline in sperm concentration heightens the urgency of clarifying microbe-mediated influences on male reproductive capacity. The synthesis of preclinical and clinical findings reveals four principal pathways by which dysbiosis compromises fertility: systemic inflammation, oxidative stress, endocrine disruption, and epigenetic alteration. Lipopolysaccharide-driven cytokinaemia, reactive oxygen species generation, hypothalamic-pituitary-gonadal axis suppression, and aberrant germ cell methylation collectively impair sperm quality and hormonal balance. Short-chain fatty acids, secondary bile acids, and indole derivatives emerge as pivotal messengers within this crosstalk. Therapeutic approaches targeting the androbactome, namely dietary optimization, probiotic or prebiotic supplementation, and fecal microbiota transplantation, have demonstrated encouraging improvements in sperm parameters and testosterone levels, yet the causal inference is constrained by predominantly cross-sectional designs and limited long-term safety data. Recognizing the androbactome as a modifiable determinant of male fertility may open new avenues for personalized diagnosis, risk stratification, and adjunctive therapy in regard to idiopathic infertility. The integration of multi-omics platforms to characterize microbial and metabolomic signatures promises to enrich diagnostic algorithms and guide precision interventions, but rigorously controlled longitudinal and interventional studies are required to secure a translational impact.},
}

Humans
Male
*Gastrointestinal Microbiome/physiology
*Infertility, Male/microbiology/metabolism
*Testis/metabolism/microbiology
Animals
*Fertility
Spermatogenesis
Dysbiosis/microbiology

@article {pmid40649705,
year = {2025},
author = {Borbélyová, V and Szabó, J and Sušienková, P and Potvin, J and Belvončíková, P and Groß, T and Jančovičová, A and Bačová, Z and Rašková, B and Szadvári, I and Antal, M and Pirník, Z and Karhánek, M and Šoltys, K and Gardlík, R and Celec, P and Ostatníková, D and Tomova, A},
title = {The Effect of Parental Faecal Microbiome Transplantation from Children with Autism Spectrum Disorder on Behavior and Gastrointestinal Manifestations in the Male Offspring of Shank3 Mice.},
journal = {International journal of molecular sciences},
volume = {26},
number = {13},
pages = {},
doi = {10.3390/ijms26135927},
pmid = {40649705},
issn = {1422-0067},
support = {APVV-20-0114//Slovak Research and Development Agency/ ; VEGA 1/0062/21//Ministry of Education, Science, Research, and Sport of the Slovak Republic/ ; },
mesh = {Animals ; *Autism Spectrum Disorder/therapy/microbiology/genetics ; *Fecal Microbiota Transplantation ; Mice ; Male ; Female ; *Nerve Tissue Proteins/genetics/metabolism ; Humans ; Behavior, Animal ; Pregnancy ; Gastrointestinal Microbiome ; Mice, Knockout ; Disease Models, Animal ; Child ; Prenatal Exposure Delayed Effects ; Microfilament Proteins ; },
abstract = {The increasing incidence of autism spectrum disorder (ASD) increases the urgency of establishing the mechanism of its development for effective prevention and treatment. ASD's etiology includes genetic predisposition and environmental triggers, both of which can play a role in the changed microbiota. Recent research has proved the impact of maternal microbiota on the neurodevelopment of the child. To investigate the co-play of genetic and microbiota factors in ASD development, we performed fecal microbiota transplantation (FMT) from children with ASD to female Shank3b[+/-] mice and studied the autism-like symptoms in the male Shank3b[-/-] and wild-type (WT) offspring. WT animals with prenatal exposure to ASD microbiota had delayed neurodevelopment and impaired food intake behavior, but also elevated plasma leptin concentration and body weight. Shank3b[-/-] mice after FMT ASD exhibited impaired learning and exacerbated anxiety-like behavior in adulthood. Interestingly, FMT ASD improved learning in adolescent Shank3b[-/-] mice. Prenatal exposure to ASD microbiota decreased the activity of hypocretin neurons of the lateral hypothalamic area in both genotypes. The combination of genetic predisposition and FMT ASD led to an increased colon permeability, evaluated by zonula occludens (ZO1, ZO3) and claudin factors. These results suggest the effect of parental FMT exposure on shaping offspring behavior in Shank3b[-/-] mice and the potential of microbiota in the modulation of ASD.},
}

Animals
*Autism Spectrum Disorder/therapy/microbiology/genetics
*Fecal Microbiota Transplantation
Mice
Male
Female
*Nerve Tissue Proteins/genetics/metabolism
Humans
Behavior, Animal
Pregnancy
Gastrointestinal Microbiome
Mice, Knockout
Disease Models, Animal
Child
Prenatal Exposure Delayed Effects
Microfilament Proteins

@article {pmid40647353,
year = {2025},
author = {Liber, A and Więch, M},
title = {The Impact of Fecal Microbiota Transplantation on Gastrointestinal and Behavioral Symptoms in Children and Adolescents with Autism Spectrum Disorder: A Systematic Review.},
journal = {Nutrients},
volume = {17},
number = {13},
pages = {},
doi = {10.3390/nu17132250},
pmid = {40647353},
issn = {2072-6643},
mesh = {Humans ; *Autism Spectrum Disorder/therapy/complications/psychology/microbiology ; *Fecal Microbiota Transplantation/methods ; Child ; Adolescent ; *Gastrointestinal Diseases/therapy/etiology ; Treatment Outcome ; Male ; Female ; Child, Preschool ; Gastrointestinal Microbiome ; *Behavioral Symptoms/therapy ; Dysbiosis/therapy ; },
abstract = {Background: Gastrointestinal (GI) symptoms, often reported by individuals with autism spectrum disorders (ASD), may impair functionality and exacerbate behavioral symptoms. Gut dysbiosis has been identified as a potential environmental factor influencing these symptoms through gut-brain axis dysregulation. Fecal microbiota transplantation (FMT) is a promising therapeutic strategy with potential to alleviate symptoms. This review systematically evaluates the efficacy and safety of FMT in GI and ASD-related symptoms. Methods: This systematic review followed PRISMA 2020 guidelines and was registered in PROSPERO. The review included clinical trials on FMT in children and adolescents with ASD, published up to October 2024. The bias assessments were performed using Cochrane tools. Outcomes focused on changes in GI and ASD-related symptoms using scales selected by the authors. Results: This systematic review included two RCTs and seven before-and-after studies. Improvements in GI and ASD-related outcomes were reported in all before-and-after studies, whereas the results of RCTs were inconsistent. The before-and-after studies showed a high risk of bias, while the RCTs demonstrated a low risk. Conclusions: Although many studies have been conducted, the methodological limitations of some and contradictory findings of others make it difficult to draw clear conclusions about the effectiveness of FMT in children with ASD. Variations in intervention protocols underscore the importance of establishing standardized FMT procedures in future rigorously designed trials.},
}

Humans
*Autism Spectrum Disorder/therapy/complications/psychology/microbiology
*Fecal Microbiota Transplantation/methods
Child
Adolescent
*Gastrointestinal Diseases/therapy/etiology
Treatment Outcome
Male
Female
Child, Preschool
Gastrointestinal Microbiome
*Behavioral Symptoms/therapy
Dysbiosis/therapy

@article {pmid40647217,
year = {2025},
author = {Szczuko, M and Grudniewska, A and Durma, A and Małecki, R and Filipczyńska, I and Franek, E and Kędzierska-Kapuza, K},
title = {Non-Pharmacological Interventions Aimed at Changing the Gut Microbiota for Preventing the Progression of Diabetic Kidney Disease.},
journal = {Nutrients},
volume = {17},
number = {13},
pages = {},
doi = {10.3390/nu17132112},
pmid = {40647217},
issn = {2072-6643},
mesh = {*Gastrointestinal Microbiome ; Humans ; *Diabetic Nephropathies/microbiology/therapy/prevention & control ; *Probiotics/therapeutic use/administration & dosage ; Disease Progression ; Fecal Microbiota Transplantation ; Animals ; Synbiotics/administration & dosage ; Dysbiosis/therapy ; Dietary Supplements ; },
abstract = {BACKGROUND: Diabetic kidney disease (DKD) affects 20-50% of individuals with diabetes. The aim of this review was to identify interventions that positively influence the gut microbiota in DKD.

METHODS: Identification of relevant studies was conducted via a systematic search of databases and registers using the PRISMA guidelines. This review examined the relevant literature published up to 5 January 2025, using a systematic search in PubMed and Scopus. The search was conducted with combinations of keywords including DKD and therapy, supplementation and gut microbiota, and supplementation or probiotics or fecal microbiota transplant. The initial search fielded 132 results from PubMed and 72 from Scopus, which was narrowed to 135 relevant studies. The exclusion criteria included non-English language studies, letters to the editor, and conference abstracts. Eligible studies were independently assessed by a minimum of three authors, with discrepancies resolved through consensus.

RESULTS: Gut microbiota-targeted interventions, including probiotics, synbiotics, and dietary modifications, show promise in modulating the gut microbiota, but evidence specific to DKD remains limited. Some natural food components such as polyphenols and anthocyanins modulate the composition of the gut microbiota translocation of uremic toxins, which slows down the progression of diabetic kidney disease. In animal models, fecal microbiota transplantation (FMT) has shown positive effects in regulating dysbiosis and beneficial effects in chronic kidney disease, but studies involving humans with DKD are insufficient.

CONCLUSIONS: Lactobacillus and Bifidobacterium strains, administered at doses ranging from 0.6 to 90 billion CFU, may help lower urea and creatinine levels, but outcomes vary by disease stage, duration of therapy, and amount used. High-fiber diets (>10.1 g/1000 kcal/day) and supplements such as resistant starch and curcumin (400-1500 mg/day) may reduce uremic toxins through gut microbiota modulation and reduction in oxidative stress. The effect of sodium butyrate requires further human studies.},
}

*Gastrointestinal Microbiome
Humans
*Diabetic Nephropathies/microbiology/therapy/prevention & control
*Probiotics/therapeutic use/administration & dosage
Disease Progression
Fecal Microbiota Transplantation
Animals
Synbiotics/administration & dosage
Dysbiosis/therapy
Dietary Supplements

@article {pmid40645350,
year = {2025},
author = {Fatima, SN and Arif, F and Khalid, R and Khan, M and Naseem, K},
title = {Immunomodulatory role of gut microbiota in autoimmune disorders and the advancement of gut microbiota based therapeutic strategies.},
journal = {Microbial pathogenesis},
volume = {207},
number = {},
pages = {107882},
doi = {10.1016/j.micpath.2025.107882},
pmid = {40645350},
issn = {1096-1208},
abstract = {This review investigates the central hypothesis that gut microbiota dysbiosis contributes to autoimmune pathogenesis via immune dysregulation, increased intestinal permeability, and aberrant metabolite signaling and many other pathways. Mechanisms such as SCFA depletion, Th17/Treg imbalance, molecular mimicry, and disrupted aryl hydrocarbon receptor (AhR) pathways plays central immunomodulatory role in the development as well as management of autoimmune disorders including RA, T1D, MS, and IBD. Emerging interventions like probiotics, prebiotics, SCFA supplementation, and FMT are critically assessed to demonstrating their modulatory effects on cytokine profiles, epithelial integrity, and Treg induction. Clinical and preclinical data support microbial restoration as a viable immunotherapeutic strategy. The review concludes that targeting gut-immune crosstalk through microbiota-directed therapies may offer precise, mechanism-based management for many autoimmune disorders.},
}

@article {pmid40644647,
year = {2025},
author = {Barragan-Carrillo, R and Zengin, ZB and Pal, SK},
title = {Microbiome Modulation for the Treatment of Solid Neoplasms.},
journal = {Journal of clinical oncology : official journal of the American Society of Clinical Oncology},
volume = {},
number = {},
pages = {JCO2500374},
doi = {10.1200/JCO-25-00374},
pmid = {40644647},
issn = {1527-7755},
abstract = {The interplay between the human gut microbiome and the immune system has sparked growing interest in microbiome modulation as a therapeutic strategy in oncology. Preclinical studies have identified specific bacterial species linked to improved responses to immune checkpoint inhibitors (ICIs), leading to clinical investigations in melanoma, renal cell carcinoma (RCC), and non-small cell lung cancer (NSCLC). The stool bacterial abundance of Ruminococcaceae, Akkermansia, and Bifidobacterium correlates with favorable clinical outcomes, whereas the disruption of the gut microbiome through antibiotics before or during ICI initiation is associated with higher rates of primary resistance and shorter survival. Biomarkers such as TOPOSCORE have been developed to better predict ICI benefits and estimate dysbiosis and treatment responses. Several microbiome-modulating strategies have shown potential in patients receiving treatment with ICIs-for instance, high dietary fiber intake may be linked to improved outcomes. As a separate strategy, certain probiotics appear to enhance clinical activity in early trials when incorporated into ICI-based regimens. Finally, fecal microbiota transplantation has shown safety and efficacy in ICI-refractory melanoma and yielded encouraging results in treatment-naïve patients with melanoma, NSCLC, and RCC. Although several compelling signals have been observed to date with microbiome manipulation, the field is lacking large, definitive randomized trials-these are indeed a prerequisite for any of the highlighted strategies to become a standard of care.},
}

@article {pmid40643902,
year = {2025},
author = {Anderer, S},
title = {Fecal Transplant Appears Noninferior to Antibiotics for Treating CDI.},
journal = {JAMA},
volume = {},
number = {},
pages = {},
doi = {10.1001/jama.2025.10327},
pmid = {40643902},
issn = {1538-3598},
}

@article {pmid40643244,
year = {2025},
author = {Seekatz, AM},
title = {Straining to define a healthy microbiome.},
journal = {mSphere},
volume = {},
number = {},
pages = {e0079724},
doi = {10.1128/msphere.00797-24},
pmid = {40643244},
issn = {2379-5042},
abstract = {In 2020, I wrote an mSphere of Influence commentary on two studies that shaped my research perspective on the human gut microbiome (McNulty et al., Sci Transl Med 3:106ra106, 2011, https://doi.org/10.1126/scitranslmed.3002701; Hamilton et al., Gut Microbes 4:125, 2013, https://doi.org/10.4161/gmic.23571). The microbiome field has continued to progress since the publication of these studies over 10 years ago, emerging as a considerable factor in almost all areas focused on disease development. My previous commentary highlighted two areas that piqued my interest early on in my career: (i) that the extant microbial community should be considered when proposing to manipulate the microbiota, such as via probiotics or fecal microbiota transplantation, and (ii) that realized (i.e., transcribed) functional changes of the microbiota may occur independent of changes in its composition. Since writing that commentary, two microbiota-based therapeutics for the treatment of Clostridioides difficile infection have been approved, highlighting the potential success of using the microbiota to treat or prevent disease. Despite these wins and ever-growing evidence of the importance of the microbiome in managing our health, translating mechanistic studies into therapeutic value has been slower. In this minireview, I expand upon two large questions that would increase our ability to translate the microbiome into therapies, highlighting both historical and recent progress.},
}

@article {pmid40642988,
year = {2025},
author = {Wang, F and Wu, Y and Ni, J and Xie, Q and Shen, J and Chen, H and Ma, C and Yao, Y and Wang, J and Xu, L and Xiang, Q and Zhao, Y and Chen, Y and Li, L},
title = {Gut microbiota links to histological damage in chronic HBV infection patients and aggravates fibrosis via fecal microbiota transplantation in mice.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0076425},
doi = {10.1128/spectrum.00764-25},
pmid = {40642988},
issn = {2165-0497},
abstract = {Gut microbiota dysbiosis has been observed in HBV-related cirrhosis, but its role in early-stage disease and its correlation with liver pathology remain unclear. Moreover, whether dysbiosis is a cause or consequence of liver cirrhosis is still debated. We recruited 20 treatment-naïve patients with chronic HBV infection, assessing liver injury via biopsy. Fecal metagenomic sequencing was used to analyze the correlation between gut microbiota and liver histology. To explore the causality, fecal samples from an HBV-related cirrhosis patient were transplanted into mice with CCl4-induced liver fibrosis. Patients with significant histological damage exhibited reduced alpha diversity and greater microbial homogeneity. Species such as Eubacterium_sp_CAG_180, Gemmiger_formicilis, and Oscillibacter_sp_ER4 had decreased abundance, while Parabacteroides_distasonis, Bacteroides_dorei, and Bacteroides_finegoldii were enriched. Mice receiving fecal transplants from the cirrhotic patient showed aggravated liver fibrosis, with increased collagen deposition; elevated ALT, AST, and ALP levels; and heightened hepatic inflammatory gene expression. Additionally, abnormal bile acid profiles with elevated unconjugated bile acids (e.g., GCA and CA) were observed. Gut microbiota dysbiosis is closely associated with liver histological damage in chronic HBV infection and may drive fibrosis progression via microbial-bile acid interactions. These findings suggest potential for gut microbiota-based assessment and treatment strategies in chronic hepatitis B.IMPORTANCEThis study elucidates a significant association between gut microbiota dysbiosis and liver histological damage in patients with chronic hepatitis B (HBV), potentially exacerbating fibrosis progression through bile acid interactions. By analyzing patient gut microbiota and conducting fecal transplant experiments in mice, researchers have identified that gut microbiota dysbiosis contributes to hepatic fibrosis during chronic HBV infection. These findings underscore the importance of the gut-liver axis in HBV disease progression, indicating that monitoring or modulating gut bacteria may facilitate early diagnosis or therapeutic interventions. This research bridges the gap in understanding whether microbial alterations drive disease progression or result from it, providing a foundation for developing therapies targeting the microbiome to mitigate liver damage in chronic HBV infections.},
}

@article {pmid40642664,
year = {2025},
author = {Horwat, P and Mariowska, A and Szymanska, A and Dzieciatkowska, M and Pierudzka, W},
title = {Multimodal Interventions Targeting Gut Microbiota and Microbial Metabolites in Cognitive Impairment.},
journal = {Cureus},
volume = {17},
number = {6},
pages = {e85688},
pmid = {40642664},
issn = {2168-8184},
abstract = {Mild cognitive impairment (MCI) is a transitional stage between normal aging and Alzheimer's disease (AD). Recent studies suggest that alterations in gut microbiota and microbial metabolites are associated with cognitive decline, highlighting the gut-brain axis as a potential therapeutic target. This narrative review explores current evidence on the relationship between gut microbiota, microbial metabolites, and MCI. It summarizes intervention strategies including probiotics, prebiotics, synbiotic, fecal microbiota transplantation, dietary modifications, medicinal herbs, phytochemicals, metformin, and lifestyle factors. Probiotic strains such as Lactobacillus and Bifidobacterium have shown cognitive benefits. Adherence to the Mediterranean and MIND diets, as well as metformin use, is associated with lower MCI risk. Novel strategies, including plant-based compounds and nature exposure, show promise in modulating gut microbiota and improving cognitive outcomes. Gut microbiota modulation represents a promising avenue for early intervention in MCI. Personalized, multifactorial approaches based on individual microbiome profiles may enhance prevention and management strategies. However, more high-quality clinical trials are needed to establish evidence-based guidelines.},
}

@article {pmid40642089,
year = {2025},
author = {Lei, W and Cheng, Y and Liu, X and Gao, J and Zhu, Z and Ding, W and Xu, X and Li, Y and Ling, Z and Jiang, R and Chen, X},
title = {Gut microbiota-driven neuroinflammation in Alzheimer's disease: from mechanisms to therapeutic opportunities.},
journal = {Frontiers in immunology},
volume = {16},
number = {},
pages = {1582119},
pmid = {40642089},
issn = {1664-3224},
mesh = {Humans ; *Alzheimer Disease/therapy/microbiology/immunology/metabolism/etiology ; *Gastrointestinal Microbiome/immunology ; Animals ; *Neuroinflammatory Diseases/therapy/microbiology ; Dysbiosis/immunology ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Brain/metabolism/immunology ; Brain-Gut Axis ; },
abstract = {Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, tau hyperphosphorylation, and chronic neuroinflammation. While neuroinflammation-mediated by microglial and astrocyte activation-has long been considered a secondary response to Aβ pathology, emerging evidence positions it as a primary driver of cognitive decline. Notably, the gut microbiota, through the microbiota-gut-brain axis (MGBA), is crucial in modulating neuroinflammation. Dysbiosis disrupts gut barrier integrity, promotes systemic inflammation, and exacerbates neuroinflammatory responses, thereby accelerating AD progression. Recent advances reveal that gut microbiota-derived metabolites (e.g., short-chain fatty acids, lipopolysaccharides) directly influence microglial activation and Aβ aggregation. These findings have opened new therapeutic possibilities, with microbiota-targeted approaches such as probiotics, prebiotics, and fecal microbiota transplantation demonstrating promising neuroprotective effects in preclinical studies by reducing neuroinflammation and preserving cognitive function. However, translating these findings into clinical applications requires further validation through randomized controlled trials. This review summarizes the current understanding of gut microbiota-driven neuroinflammation in AD, from molecular mechanisms to potential therapeutic strategies. Targeting the MGBA represents a paradigm shift in AD management, emphasizing the modulation of neuroinflammation and pathological progression through gut microbiota interventions. The discussion also addresses existing research challenges and outlines future directions to advance this promising field.},
}

Humans
*Alzheimer Disease/therapy/microbiology/immunology/metabolism/etiology
*Gastrointestinal Microbiome/immunology
Animals
*Neuroinflammatory Diseases/therapy/microbiology
Dysbiosis/immunology
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Brain/metabolism/immunology
Brain-Gut Axis

@article {pmid40641916,
year = {2025},
author = {Daniluk, U and Świdnicka-Siergiejko, A and Daniluk, J and Rusak, M and Dąbrowska, M and Guzińska-Ustymowicz, K and Pryczynicz, A and Dąbrowski, A},
title = {The development of pancreatic cancer is accompanied by significant changes in the immune response in genetically predisposed mice.},
journal = {Frontiers in oncology},
volume = {15},
number = {},
pages = {1603293},
pmid = {40641916},
issn = {2234-943X},
abstract = {PURPOSE: The pathogenesis of pancreatic cancer (PC) is extremely complex and involves genetic and environmental factors, as well as significant changes in the immune response to tumor cells from the loss of immune surveillance to the development of immunotolerance to cancer. Currently available literature data on this subject is inconsistent. The purpose of our study was to evaluate the status of dendritic cells (DC) and other immune cells in the pancreas and blood of mice genetically predisposed to pancreatic cancer (Kras[G12D] mutation). The second objective was to assess the impact of fecal microbiota transplantation (FMT) from PC mice on pancreatic tumor development and alterations in pancreatic and blood immune cell counts in mice genetically predisposed to PC.

METHODS: We used LSL-K-Ras[G12D] mice, which possess the conditional knock-in mutant K-Ras[G12D] driven by its endogenous promoter and Ela-CreERT mice, which express tamoxifen-regulated CreERT specifically in pancreatic acinar cells under the control of a full-length elastase gene promoter. The immunophenotype of immune cells separated from pancreatic tissue and circulating blood was analyzed with the use of multicolor flow cytometry and immunochemistry staining. Fecal pellets from LSL-K-Ras[G12D] mice, that developed PC after the cerulein (CER) treatment, were collected and transplanted into animals previously treated with the antibiotic.

RESULTS: Using immunohistochemistry and flow cytometry, we found that in mice genetically predisposed to PC, cerulein (CER) administered intraperitoneally induced tumor growth and inflammatory cell infiltration in pancreatic tissue, but without affecting immune cell differentiation in the blood. In contrast, orally administered FMT activated the immune system in the gastrointestinal tract, leading to generalized immune cell activation, as observed in the blood, and local infiltration of cells in the pancreatic tissue of Kras mutant mice that developed pancreatic tumors. Interestingly, immunohistochemical evaluation of pancreatic tissue revealed that the Kras mutation alone causes increased infiltration of CD11b[+], CD20[+], CD3[+], CD4[+], and CD8[+] cells. After FMT, there was a trend toward an increased intensity of infiltration by these immune cells, with the exception of CD11b[+].

CONCLUSIONS: Our data suggest that pancreatic cancer development in genetically predisposed mice is accompanied by profound changes in immune cell composition. Treatment with tumor-inducing agents such as CER or FMT from tumor-bearing mice, accelerated PC progression. The type of immune system response, systemic or local, in mice with pancreatic cancer depends on the route of entry of the inflammatory agent. Oral administration of FMT activated the systemic immune response, in contrast to the intraperitoneal injection of CER.},
}

@article {pmid40641009,
year = {2025},
author = {Siegel, R and Sibert, NT and Breidenbach, C and Gani, C and Neumann, PA and Benz, SR and Post, S and Seufferlein, T and Kolb, V and Behrend, M and Blossey, RD and Bunse, J and Dahlke, M and Diller, R and Emmanouilidis, N and Ettrich, TJ and Fahlke, J and Flemming, S and Freitag, B and Fuchs, M and Haeder, L and Hollerbach, S and Höppner, J and Kim, M and Klink, C and Knuth, J and Koeppen, S and Köninger, J and Kolbe, EW and Kühn, F and Mussa, S and Oehring, R and Petzoldt, S and Piso, P and Prause, C and Prinz, C and Reißfelder, C and Riechmann, M and Ritz, JP and Rolinger, J and Rosenberg, R and Scheuerlein, H and Schilawa, D and Schneider, PM and Schwandner, T and Siech, M and Steinemann, D and Stöltzing, O and von Haeften, E and Weihs, D and Wiegering, A and Zielinski, CB and Kowalski, C},
title = {Impact of preoperative radiotherapy on patient-reported outcomes in rectal cancer.},
journal = {Colorectal disease : the official journal of the Association of Coloproctology of Great Britain and Ireland},
volume = {27},
number = {7},
pages = {e70158},
doi = {10.1111/codi.70158},
pmid = {40641009},
issn = {1463-1318},
support = {//Innovation Fund of the German Federal Joint Committee (Innovationsausschuss beim Gemeinsamen Bundesausschuss, G BA)/ ; },
mesh = {Humans ; *Rectal Neoplasms/surgery/radiotherapy ; *Patient Reported Outcome Measures ; Male ; Female ; Middle Aged ; Prospective Studies ; Quality of Life ; Aged ; *Preoperative Care/methods ; *Neoadjuvant Therapy/methods/adverse effects ; Postoperative Complications/etiology ; Proctectomy ; Radiotherapy, Adjuvant/adverse effects ; Fecal Incontinence/etiology ; Surveys and Questionnaires ; Adult ; Treatment Outcome ; },
abstract = {AIM: To prospectively evaluate the effect of preoperative radiotherapy followed by surgery versus surgery alone on patient-reported outcomes (PROs) 1 year after surgery.

METHOD: Prospective observational cohort study in 127 colorectal cancer centres. Patients with rectal cancer completed European Organization for Research and Treatment of Cancer Quality of Life Questionnaire Core (EORTC-QLQ-C30) and Colorectal module (-CR29) questionnaires (thus providing PROs) before initialization of treatment [baseline (T0)] and at 12 months after surgery [follow up (T1)]. The PRO data together with sociodemographic information were linked to clinical data. Relevant confounders were identified using directed acyclic graphs. The effect of preoperative radiotherapy on selected PROs 12 months after surgery was estimated using adjusted tobit regression models.

RESULTS: Of 1635 patients with rectal cancer for whom both baseline and follow-up PROs were available, 565 (35%) received preoperative radiotherapy. Twelve months after surgery, patients with surgery alone reported better scores for global health status/Quality of Life, urinary incontinence, faecal incontinence (patients without stoma), dyspareunia (female patients) and impotence (male patients) than did patients receiving preoperative radiotherapy. The statistically significant effects ranged between 33.20 (p < 0.001, R[2] = 0.19) for impotence and 39.01 (p = 0.001, R[2] = 0.10) for dyspareunia. For global health status/QoL and urinary incontinence, no statistically significant effect could be found.

CONCLUSION: Radiotherapy in addition to surgery negatively affects selected PROs 1 year after surgery in patients with rectal cancer. Compared with surgery alone, patients report profoundly impaired bowel and sexual function after preoperative radiotherapy. However, global health status/QoL was not affected statistically significantly. These results are an important argument for limiting preoperative radiotherapy to patients with a high risk of recurrence of rectal cancer and may facilitate informed decision-making.

TRIAL REGISTRATION: German Clinical Trial Registry Number DRKS00008724 (https://drks.de/search/de/trial/DRKS00008724).},
}

Humans
*Rectal Neoplasms/surgery/radiotherapy
*Patient Reported Outcome Measures
Male
Female
Middle Aged
Prospective Studies
Quality of Life
Aged
*Preoperative Care/methods
*Neoadjuvant Therapy/methods/adverse effects
Postoperative Complications/etiology
Proctectomy
Radiotherapy, Adjuvant/adverse effects
Fecal Incontinence/etiology
Surveys and Questionnaires
Adult
Treatment Outcome

@article {pmid40640940,
year = {2025},
author = {Wang, N and Sun, C and Yang, Y and Zhang, D and Huang, L and Xu, C and Wang, M and Xu, M and Yan, T and Wu, Y and Xu, L and Ju, Y and Sun, H and Guo, W},
title = {Gut microbiota-derived indoleacetic acid attenuates neuroinflammation and neurodegeneration in glaucoma through ahr/rage pathway.},
journal = {Journal of neuroinflammation},
volume = {22},
number = {1},
pages = {179},
pmid = {40640940},
issn = {1742-2094},
support = {SHSMU-ZDCX20210902//Innovative Research Team of High-level Local University in Shanghai/ ; 82171046//National Natural Science Foundation of China/ ; BYH20220403//Post Graduate Medical Education Program 2022/ ; 20DZ2270800//Research Grant of the Shanghai Science and Technology Committee/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; Animals ; *Indoleacetic Acids/metabolism/pharmacology/therapeutic use ; Mice ; Humans ; Male ; *Receptors, Aryl Hydrocarbon/metabolism ; *Glaucoma/metabolism/pathology/microbiology ; *Neuroinflammatory Diseases/metabolism ; Signal Transduction/physiology/drug effects ; Mice, Inbred C57BL ; Female ; Fecal Microbiota Transplantation ; Microglia/metabolism/drug effects ; Middle Aged ; Aged ; },
abstract = {BACKGROUND: Gut microbiota has emerged as a promising therapeutic target for neurodegenerative disorders through regulation of neuroinflammatory responses, while its role in optic nerve degeneration remains incompletely characterized. This study elucidates the neuroprotective role of gut microbiota derived tryptophan metabolites in glaucoma through gut-eye communication and inhibition of microglia-mediated neuroinflammation.

METHODS: Gut microbiota profiling (16 S rRNA sequencing) and serum indoleacetic acid (IAA) quantification were performed in glaucoma patients versus controls. Microbiota-metabolite relationships were further validated through fecal microbiota transplantation (FMT). The neuroprotective and anti-neuroinflammatory effect of Bacteroides fragilis (B. fragilis) and IAA was assessed in both microbead-induced ocular hypertension mice model and in vitro BV-2 microglial cell inflammation model via immunofluorescence, qPCR, Western blot and mice behavioral assays. To explore the underlying mechanisms, retinal transcriptomics and microglia-neuron co-cultures were also employed.

RESULT: Glaucoma patients exhibited gut dysbiosis characterized by depleted tryptophan-metabolizing bacteria (B. fragilis, Bacteroides thetaiotaomicron, Anaerostipes hadrus) and reduced serum IAA levels. Mice receiving FMT from glaucoma patients exhibited lower systemic IAA levels. In in vivo and in vitro models, B. fragilis or IAA restored AhR activation, suppressed inflammation by inhibiting microglial activation and the release of pro-inflammatory mediators throughout the retina, reduced retinal ganglion cells (RGCs) loss and preserved visual function. Mechanistically, IAA attenuated RAGE/NF-κB pathway activation via AhR-dependent signaling, conferring neuroprotection.

CONCLUSION: Our study proposes a novel AhR-mediated gut microbiota-eye axis in glaucoma pathogenesis and demonstrates that IAA serves as an effective neuroprotective strategy with clinical potential for managing RGCs neurodegeneration.},
}

*Gastrointestinal Microbiome/physiology
Animals
*Indoleacetic Acids/metabolism/pharmacology/therapeutic use
Mice
Humans
Male
*Receptors, Aryl Hydrocarbon/metabolism
*Glaucoma/metabolism/pathology/microbiology
*Neuroinflammatory Diseases/metabolism
Signal Transduction/physiology/drug effects
Mice, Inbred C57BL
Female
Fecal Microbiota Transplantation
Microglia/metabolism/drug effects
Middle Aged
Aged

@article {pmid40639338,
year = {2025},
author = {Lesmana, I and Qian, C and Hsiao, EY},
title = {Fibromyalgia pain may have a gut solution.},
journal = {Neuron},
volume = {113},
number = {13},
pages = {2029-2031},
doi = {10.1016/j.neuron.2025.06.005},
pmid = {40639338},
issn = {1097-4199},
mesh = {*Fibromyalgia/therapy/microbiology ; Humans ; Animals ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Mice ; *Pain/microbiology ; },
abstract = {In this issue of Neuron, Cai et al.[1] demonstrated that transferring fecal microbiota from fibromyalgia patients to mice confers pain hypersensitivity and depression-like behavior, which is reversed by fecal microbiota transplant from healthy donors. Fibromyalgia patients experience significant symptom relief after fecal microbiota transplantation.},
}

*Fibromyalgia/therapy/microbiology
Humans
Animals
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Mice
*Pain/microbiology

@article {pmid39172632,
year = {2025},
author = {Blount, KF and Papazyan, R and Ferdyan, N and Srinivasan, K and Gonzalez, C and Shannon, WD and Fuchs, BC},
title = {Microbiome and Metabolome Restoration After Administration of Fecal Microbiota, Live-jslm (REBYOTA) for Preventing Recurrent Clostridioides difficile Infection.},
journal = {The Journal of infectious diseases},
volume = {231},
number = {6},
pages = {e1022-e1033},
doi = {10.1093/infdis/jiae418},
pmid = {39172632},
issn = {1537-6613},
support = {//Rebiotix, Inc/ ; },
mesh = {Humans ; *Clostridium Infections/prevention & control/microbiology ; Male ; Female ; Double-Blind Method ; *Metabolome ; *Feces/microbiology ; Clostridioides difficile ; Middle Aged ; *Fecal Microbiota Transplantation/methods ; *Gastrointestinal Microbiome ; Adult ; Bile Acids and Salts/analysis ; Aged ; Dysbiosis/microbiology ; Treatment Outcome ; *Probiotics/administration & dosage ; },
abstract = {BACKGROUND: Microbiota-based treatments are effective in preventing recurrent Clostridioides difficile infection. Fecal microbiota, live-jslm (REBYOTA; RBL, previously RBX2660) was shown to prevent recurrent C difficile infection in a phase 3 clinical trial (PUNCH CD3) based on a randomized, double-blinded, placebo-controlled design.

METHODS: Stool samples from participants in PUNCH CD3 who received a single blinded dose of rectally administered RBL or placebo were sequenced to determine microbial community composition and calculate the Microbiome Health Index for postantibiotic dysbiosis. The composition of bile acids (BAs) in the same samples was quantified by liquid chromatography-mass spectrometry. Relationships between BA composition and microbiota community structure and correlations with treatment outcomes were assessed.

RESULTS: Before administration, Gammaproteobacteria and Bacilli dominated the microbiota community, and primary BAs were more prevalent than secondary BAs. Clinical success after administration correlated with shifts to predominantly Bacteroidia and Clostridia, a significant increase in Microbiome Health Index for postantibiotic dysbiosis, and a shift from primary to secondary BAs. Several microbiota and BA changes were more extensive in RBL-treated responders as compared with placebo-treated responders, and microbiota changes correlated with BA changes.

CONCLUSIONS: Clinical response and RBL administration were associated with significant restoration of microbiota and BA composition.

CLINICAL TRIALS REGISTRATION: NCT03244644 (https://clinicaltrials.gov/ct2/show/NCT03244644).},
}

Humans
*Clostridium Infections/prevention & control/microbiology
Male
Female
Double-Blind Method
*Metabolome
*Feces/microbiology
Clostridioides difficile
Middle Aged
*Fecal Microbiota Transplantation/methods
*Gastrointestinal Microbiome
Adult
Bile Acids and Salts/analysis
Aged
Dysbiosis/microbiology
Treatment Outcome
*Probiotics/administration & dosage

@article {pmid40639240,
year = {2025},
author = {Zhai, L and Zheng, Y and Lo, CW and Xu, S and Jiang, X and Liu, Q and Ching, JY and Ning, Z and Bao, G and Yang, W and Zhang, Q and Cheng, CW and Lam, WC and Chan, KL and Zhang, X and Lam, PY and Wu, XY and Zhong, LLD and Cao, PH and Koh, M and Cheong, PK and Lin, Z and Lin, C and Zhao, L and Wong, XHL and Wu, JC and Bian, Z},
title = {Butyrate-producing commensal bacteria mediates the efficacy of herbal medicine JCM-16021 on abdominal pain in diarrhea-predominant irritable bowel syndrome: a randomized clinical trial.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157040},
doi = {10.1016/j.phymed.2025.157040},
pmid = {40639240},
issn = {1618-095X},
abstract = {BACKGROUND: Irritable bowel syndrome with diarrhea (IBS-D) presents significant treatment challenges due to limited therapeutic options that effectively target the underlying pathophysiological mechanisms. In this study, we performed a multi-center, double-blind randomized placebo-controlled trial to investigate the efficacy and safety of herbal medicine JCM-16021 on IBS-D with a focus on its effects on gut microbiota.

RESULTS: Our study assessed the clinical efficacy and safety of JCM-16021 in alleviating abdominal pain in IBS-D patients. The results suggested that JCM-16021 is both effective and safe, with its therapeutic effects closely linked to the modulation of short-chain fatty acid (SCFA) producers. Through fecal microbiota transplantation (FMT) experiments in mice, we showed that SCFA producers mediate the alleviation of abdominal pain symptoms by the JCM-16021 treatment. In a TNBS-induced mouse model of IBS, we showed that butyrate producers enriched by JCM-16021 significantly ameliorate abdominal pain. Importantly, baseline gut microbial profiles, such as the presence of Eubacterium rectale in IBS-D patients are predictive of their responses to JCM-16021 treatment.

CONCLUSIONS: Our findings not only affirm the efficacy of JCM-16021 in mitigating abdominal pain in IBS-D patients but also highlight a microbiota-dependent mechanism, underscoring the therapeutic potential of gut microbiota modulation in treating gastrointestinal disorders. By combining clinical trials in humans with biological experiments in mice, this study establishes a translational approach to investigate the role of gut microbiota in the treatment of herbal medicine.

CLINICALTRIALS: gov no: NCT03457324.},
}

@article {pmid40637385,
year = {2025},
author = {Yang, L and Yang, J and Zhang, T and Xie, X and Wu, Q},
title = {Gut microbiota: a novel strategy affecting atherosclerosis.},
journal = {Microbiology spectrum},
volume = {},
number = {},
pages = {e0048224},
doi = {10.1128/spectrum.00482-24},
pmid = {40637385},
issn = {2165-0497},
abstract = {Atherosclerosis is a common chronic inflammatory cardiovascular disease affecting both coronary and peripheral arteries, which is influenced by multiple factors. It is increasingly evident that gut microbes and their byproducts play a crucial role in the development of atherosclerosis. The most representative feature of microbial dysbiosis in coronary artery disease patients is the reduction of the abundance of the phylum Bacteroidetes and the increase of the abundance of the phylum Firmicutes, which may cause changes in functional genes and metabolites. The gut microbiota and its metabolites influence the early, intermediate, and late stages of atherosclerosis mainly by inhibiting or promoting inflammatory responses. In addition, the reshaping of gut microbiota through probiotics, prebiotics, and fecal microbiota transplantation (FMT) is discussed as an alternative to traditional therapeutic methods. By summarizing how gut microbiota and their metabolites affect the process of atherosclerosis, we can better understand the complex relationship between gut microbiota and atherosclerosis.IMPORTANCEAtherosclerosis is an inflammatory cardiovascular disease, making it crucial to understand its pathogenesis and develop effective treatments. This review thoroughly examines the literature, emphasizing the gut microbiome as a key factor influencing atherosclerosis. It also explores how the gut microbiota and its metabolites impact the primary, intermediate, and advanced stages of atherosclerosis and proposes that remodeling the gut microbiota is a promising strategy for improving atherosclerosis.},
}

@article {pmid40637175,
year = {2025},
author = {Fahim, SM and Huey, SL and Palma Molina, XE and Agarwal, N and Ridwan, P and Ji, N and Kibbee, M and Kuriyan, R and Finkelstein, JL and Mehta, S},
title = {Gut microbiome-based interventions for the management of obesity in children and adolescents aged up to 19 years.},
journal = {The Cochrane database of systematic reviews},
volume = {7},
number = {7},
pages = {CD015875},
pmid = {40637175},
issn = {1469-493X},
mesh = {Humans ; Adolescent ; Child ; Randomized Controlled Trials as Topic ; *Pediatric Obesity/therapy/microbiology ; *Gastrointestinal Microbiome ; Probiotics/therapeutic use ; Child, Preschool ; Young Adult ; Prebiotics/administration & dosage ; Synbiotics/administration & dosage ; Infant ; Fecal Microbiota Transplantation ; Body Mass Index ; Overweight/therapy ; },
abstract = {BACKGROUND: The epidemic of overweight and obesity affects more than 390 million children and adolescents aged 5 to 19 years and 37 million children under five years of age. Overweight and obesity are associated with both short- and long-term consequences, including chronic inflammation, metabolic diseases, as well as alterations in the gut microbiome composition. Gut microbiome-based approaches may impact microbiome-related metrics such as diversity or the abundance of intestinal bacteria, which may be linked to obesity-related outcomes. However, evidence regarding the effect of gut microbiome-based interventions for the management of obesity is limited.

OBJECTIVES: To assess the effects of gut microbiome-based interventions in the management of overweight or obesity in children and adolescents in all their diversity aged 0 to 19 years.

SEARCH METHODS: We searched CENTRAL, MEDLINE, CINAHL, Web of Science Core Collection, BIOSIS Previews, Global Index Medicus (all regions), IBECS, SciELO, PAHO, PAHO IRIS, WHO IRIS, WHOLIS, Bibliomap, TRoPHI as well as ICTRP Search Portal and ClinicalTrials.gov. The date of the last search for all databases was 24 January 2025. We did not apply any language restrictions.

SELECTION CRITERIA: We included randomised controlled trials that evaluated gut microbiome-based interventions [i.e. prebiotics, probiotics, synbiotics, short-chain fatty acids (SCFAs), and faecal microbiota transplantation (FMT)] compared to standard-of-care, placebo, or control interventions in children and adolescents aged 0 to 19 years with overweight or obesity.

DATA COLLECTION AND ANALYSIS: Two review authors independently screened titles and abstracts and full texts, extracted data, and assessed the risk of bias using the Cochrane Risk of Bias 2 tool and certainty of the evidence using Grading of Recommendations Assessment, Development and Evaluation (GRADE), a framework for assessing the certainty of evidence and making recommendations in systematic reviews. Random-effects meta-analyses were performed unless only one study per outcome was available, for which fixed-effect analyses were performed.

MAIN RESULTS: We found 17 studies (838 participants) from various countries, evaluating the effects of prebiotics, probiotics, synbiotics, SCFAs, and FMT on body mass index (BMI), body weight, waist circumference, total body fat percentage (%TBF), systolic and diastolic blood pressure, and adverse events. Of the 17 studies included, five studies were in adolescents aged 10 to 19 years, and 12 studies were in children and adolescents spanning both age groups, 0 to 19 years. Upon contacting authors for data grouped by age of the participants, no studies provided separate outcomes data for children and adolescents. The included studies were funded by either academic funding sources or grants from the public and private sectors. Additionally, 15 studies were classified as currently being conducted ('ongoing'). The certainty of evidence throughout was very low. In adolescents 10 to 19 years of age, probiotics compared to placebo or no intervention may have little to no effect on BMI, body weight, waist circumference, %TBF, blood pressure, and adverse events. Similarly, FMT compared to placebo may have little to no effect on waist circumference, %TBF, blood pressure, and adverse events in this age group. According to one study with 41 participants and in children and adolescents 0 to 19 years of age, intervention with prebiotics compared to placebo may result in a small reduction in BMI (mean difference = -0.70, 95% CI = -1.25 to -0.15) and body weight (mean difference = -1.5, 95% CI = -2.61 to -0.39). Prebiotics compared to placebo may have little to no effect on waist circumference, %TBF, systolic blood pressure, and adverse events. No data were available on the effect of prebiotics on diastolic blood pressure. Probiotics compared to placebo may have little to no effect on BMI, body weight, waist circumference, %TBF, blood pressure, and adverse events in children and adolescents (0 to 19 years). Synbiotics compared to placebo may result in a reduction in systolic blood pressure (mean difference = -40.00, 95% CI = -50.63 to -29.37) in children and adolescents (0 to 19 years); according to one study with 56 participants. The evidence is very uncertain about the effects of synbiotics compared to a placebo on BMI, body weight, waist circumference, blood pressure, and adverse events. No data were available on the effect of synbiotics compared to placebo on %TBF. Synbiotics, compared to probiotics, may have little to no effect on waist circumference, %TBF, and adverse events. No data were available on the effect of synbiotics compared to probiotics on BMI, body weight, and blood pressure. According to one study with 48 participants and very low-certainty of evidence, SCFAs compared to placebo may result in a reduction in waist circumference (mean difference = -5.08, 95% CI = -7.40 to -2.76) and BMI (mean difference = -2.26, 95% CI = -3.24 to -1.28) in children and adolescents (0-19 years). SCFAs compared to placebo may have little to no effect on adverse events. No data were available on the effect of SCFAs on body weight, %TBF, and blood pressure. Adverse events, i.e. abdominal cramps, abdominal discomfort, abdominal pain, diarrhoea, vomiting, and migraine, were reported in the prebiotics group but with very low incidence. Additionally, adverse events such as nausea and headache were reported in the SCFAs group, but with low incidence.

AUTHORS' CONCLUSIONS: In adolescents aged 10 to 19 years, gut microbiome-based interventions may result in little to no difference in obesity-related outcomes. In children and adolescents aged 0 to 19 years, prebiotics may result in a small reduction in BMI and body weight; synbiotics may result in a reduction in systolic blood pressure, and SCFAs may result in a reduction in BMI and waist circumference, albeit the certainty of evidence was very low. The evidence was of very low certainty due to few studies per comparison, small sample sizes, short intervention durations, and insufficient reporting of adverse events. More rigorous research examining different types of gut microbiome-based interventions for the management of obesity is required in children and adolescents, both in clinical and community settings. Future trials should also report methods related to randomisation, blinding, and compliance, as well as include prespecified analysis plans.},
}

Humans
Adolescent
Child
Randomized Controlled Trials as Topic
*Pediatric Obesity/therapy/microbiology
*Gastrointestinal Microbiome
Probiotics/therapeutic use
Child, Preschool
Young Adult
Prebiotics/administration & dosage
Synbiotics/administration & dosage
Infant
Fecal Microbiota Transplantation
Body Mass Index
Overweight/therapy

@article {pmid40635758,
year = {2025},
author = {Pan, J and Lin, S and Qian, Q and Fu, S and Liu, X},
title = {Gut-brain axis in post-traumatic stress disorder: microbial - mediated mechanisms and new therapeutic approaches - A narrative review.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1621678},
pmid = {40635758},
issn = {1663-9812},
abstract = {Post-traumatic stress disorder (PTSD) is a severe mental disorder that occurs after experiencing or witnessing a traumatic event. Not only does this disorder severely impair the quality of life and emotional wellbeing of patients, but in recent years the global rate of PTSD diagnoses has increased to 1.5-2 times, and the prevalence of PTSD associated with COVID-19 events in particular has surged to 10%-25%, underscoring the urgency of developing effective treatments. The lifetime prevalence of PTSD in the general population is estimated to be approximately 3.9%, while in high-risk populations, such as war veterans, it can be as high as 30%. As a key pathway connecting the central nervous system to peripheral organs, the gut-brain axis has received increasing attention for its role in PTSD. Although the gut-brain axis has been shown to be associated with several psychiatric disorders, especially depression, its specific role in PTSD remains undercharacterized. Existing studies suggest that specific strains of Lactobacillus (e.g., Lactobacillus reuteri) may alleviate inflammatory responses and improve PTSD-like behaviors by down-regulating the expression of pro-inflammatory factors (IL-6 and TNF-α). In this study, we used a narrative review approach to sort out the research progress of gut microbiota alteration in PTSD, and compared the characteristics of changes in specific microbial taxa (e.g., Bacteroides, Lactobacillus, etc.), the index of microbiota diversity (α/β diversity), and the levels of inflammatory markers (e.g., IL-6, TNF-α) between the animal model and the human patients, respectively, in order to We further explored the potential pathogenic mechanisms mediated by microorganisms, such as influencing the vagal pathway, hypothalamic-pituitary-adrenal (HPA) axis function, immune system and other processes involved in the pathology of PTSD, and summarized the intervention strategies targeting gut microecology, such as probiotic supplementation, dietary interventions and fecal bacteria transplantation.},
}

@article {pmid40635387,
year = {2025},
author = {Gragnaniello, V and Cananzi, M and Cavaliere, A and Loro, C and Cazzorla, C and Gueraldi, D and Puma, A and Burlina, AB},
title = {Early Enzyme Replacement Therapy Does Not Prevent the Protein Losing Enteropathy Syndrome in Neurovisceral Gaucher Disease.},
journal = {American journal of medical genetics. Part A},
volume = {},
number = {},
pages = {e64184},
doi = {10.1002/ajmg.a.64184},
pmid = {40635387},
issn = {1552-4833},
abstract = {Gaucher disease (GD) is a rare lysosomal storage disorder characterized by multisystemic involvement. With the advent of enzyme replacement therapy (ERT), patient survival has improved, revealing new long-term complications. We report a case of a 4-year-old male with severe neurovisceral GD who developed protein-losing enteropathy (PLE) secondary to mesenteric lymphadenopathy, despite ERT starting in the neonatal period. Furthermore, we review the literature related to this rare complication. The patient presented with severe recurrent diarrhea, abdominal distension, weight loss, and malnutrition. Abdominal CT revealed multiple enlarged mesenteric lymph nodes with calcification. Laboratory findings showed lymphopenia and increased fecal alpha-1-antitrypsin. Other causes of diarrhea were excluded. Treatment with a specific diet (high-protein, MCT-enriched) and a course of budesonide resulted in persistent clinical improvement and normalization of laboratory parameters. This case highlights the emergence of gastrointestinal complications in patients with neurovisceral GD on long-term ERT, particularly the development of PLE due to mesenteric lymphadenopathy. It underscores the need for vigilance in monitoring GD patients for such complications and demonstrates the potential efficacy of dietary interventions and anti-inflammatory therapy in managing PLE in this context. The case also emphasizes the limitations of current ERT in addressing all aspects of GD, particularly in sequestered sites like lymph nodes, and calls for new therapeutic strategies to address these challenges.},
}

@article {pmid40634307,
year = {2025},
author = {De Sciscio, M and Bryant, RV and Haylock-Jacobs, S and Day, AS and Pitchers, W and Iansek, R and Costello, SP and Kimber, TE},
title = {Faecal microbiota transplant in Parkinson's disease: pilot study to establish safety & tolerability.},
journal = {NPJ Parkinson's disease},
volume = {11},
number = {1},
pages = {203},
pmid = {40634307},
issn = {2373-8057},
support = {2021/23-QA253//Hospital Research Foundation/ ; 2021/23-QA253//Hospital Research Foundation/ ; 2021/23-QA253//Hospital Research Foundation/ ; },
abstract = {Emerging evidence suggests gut microbiota differences in Parkinson's Disease (PD) may impact disease progression and treatment. Faecal Microbiota Transplantation (FMT) offers a potential therapeutic approach. We conducted an open-label pilot study to assess the safety, tolerability, and symptom impact of FMT in 12 patients with mild to moderate PD, administered via enema for 6 months. FMT was safe and well tolerated, causing only mild, transient gastrointestinal symptoms. While no significant motor symptom changes were observed, there was a trend toward reduced daily OFF time at 2 months. Whilst no sustained improvement in non-motor symptoms was found after 6 months, transient improvements in quality of life and non-motor scores were noted at 2 months; these gains regressed by study end. Overall, extended FMT therapy in PD appears safe and tolerable, with reduction in daily motor OFF time and self-reported non-motor symptoms that was not sustained throughout the 6-months of treatment.},
}

@article {pmid40198765,
year = {2025},
author = {Saha, S and Rehman, L and Rehman, A and Darbaniyan, F and Weber, DM and Becnel, M and Gaballa, M and Thomas, SK and Lee, HC and Chang, CC and Arora, R and Menges, M and Corallo, S and Davila, ML and Locke, FL and Tanner, MR and Neelapu, SS and Shpall, EJ and Flowers, CR and Orlowski, RZ and Jenq, RR and Jain, MD and Peterson, C and Hansen, DK and Saini, NY and Patel, KK},
title = {Longitudinal analysis of gut microbiome and metabolome correlates of response and toxicity with idecabtagene vicleucel.},
journal = {Blood advances},
volume = {9},
number = {14},
pages = {3429-3440},
doi = {10.1182/bloodadvances.2024014476},
pmid = {40198765},
issn = {2473-9537},
mesh = {Humans ; *Gastrointestinal Microbiome ; *Metabolome ; *Immunotherapy, Adoptive/adverse effects/methods ; Male ; Female ; Middle Aged ; Aged ; Longitudinal Studies ; Feces/microbiology ; Receptors, Chimeric Antigen ; },
abstract = {Increasing evidence suggests that the gut microbiome may influence the responses and toxicities associated with chimeric antigen receptor T-cell (CAR-T) therapy. We conducted whole-genome shotgun sequencing on stool samples (N = 117) collected at various times from patients with multiple myeloma (n = 33) who underwent idecabtagene vicleucel (ide-cel) anti-B-cell maturation antigen CAR-T therapy. We observed a significant decrease in bacterial diversity after ide-cel infusion, along with significant differences in the bacterial composition linked to therapy response and toxicities. Specifically, we found significant enrichment of Flavonifractor plautii, Bacteroides thetaiotaomicron, Blautia fecis, and Dysosmobacter species in ide-cel responders. A notable finding was the link of major microbiome disruption, defined as the presence of dominant specific taxa (>35% prevalence), and increased facultative pathobionts, like Enterococcus, with ide-cel toxicities, especially cytokine release syndrome (CRS). Patients with genus dominance in baseline samples had a higher incidence of grade 2 or higher CRS at 46.2% than those without genus dominance (11.1%; P = .043). In addition, network analysis and mass spectrometric assessment of stool metabolites revealed important associations and pathways, such as F plautii being linked to increased indole metabolites and pathways in responders. Our findings uncovered novel microbiome associations between ide-cel responses and toxicities that may be useful for developing modalities to improve CAR-T outcomes.},
}

Humans
*Gastrointestinal Microbiome
*Metabolome
*Immunotherapy, Adoptive/adverse effects/methods
Male
Female
Middle Aged
Aged
Longitudinal Studies
Feces/microbiology
Receptors, Chimeric Antigen

@article {pmid40634168,
year = {2025},
author = {Lee, PC and Chang, TE and Wang, YP and Lee, KC and Lin, YT and Yang, UC and Huang, HC and Huang, YH and Luo, JC and Hou, MC},
title = {Response to commentary on 'Alteration of gut microbial composition associated with the therapeutic efficacy of fecal microbiota transplantation in Clostridium difficile infection'.},
journal = {Journal of the Formosan Medical Association = Taiwan yi zhi},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jfma.2025.05.037},
pmid = {40634168},
issn = {0929-6646},
}

@article {pmid40632357,
year = {2025},
author = {Arif, TB and Damianos, JA and Rahman, AU and Hasnain, N},
title = {Fecal Microbiota Transplantation for Disorders of Gut-Brain Interaction: Current Insights, Effectiveness, and Future Perspectives.},
journal = {Current gastroenterology reports},
volume = {27},
number = {1},
pages = {50},
pmid = {40632357},
issn = {1534-312X},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods ; *Dysbiosis/therapy/complications/microbiology ; *Gastrointestinal Microbiome ; *Brain-Gut Axis ; *Gastrointestinal Diseases/therapy/microbiology ; },
abstract = {PURPOSE OF REVIEW: Dysbiosis can disrupt intestinal barrier integrity and impact the immune and nervous systems, playing a significant role in developing disorders of gut-brain interaction (DGBI). This review aims to provide a comprehensive understanding of dysbiosis and its role in DGBI while examining the latest advancements in fecal microbiota transplantation (FMT). It also highlights key challenges in the field and outlines critical directions for future research to optimize FMT strategies, ultimately improving patient outcomes in this evolving treatment area.

RECENT FINDINGS: In DGBI, dysbiosis triggers immune responses, increases gut permeability, and disrupts nervous system signaling, with contributing factors including diet, antibiotics, stress, and infections. Individuals with DGBI exhibit distinct microbial imbalances, such as an increased Firmicutes-to-Bacteroidetes ratio and reduced beneficial bacteria. FMT has shown mixed results, with factors like patient selection, treatment protocols, and microbiome diversity influencing outcomes. While FMT can improve symptoms in refractory irritable bowel syndrome (IBS), effects may fade over time, requiring repeat treatments. Future FMT approaches should focus on targeted microbial interventions, considering the role of archaea, fungi, and microbial metabolites, while prioritizing optimal donor selection and large-scale trials for long-term efficacy. Despite the promising findings, FMT has not yet been widely endorsed in clinical guidelines due to the variability and heterogeneity of the data available. While much of the research has focused on IBS, studies have also explored the impact of FMT on other conditions such as functional diarrhea, functional constipation, and functional dyspepsia, which all exhibit altered microbial profiles.},
}

Humans
*Fecal Microbiota Transplantation/methods
*Dysbiosis/therapy/complications/microbiology
*Gastrointestinal Microbiome
*Brain-Gut Axis
*Gastrointestinal Diseases/therapy/microbiology

@article {pmid40631858,
year = {2025},
author = {Qu, S and Gu, Y and Hou, X and Wei, M and Wang, M and Su, Y and Miao, Y and Yang, J and Sun, Y and Zeng, Z},
title = {Dual associations of gut and oral microbial networks with kidney transplantation.},
journal = {mSystems},
volume = {},
number = {},
pages = {e0025225},
doi = {10.1128/msystems.00252-25},
pmid = {40631858},
issn = {2379-5077},
abstract = {UNLABELLED: Gut and oral microbiomes play an essential role in the occurrence and development of kidney disease, but their changes after kidney transplantation in patients with end-stage renal disease and their relationships with host health remain unclear. Through shotgun metagenomic sequencing of fecal and saliva samples, we found that for both gut and oral microbiome, the initial loss of species diversity after kidney transplantation led to a reduction in network nodes and interactions, but strengthened the connections among the remaining species, which started to get a recovery approximately 7-14 days later. Different network modules tended to exhibit unique functions and showed different responses to transplantation. These network changes were significantly correlated with clinical indicators, especially with estimated glomerular filtration rate, suggesting that microbial networks contributed to regulating kidney function and host health from dual dimensions. Our study provides novel insights into associating microbiomes with patient recovery after kidney transplantation and offers new diagnostic strategies.

IMPORTANCE: Understanding the dynamics of gut and oral microbiomes after kidney transplantation is crucial for improving post-transplant outcomes and managing potential complications. Through shotgun metagenomic sequencing of fecal and saliva samples from patients following kidney transplantation, our study emphasizes that, in addition to focusing on the various microbial species themselves, the topological properties of gut and oral microbial networks are also critically important for kidney function. We aim to explore the relationship between host health and the oral and gut microbiomes following kidney transplantation from an ecological perspective and extend to other diseases to advance the study of the microbiome and its clinical impact.},
}

@article {pmid40630283,
year = {2025},
author = {Ness, C and Svistounov, D and Solbu, MD and Petrenya, N and Boardman, N and Ytrehus, K and Jenssen, TG and Holmes, A and Simpson, SJ and Zykova, SN},
title = {Gut Microbiome Diversity and Uric Acid in Serum and Urine.},
journal = {Kidney international reports},
volume = {10},
number = {6},
pages = {1683-1693},
pmid = {40630283},
issn = {2468-0249},
abstract = {INTRODUCTION: An increasing body of evidence has shown the importance of the gut microbiota in modulating serum uric acid (SUA) levels. In this study, we aimed to determine the association between gut microbiome diversity, diet, SUA, and fractional excretion of uric acid (FEUA) in the kidney.

METHODS: A cross-sectional study was conducted in 53 adults with normal or elevated SUA and estimated glomerular filtration rate (eGFR) range from 37 to 124 ml/min per 1.73 m[2]. Fecal microbiome composition was analyzed using 16S ribosomal RNA sequencing; and alpha diversity was expressed as reverse Simpson, Shannon, and Richness indices. Dietary data were collected, and dietary patterns were identified using principal component analysis. Unadjusted linear regression and models adjusted for sex, waist-hip ratio (WHR), and eGFR were used to study the association between gut microbial diversity, dietary pattern scores, and SUA/FEUA.

RESULTS: Shannon index was negatively associated with SUA after multiple adjustment (β -36.4, 95% CI [-66.2 to -6.7], P = 0.017; adjusted R[2] = 0.62, P < 0.001). Sex (standardized β = 0.52) and WHR (standardized β = 0.35) had the highest effect on SUA, followed by Shannon diversity index (standardized β = -0.22). We found that Shannon index (standardized β = 0.49, P < 0.001) was positively associated with FEUA after adjustment for sex and "sweet" dietary pattern. This model explained 40% of the variability in FEUA (P < 0.001). None of the dietary patterns were associated with SUA or FEUA.

CONCLUSION: A higher gut microbial diversity was associated with lower SUA and more efficient elimination of uric acid by the kidneys. There is a need for studies assessing efficacy and safety of interventions on the gut microbiome as a treatment of hyperuricemia.},
}

@article {pmid40630180,
year = {2025},
author = {Zhang, Z and Wang, R and Li, M and Lu, M},
title = {Current insights and trends in atopic dermatitis and microbiota interactions: a systematic review and bibliometric analysis.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1613315},
pmid = {40630180},
issn = {1664-302X},
abstract = {BACKGROUND: Atopic dermatitis (AD) is a prevalent chronic inflammatory skin condition influenced by immune dysfunction, genetics, and environmental factors, with emerging evidence highlighting the critical role of skin and gut microbiota in its pathogenesis. This article uniquely integrates a systematic review with bibliometric analysis to map the research landscape of AD and microbiota interactions, offering a comprehensive synthesis of trends and future directions.

METHODS: We conducted a bibliometric analysis using the Web of Science Core Collection, retrieving 1,196 English-language articles and reviews published between 2009 and 2024, employing a detailed search strategy targeting AD and microbiota-related terms. Data were analyzed with tools like CiteSpace, VOSviewer, and Biblioshiny to assess publication trends, geographical contributions, institutional outputs, journal impacts, author networks, reference citations, and keyword evolution.

RESULTS: Research on AD and microbiota has surged since 2016, peaking at 168 publications in 2021, with the USA leading in output (360 papers) and citations (24,655). The University of Copenhagen and the Journal of Allergy and Clinical Immunology emerged as top contributors, while authors like Gallo, Richard L., and Kong, Heidi H. drove influential studies. Key findings underscore the skin and gut microbiomes as research hotspots, with Staphylococcus aureus and the gut-skin axis dominating discussions. Emerging trends from 2020 to 2024 focus on adult AD severity, prebiotics, and personalized interventions like fecal microbiota transplantation (FMT), supported by multi omics data.

CONCLUSION: This study illuminates the dynamic growth and global collaboration in AD and microbiota research, emphasizing microbial dysbiosis and immune modulation as pivotal to AD management. These insights pave the way for precision medicine and dietary interventions, promising enhanced therapeutic strategies and improved patient outcomes through continued multidisciplinary efforts.},
}

@article {pmid40625834,
year = {2025},
author = {Xie, W and Yan, X and Yang, X and Sun, H and Zhang, W},
title = {The regulation of neuroinflammatory response after stroke by intestinal flora microorganisms.},
journal = {Frontiers in cellular and infection microbiology},
volume = {15},
number = {},
pages = {1594834},
pmid = {40625834},
issn = {2235-2988},
mesh = {Humans ; *Gastrointestinal Microbiome/immunology ; Animals ; Probiotics/therapeutic use ; *Neuroinflammatory Diseases/immunology/therapy/microbiology ; Fecal Microbiota Transplantation ; *Stroke/immunology/microbiology ; Brain-Gut Axis/immunology ; Immunity, Innate ; Brain/immunology ; Prebiotics/administration & dosage ; Adaptive Immunity ; Inflammation ; Blood-Brain Barrier ; Anti-Bacterial Agents/therapeutic use ; },
abstract = {Ischemic stroke (IS) is a severe central nervous system disorder characterized by high incidence, disability, mortality, and recurrence rates, along with numerous complications. The microbiota-gut-brain axis (MGBA) represents a bidirectional communication pathway between the brain and the gut, which can influence the onset and progression of IS through neural, immunoregulatory, and gut metabolite pathways. Recent preclinical and clinical evidence supports the use of fecal microbiota transplantation (FMT), probiotics and prebiotics, dietary interventions, and antibiotics as strategies to suppress neuroinflammation in IS, protect the blood-brain barrier, modulate immune responses, and improve stroke outcomes. In this review, we summarize the manifestations of innate inflammation and adaptive immunity following the onset of IS, highlight the interactions between the MGBA and post-stroke neuroinflammation, and discuss current therapeutic measures, thus providing insights for the development of novel treatment strategies in the future.},
}

Humans
*Gastrointestinal Microbiome/immunology
Animals
Probiotics/therapeutic use
*Neuroinflammatory Diseases/immunology/therapy/microbiology
Fecal Microbiota Transplantation
*Stroke/immunology/microbiology
Brain-Gut Axis/immunology
Immunity, Innate
Brain/immunology
Prebiotics/administration & dosage
Adaptive Immunity
Inflammation
Blood-Brain Barrier
Anti-Bacterial Agents/therapeutic use

@article {pmid40388103,
year = {2025},
author = {Dukaew, N and Noppakun, K and Thongkumkoon, P and Na Takuathung, M and Inpan, R and Kongta, N and Suyayai, N and Manoree, C and Koonrungsesomboon, N},
title = {Associations between the gut microbiota and the metabolism rate of tacrolimus in kidney transplant recipients during the early posttransplant period.},
journal = {Archives of pharmacal research},
volume = {48},
number = {6},
pages = {549-562},
pmid = {40388103},
issn = {1976-3786},
support = {1196/2564//Kidney Foundation of Thailand/ ; 115-2564//Faculty of Medicine, Chiang Mai University/ ; },
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/drug effects ; *Tacrolimus/pharmacokinetics/metabolism ; *Kidney Transplantation ; *Immunosuppressive Agents/pharmacokinetics/metabolism/administration & dosage ; Male ; Female ; Middle Aged ; Adult ; Feces/microbiology ; RNA, Ribosomal, 16S/genetics ; },
abstract = {The use of tacrolimus (TAC), a critical immunosuppressant post transplantation, is complicated by its high pharmacokinetic variability. While the gut microbiota has gained attention as a potential contributor, few studies have assessed its role in TAC metabolism variability. This study investigated the associations between the gut microbiota and TAC metabolism rates in kidney transplant recipients during the first month post transplantation-a crucial period for adjusting TAC to achieve therapeutic levels. We recruited 20 kidney transplant recipients and profiled their gut microbiota diversity and composition from stool samples collected before transplantation and at weeks 1 and 4 post transplantation via 16S rRNA sequencing. The TAC pharmacokinetic parameters were also collected. Associations between TAC metabolism status or pharmacokinetic parameters and gut microbiota diversity and composition were evaluated. Recipients with a fast TAC metabolism rate (C0/D ratio < 1.05 ng/mL × 1/mg) presented significantly greater changes in both bacterial alpha and beta diversity metrics at 1 week post transplantation than did those with a slow metabolism rate (C0/D ratio ≥ 1.05 ng/mL × 1/mg). Compared with slow metabolizers, fast metabolizers were associated with a significant increase in the abundance of three bacterial genera (Faecalibacterium, Clostridia vadinBB60, and Ruminococcus) and a significant decrease in the abundance of two bacterial species (Bacteroides plebeius and Parabacteroides goldsteinii). This study revealed links between gut microbiota diversity and composition and TAC metabolism rates in kidney transplant recipients during the early posttransplant period, underscoring the importance of investigating the gut microbiota as a contributor to TAC pharmacokinetic variability. Clarifying this causal relationship could better predict inter- and intraindividual TAC pharmacokinetic variability.},
}

Humans
*Gastrointestinal Microbiome/physiology/drug effects
*Tacrolimus/pharmacokinetics/metabolism
*Kidney Transplantation
*Immunosuppressive Agents/pharmacokinetics/metabolism/administration & dosage
Male
Female
Middle Aged
Adult
Feces/microbiology
RNA, Ribosomal, 16S/genetics

@article {pmid40625618,
year = {2025},
author = {Hu, Y and Zheng, S and Xu, J and Zhao, Y and Wang, J and Fang, Z and Zhou, L},
title = {Gestational diabetes mellitus alters neonatal gut microbiota and increases infection susceptibility.},
journal = {Frontiers in microbiology},
volume = {16},
number = {},
pages = {1600325},
pmid = {40625618},
issn = {1664-302X},
abstract = {INTRODUCTION: Gestational diabetes mellitus (GDM) affects up to 27.6% of pregnancies in certain regions and is associated with a two- to threefold increased risk of neonatal infections. Although maternal gut microbiota undergoes significant remodeling during pregnancy, the specific mechanisms governing GDM-induced microbial reprogramming in offspring and its implications for susceptibility to infections remain unclear. This study aimed to investigate the impact of GDM on the composition of neonatal gut microbiota, metabolomic profiles, and susceptibility to infections using a translational approach.

METHOD: We recruited pregnant women with and without GDM at the JinHua Municipal Central Hospital in China. Meconium and blood samples were collected from newborns within 24 h of birth. The composition of the gut microbiota was analyzed using 16S rDNA amplicon sequencing, and short-chain fatty acids (SCFAs) were quantified using gas chromatography-mass spectrometry. Serum inflammatory markers, including interleukin-6 (IL-6), C-reactive protein (CRP), lipopolysaccharides (LPS), and procalcitonin (PCT), were measured by enzyme-linked immunosorbent assay. To establish causality, fecal microbiota transplantation (FMT) was conducted in antibiotic-treated mice using pooled samples from healthy and GDM-exposed neonates, followed by assessment of inflammatory markers and intestinal barrier integrity.

RESULTS AND DISCUSSION: GDM significantly reduced the diversity of neonatal gut microbiota and altered its composition, characterized by a depletion of beneficial taxa (Bifidobacterium, Blautia, Faecalibacterium) and an enrichment of potential pathogens (Stenotrophomonas, Chryseobacterium). These alterations were accompanied by significant reductions in fecal SCFAs, particularly acetate (49.30%), butyrate (41.00%), and propionate (17.83%). GDM-exposed neonates exhibited elevated serum inflammatory markers, including IL-6, CRP, LPS, and PCT, which correlated negatively with beneficial bacteria and positively with opportunistic pathogens. FMT experiments demonstrated that mice receiving GDM-associated microbiota developed increased systemic inflammation and compromised intestinal barrier function, as evidenced by the downregulation of tight junction proteins (ZO-1, occludin, claudin-1, mucin1). These findings suggest that GDM-induced alterations in neonatal gut microbiota composition and metabolite production may compromise intestinal barrier function and increase susceptibility to infections, highlighting the potential for microbiome-targeted interventions to mitigate infection risk in GDM-exposed neonates.},
}

@article {pmid40625306,
year = {2025},
author = {Wu, J and Xiang, J and Song, P and Bai, Y and Che, Q and Cao, H and Guo, J and Su, Z},
title = {GOS-Modulated Gut Microbiota in Mice Ameliorates Obesity in High-Fat Diet-Fed Mice Through the Gut-Liver Axis and Bile Acid Pathway.},
journal = {Journal of food science},
volume = {90},
number = {7},
pages = {e70361},
doi = {10.1111/1750-3841.70361},
pmid = {40625306},
issn = {1750-3841},
support = {202103000089//the Science and Technology Program of Guangzhou, China/ ; //the Guangdong Demonstration BASe for Joint Cultivation of Postgraduates (2023)/ ; 2020B1515020026//the Science Foundation for Distinguished Young Scholars of Guangdong, China/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; *Bile Acids and Salts/metabolism ; Diet, High-Fat/adverse effects ; *Obesity/metabolism/microbiology ; Mice ; *Liver/metabolism/drug effects ; Mice, Inbred C57BL ; Male ; Lipid Metabolism/drug effects ; *Oligosaccharides/pharmacology/administration & dosage ; Fibroblast Growth Factors/metabolism ; Signal Transduction/drug effects ; Feces/microbiology ; Mice, Obese ; },
abstract = {This work is meant to study the effect of galacto-oligosaccharide (GOS) intervention in the fecal microbiota of obese mice on lipid metabolism and anti-obesity in mice. A pseudo-germ-free mice model was established by administration of a mixture of antibiotics. The fecal microbiota of GOS-fed obese mice are transplanted into pseudo-germ-free mice. To investigate the effects of GOS intervention on lipid metabolism, lipid quadruple, bile acid metabolism, and intestinal microbiota in obese mice. At the same time, the expression of BAS synthase and the effects of FXR-SHP and FXR-FGF15-FGFR4 signaling pathways on BAS homeostasis were also explored. The fecal microbiota of obese mice intervened by GOS could reshape the structure of intestinal microbiota, regulate the synthesis of bile acids in the enterohepatic circulation and the expression of transport-related factors, and promote metabolic ability to exert anti-obesity effects.},
}

Animals
*Gastrointestinal Microbiome/drug effects
*Bile Acids and Salts/metabolism
Diet, High-Fat/adverse effects
*Obesity/metabolism/microbiology
Mice
*Liver/metabolism/drug effects
Mice, Inbred C57BL
Male
Lipid Metabolism/drug effects
*Oligosaccharides/pharmacology/administration & dosage
Fibroblast Growth Factors/metabolism
Signal Transduction/drug effects
Feces/microbiology
Mice, Obese

@article {pmid40624229,
year = {2025},
author = {Lau, HC and Zhang, X and Yu, J},
title = {Gut microbiome in metabolic dysfunction-associated steatotic liver disease and associated hepatocellular carcinoma.},
journal = {Nature reviews. Gastroenterology & hepatology},
volume = {},
number = {},
pages = {},
pmid = {40624229},
issn = {1759-5053},
abstract = {Metabolic dysfunction-associated steatotic liver disease (MASLD) is the most prevalent chronic liver disease worldwide, affecting billions of the global population. It can gradually progress to more severe diseases, including steatohepatitis, cirrhosis and hepatocellular carcinoma. Studies have highlighted the importance of the gut microbiome in the pathogenesis and progression of MASLD. On the other hand, increasing evidence has revealed the clinical potential of targeting the gut microbiome to treat MASLD. In this Review, we summarize gut microbial alterations in MASLD, metabolic dysfunction-associated steatohepatitis and hepatocellular carcinoma. The mechanisms by which a dysregulated gut-liver axis contributes to disease progression are also described, including intestinal barrier dysfunction, chronic inflammation, and altered metabolic pathways (for example, bile acids) and microbial-derived metabolites (for example, short-chain fatty acids, tryptophan derivatives and endogenous ethanol). In addition, we discuss the clinical implications of utilizing the gut microbiome as a diagnostic biomarker and the therapeutic approaches to treat MASLD and related diseases such as faecal microbiota transplantation, probiotics and engineered bacteria, prebiotics and postbiotics, microbial-derived metabolites, antimicrobials and bacteriophages. Finally, we discuss current challenges in basic and translational research on the microbiome in MASLD and propose future directions to drive progress in this field.},
}

@article {pmid40623769,
year = {2025},
author = {Basoya, R and Singh, B and Basi, A and Aggarwal, S},
title = {Role of microbiome in cancer progression.},
journal = {International review of cell and molecular biology},
volume = {394},
number = {},
pages = {79-106},
doi = {10.1016/bs.ircmb.2024.12.013},
pmid = {40623769},
issn = {1937-6448},
mesh = {Humans ; *Neoplasms/microbiology/pathology/therapy ; *Disease Progression ; *Microbiota ; Animals ; },
abstract = {The human microbiome plays a crucial role in maintaining health and preventing disease. Dysbiosis, or imbalance, in the microbiome, has been linked to various diseases, including cancer. This chapter explores the influence of microbiomes on different organs, immune system modulation, and cancer development. Specific microorganisms, such as Helicobacter pylori, Escherichia coli, and human papillomavirus (HPV), contribute to gastric, colorectal, and cervical cancer through mechanisms like immunomodulation and proliferative signaling pathways. Dysbiosis-induced cancer progression involves NF-κB, Wnt/β-catenin, and JAK/STAT signaling. Recent studies highlight the microbiome's potential in cancer diagnosis and immunotherapy. Fecal Microbiota Transplantation (FMT) and predictive biomarkers, such as Porphyromonas gingivalis and Escherichia-Shigella, show promise in treating colorectal cancer. The microbiome influences tumor biology and immune response, affecting immunotherapeutic efficacy. Understanding microbiome-cancer interactions offers new opportunities for improved diagnosis and personalized therapy. This chapter provides comprehensive insights into the role of microbiome in cancer progression, emphasizing the importance of microbiome research in developing effective cancer treatments.},
}

Humans
*Neoplasms/microbiology/pathology/therapy
*Disease Progression
*Microbiota
Animals

@article {pmid40621498,
year = {2025},
author = {Chong, J and Zhou, Y and Li, Z and Li, X and Zhang, J and Cao, H and Ma, J and Ge, L and Zhong, H and Sun, J},
title = {Hyodeoxycholic acid modulates gut microbiota and bile acid metabolism to enhance intestinal barrier function in piglets.},
journal = {Frontiers in veterinary science},
volume = {12},
number = {},
pages = {1610956},
pmid = {40621498},
issn = {2297-1769},
abstract = {Oral bile acids, particularly hyodeoxycholic acid (HDCA), serve as critical drivers for gut microbial community maturation in mice. In the first study, Cy5-labeled HDCA combined with fluorescence imaging revealed rapid gastrointestinal transit of HDCA in piglets, contrasting with its delayed absorption observed in mice. In the second study, the effects of the oral HDCA supplementation on microbiota-host metabolic interactions were investigated using four piglet model groups: OPM-HDCA (naturally born, raised germ-free (GF), and orally administered HDCA), OPM-CON (naturally born, raised GF, and orally administered PBS), SPF-HDCA (naturally born, raised GF, and received fecal microbiota transplantation (FMT) and HDCA), and SPF-CON (naturally born, raised GF with FMT but no HDCA). The results demonstrated that HDCA administration at 0.2 mg/mL suppressed body weight gain in piglets, which was alleviated by FMT. HDCA significantly altered gut microbiota composition in SPF piglets, markedly increasing the Lactobacillus abundance (37.97% vs. 5.28% in SPF-CON) while decreasing the proportion of Streptococcus (28.34% vs. 38.65%) and pathogenic family Erysipelotrichaceae (0.35% vs. 17.15%). Concurrently, HDCA enhanced intestinal barrier integrity by upregulating tight junction proteins (ZO-1, Claudin, Occludin) and suppressing pro-inflammatory cytokines (TNF-α, IL-1β). Additionally, HDCA significantly upregulated ileal gene expression of CYP7A1 (cytochrome P450 family 7 subfamily A member 1) and TGR5 (G protein-coupled bile acid receptor 1) in both SPF-HDCA and OPM-HDCA groups compared to their respective controls (p < 0.05). These findings demonstrate that HDCA exerts microbiota-dependent effects on growth performance, intestinal barrier function, and bile acid metabolism in piglets. Although 0.2 mg/mL HDCA treatment suppressed body weight gain, it potentially enhanced intestinal barrier integrity by activating the TGR5 signaling pathway and increasing the abundance of beneficial bacteria such as Lactobacillus. These results also highlight the critical role of early-life gut microbiota in nutritional interventions, providing a basis for developing precision nutritional strategies targeting intestinal microbial ecology in piglets.},
}

@article {pmid40620607,
year = {2025},
author = {Liu, J and Chen, Y and Wan, Q},
title = {Immune Cell Characteristics in a Gut-Kidney Axis-Induced Mouse Model of IgA Nephropathy: The Upregulated Dendritic Cells and Neutrophils.},
journal = {Journal of inflammation research},
volume = {18},
number = {},
pages = {8579-8592},
pmid = {40620607},
issn = {1178-7031},
abstract = {BACKGROUND: IgA nephropathy (IgAN) is the leading type of primary glomerulonephritis, significantly contributing to chronic kidney disease (CKD) and renal failure. The pathogenesis of IgAN is the multi-hit hypothesis regarding overproduction and accumulation of galactose-deficient (Gd-IgA1). Recent findings have revealed gut microbiota dysbiosis and immune responses are essential in the development of IgAN, attracting increasing attention. This study aimed to map mucosal immune cells in IgAN influenced by gut microbiota, investigating the role of innate immune cells in kidney damage.

METHODS: Fecal samples were acquired from both patients and controls for subsequent animal experiments. Mice received a broad-spectrum antibiotic cocktail to eliminate their intestinal microflora, followed by a gavage with fecal microbiota from clinical individuals. Murine intestinal and kidney tissues were collected for flow cytometry. Intestine and kidney histopathology, immunofluorescence, and inflammatory cytokine expression were assessed in the murine models. The mucosal epithelium's structure and function, along with the innate immune cell response, were analyzed.

RESULTS: Mice exhibited the IgAN phenotype following colonization with gut microbiota from IgAN patients. These mice (IgAN-FMT mice) showed renal dysfunction and increased pathology of tissue injury in both intestine and kidneys. IgAN-FMT mice showed heightened pro-inflammatory cytokine (IL-6 and TNF-α) activity, greater antibody (IgA and complement C3) deposition and decreased expression of mucosal barrier protein (ZO-1, Occludin) compared to the control group. Furthermore, CD11c[+]dendritic cells were more abundant in the murine intestine and kidneys compared to the control group.

CONCLUSION: The gut-kidney axis, including microbiota homeostasis and innate immune cell response, contributes to the pathogenesis of IgAN. Gut dysbiosis and hyperactivated immune cells like CD11c[+]dendritic cells can affect the mucosal barrier and exacerbate the renal damage, being novel insights into immunotherapeutic strategies for IgAN.},
}

@article {pmid40620312,
year = {2025},
author = {Sopel, A and Szczuciński, W and Gosiewski, T and Salamon, D},
title = {The role of fecal microbiota transplantation in selected neurodegenerative diseases and neurodevelopmental disorders.},
journal = {Przeglad gastroenterologiczny},
volume = {20},
number = {2},
pages = {127-141},
pmid = {40620312},
issn = {1895-5770},
abstract = {Fecal microbiota transplantation (FMT) is a medical procedure that allows to establish a stable and healthy intestinal microbiota in various diseases believed to be related to a gut dysbiosis. Currently, FMT is successfully used to treat recurrent Clostridioides difficile infection. However, in recent years there has been evidence that changes in composition of gut microbiota may also be relevant in the pathogenesis of several neuropsychiatric and neurodevelopmental conditions including Alzheimer's disease, multiple sclerosis, Parkinson's disease, autism spectrum disorders and schizophrenia. This review focuses on exploring the complex connection between gut microbiota and pathogenesis of these neurological conditions. It also presents current research on a possible use of FMT as a therapeutic intervention targeting the gut-brain axis.},
}

@article {pmid40619214,
year = {2025},
author = {Bai, X and Ihara, E and Tanaka, Y and Minoda, Y and Wada, M and Hata, Y and Esaki, M and Ogino, H and Chinen, T and Ogawa, Y},
title = {The interplay of gut microbiota and intestinal motility in gastrointestinal function.},
journal = {Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi},
volume = {61},
number = {},
pages = {51-58},
doi = {10.1540/jsmr.61.51},
pmid = {40619214},
issn = {1884-8796},
mesh = {Humans ; *Gastrointestinal Motility/physiology ; *Gastrointestinal Microbiome/physiology ; Bile Acids and Salts/metabolism ; Animals ; Irritable Bowel Syndrome/microbiology/physiopathology/therapy ; Probiotics/therapeutic use ; *Gastrointestinal Tract/microbiology/physiology ; Interstitial Cells of Cajal/physiology ; Fecal Microbiota Transplantation ; Prebiotics ; Constipation/microbiology ; Gastrointestinal Diseases/microbiology/therapy ; Fatty Acids, Volatile/metabolism ; },
abstract = {The relationship between gut microbiota and intestinal motility is crucial for maintaining gastrointestinal health. Intestinal motility refers to the coordinated movements of the digestive tract, essential for effective digestion, nutrient absorption, and timely waste elimination. Recent studies have demonstrated that microbiota play a crucial role not only in the maturation of intestinal motility but also in the ongoing maintenance of established motility patterns. Disruptions in motility can lead to various disorders, such as chronic constipation, irritable bowel syndrome, and chronic idiopathic pseudo-obstruction. Gut microbiota significantly influence intestinal motility through mechanisms like bile acid metabolism and the production of short-chain fatty acids. In patients with diarrhea-predominant irritable bowel syndrome, elevated primary-to-secondary bile acid ratios suggest a complex interaction between gut bacteria and bile acids that can enhance motility via receptors like TGR5. Additionally, the role of interstitial cells of Cajal in facilitating non-neuronal contractions has revolutionized our understanding of motility regulation, highlighting both neural and non-neural factors. Various therapeutic approaches, including prebiotics, probiotics, and fecal microbiota transplantation, have been explored to improve intestinal motility, although their effectiveness has been limited. Advancements in gene-related research and innovative diagnostic methods are vital for a deeper understanding of how the gut microbiome regulates motility. This review synthesizes current knowledge on the interplay between gut microbiota and intestinal motility, emphasizing the need for interdisciplinary research to develop effective treatments targeting gut microbiota for gastrointestinal disorders. By unraveling these complex interactions, we can pave the way for novel therapeutic strategies that enhance intestinal health and improve the quality of life for those affected by motility-related disorders.},
}

Humans
*Gastrointestinal Motility/physiology
*Gastrointestinal Microbiome/physiology
Bile Acids and Salts/metabolism
Animals
Irritable Bowel Syndrome/microbiology/physiopathology/therapy
Probiotics/therapeutic use
*Gastrointestinal Tract/microbiology/physiology
Interstitial Cells of Cajal/physiology
Fecal Microbiota Transplantation
Prebiotics
Constipation/microbiology
Gastrointestinal Diseases/microbiology/therapy
Fatty Acids, Volatile/metabolism

@article {pmid40618491,
year = {2025},
author = {Tian, Y and Meng, J and Zhang, D and Zhai, B and Cheng, J and Zou, J and Shi, Y and Guo, D},
title = {Wendan Decoction exerts therapeutic effects on insomnia by regulating gut microbiota and tryptophan metabolism.},
journal = {Phytomedicine : international journal of phytotherapy and phytopharmacology},
volume = {145},
number = {},
pages = {157028},
doi = {10.1016/j.phymed.2025.157028},
pmid = {40618491},
issn = {1618-095X},
abstract = {BACKGROUND: Insomnia has been a public problem threatening human health. Wendan Decoction (WDD) has good therapeutic effects on insomnia. However, its mechanism to improve sleep remains unclear.

PURPOSE: To investigate the potential mechanism of WDD in treating insomnia from the perspective of gut microbiota and metabolism.

METHODS: The chemical composition of WDD was analyzed by UHPLCOrbitrap Exploris/MS. The efficacy of WDD on PCPA-induced insomnia rats was evaluated through behavioral tests, ELISA, histopathological examination, immunofluorescence and western blotting. 16S rRNA sequencing, untargeted metabolomics, and network pharmacology were integrated to explore the mechanism of WDD in treating insomnia. The role of gut microbiota in WDD treatment was validated by antibiotic treatment and fecal microbiota transplantation (FMT). Targeted metabolomics was used to detect changes in fecal tryptophan metabolites after FMT. Additionally, RT-qPCR and western blotting were used to investigate the potential mechanisms.

RESULTS: WDD effectively shortened sleep latency, prolonged sleep duration, alleviated anxiety-like behaviors, attenuated neuronal damage, and modulated neurotransmitter levels in rats with insomnia. Moreover, WDD alleviated intestinal damage, reduced the number of Iba-1 positive cells, increased IL-10 levels and decreased IL-6, IL-1β, TNF-α and LPS levels in the colon, serum and hippocampus. It also increased the expression of Occludin, Claudin-1, and ZO-1 in both the colon and brain. 16S rRNA sequencing suggested that WDD improved gut microbiota disorders. Untargeted metabolomics and network pharmacology jointly suggested that WDD could regulate tryptophan metabolism. Antibiotic treatment and FMT confirmed the involvement of gut microbiota in the therapeutic effects of WDD in alleviating insomnia. Changes of tryptophan metabolites in feces, serum, and hippocampus confirmed the regulatory effect of WDD on tryptophan metabolism. Further mechanistic analysis suggested that WDD may correct the abnormal kynurenine pathway of tryptophan metabolism through inhibition of the expression of indoleamine 2,3-dioxygenase 1 and kynurenine-3-monooxygenase.

CONCLUSION: WDD can modulate the neurotransmitter disorders, reduce inflammatory cytokine levels, and strengthen the intestinal barrier and blood-brain barrier by regulating gut microbiota and tryptophan metabolism, thereby improving sleep. This study provides evidence for the potential therapeutic effect of WDD on insomnia via the microbiota-gut-brain axis.},
}

@article {pmid40618377,
year = {2025},
author = {Le, TT and Hoang, TN and Do, DH and Nguyen, XH and Huynh, C and Viet, HD and Dat, VQ and Zengler, K and Gilbert, JA and Avedissian, SN and Tran, TM and Le, J},
title = {Current state of microbiota clinical applications in neonatal and pediatric bacterial infections.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2529400},
doi = {10.1080/19490976.2025.2529400},
pmid = {40618377},
issn = {1949-0984},
mesh = {Humans ; Infant, Newborn ; Child ; *Bacterial Infections/microbiology/therapy ; Dysbiosis/microbiology/therapy ; *Gastrointestinal Microbiome ; Anti-Bacterial Agents/therapeutic use ; Fecal Microbiota Transplantation ; Probiotics/therapeutic use ; Infant ; Bacteria/classification/isolation & purification/genetics ; Child, Preschool ; },
abstract = {The microbiota plays a crucial role in pediatric health by shaping immune development and influencing infection susceptibility. In infants and children, an immature microbiota may compromise immune defense, increasing the risk of bacterial infections. This review evaluates clinical trials on the microbiota's role in neonatal and pediatric bacterial infections, including sepsis, infections in pediatric cancer patients, and Clostridioides difficile-associated dysbiosis. We summarized original research articles published from 2000 to May 2024 on the microbiota and bacterial infections in neonates and children. A balanced microbiota is essential for infection prevention, particularly in premature infants and immunocompromised children. Studies of microbiome signatures in the gut, oral cavity, and nasopharynx have highlighted how microbiota composition influences infection risk, treatment response, and adverse effects from antibiotics and chemotherapy. Disruptions from antibiotic exposure, chemotherapy, and hematopoietic stem cell transplantation frequently lead to dysbiosis, characterized by depletion of commensal bacteria and overgrowth of pathobionts, including antibiotic-resistant strains such as C. difficile. Conversely, microbiota-restorative interventions, such as probiotics and fecal microbiota transplantation, show promise in reducing bacterial infections by enhancing microbial resilience. The microbiota plays a critical role in predicting and potentially treating bacterial infections in children. While antibiotics remain essential, their widespread use has significant consequences for microbiota health. Striking a balance between effective infection control and microbiota preservation is crucial, particularly in vulnerable pediatric populations. Implementing judicious antibiotic use and exploring microbiota-based therapies may mitigate long-term microbiota disruptions, ultimately improving infection outcomes and overall pediatric health.},
}

Humans
Infant, Newborn
Child
*Bacterial Infections/microbiology/therapy
Dysbiosis/microbiology/therapy
*Gastrointestinal Microbiome
Anti-Bacterial Agents/therapeutic use
Fecal Microbiota Transplantation
Probiotics/therapeutic use
Infant
Bacteria/classification/isolation & purification/genetics
Child, Preschool

@article {pmid40618373,
year = {2025},
author = {Li, L and Yang, Z and Yi, Y and Song, Y and Zhang, W},
title = {Gut microbiota and radiation-induced injury: mechanistic insights and microbial therapies.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2528429},
doi = {10.1080/19490976.2025.2528429},
pmid = {40618373},
issn = {1949-0984},
mesh = {Humans ; *Gastrointestinal Microbiome/physiology/radiation effects ; *Radiation Injuries/therapy/microbiology ; Animals ; Fecal Microbiota Transplantation ; Probiotics ; Signal Transduction ; Oxidative Stress ; Neoplasms/radiotherapy ; Radiotherapy/adverse effects ; Prebiotics ; },
abstract = {Radiotherapy represents a crucial therapeutic modality in cancer treatment, yet its efficacy is frequently limited by radiation-induced toxicity. Growing evidence indicates that gut microbiota and their metabolites serve as key regulators of both radioprotective and radiosensitizing effects. This review systematically examines three fundamental regulatory mechanisms through which gut microbiota and its metabolites mitigate radiation-induced injury: (1) modulation of intestinal epithelial cell regeneration and tumor cell apoptosis via Wnt/β-catenin and PI3K/AKT/mTOR pathways; (2) immunomodulation via Toll-like receptor activation and NF-κB signaling; (3) oxidative stress management via Nrf2 signaling. We also evaluate various microbiota-targeted interventions, ranging from probiotics and prebiotics to fecal microbiota transplantation and emerging engineered microbial therapies, highlighting their potential in clinical radiotherapy. Finally, we emphasize current limitations and future research directions, underscoring the need to overcome existing challenges in microbiome analysis and therapeutic durability to fully realize the potential of precision radio-microbiome medicine, which may provide valuable references for developing personalized radiotherapy strategies based on gut microbiota and their metabolites.},
}

Humans
*Gastrointestinal Microbiome/physiology/radiation effects
*Radiation Injuries/therapy/microbiology
Animals
Fecal Microbiota Transplantation
Probiotics
Signal Transduction
Oxidative Stress
Neoplasms/radiotherapy
Radiotherapy/adverse effects
Prebiotics

@article {pmid40617533,
year = {2025},
author = {Chen, L and Li, B and Zu, M and Reis, RL and Kundu, SC and Xiao, B},
title = {Advances and mechanisms of gut microbiota modulation in enhancing immune checkpoint inhibitor efficacy.},
journal = {Seminars in cancer biology},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.semcancer.2025.06.012},
pmid = {40617533},
issn = {1096-3650},
abstract = {The gut microbiota is crucial for maintaining human health by regulating immune homeostasis and metabolic function. Immune checkpoint inhibitors (ICIs) have emerged as a cornerstone of cancer immunotherapy, yet their effectiveness is often hampered by treatment resistance and immune-related adverse events (irAEs). Increasing evidence highlights gut microbiota as a critical determinant of ICI efficacy. Here, we summarize the advances from preclinical mouse models and clinical trials to systematically illustrate how gut microbiota modulation strategies, such as fecal microbiota transplantation, specific microorganism supplementation, dietary and lifestyle interventions, and prebiotic/postbiotic supplementation, can enhance ICI therapeutic outcomes and mitigate irAEs. Mechanistically, the gut microbiota shape host immune responses, influencing innate, adaptive, and mucosal immunity, as well as immune checkpoint expression, through microbial translocation, microbiota-derived metabolites, and extracellular vesicles. This review elucidates the intricate interplay between gut microbiota and ICI treatment responses, laying a theoretical groundwork for developing personalized microbiota-based strategies to optimize cancer immunotherapy.},
}

@article {pmid40617323,
year = {2025},
author = {Lu, Y and Zhang, Z and Chen, L and Xue, P and Zhang, Y and Li, Y and Guo, H},
title = {Prospect of interdisciplinary research on gut microbiota and colorectal cancer immunotherapy.},
journal = {Critical reviews in oncology/hematology},
volume = {},
number = {},
pages = {104832},
doi = {10.1016/j.critrevonc.2025.104832},
pmid = {40617323},
issn = {1879-0461},
abstract = {Immune checkpoint blockade (ICB) is considered as a promising therapy in a variety of cancers, while colorectal cancer (CRC) is mostly resistant to it. The ICB efficacy is proved to be associated with gut microbiota. However, the research on improving ICB outcomes of CRC by microbes or their metabolites is obstructed compared to other types of cancers. Through summarizing the main progress and limitations in previous work, we provide our proposal for further study on CRC. For preclinical basic investigation, microbial tryptophan metabolism regulates ICB therapy outcomes particularly in CRC and requires specific focus. For clinical trials, sources of recruited cohorts and donators of fecal microbiota transplantation can be diversified. For future application, interdisciplinary methods and models coupled with advanced technologies are suggested for designing precise intervention strategies based on prebiotics.},
}

@article {pmid40617308,
year = {2025},
author = {Dan, W and Xiong, C and Zhou, G and Chen, J and Pan, F},
title = {Gut microbiota as a mediator of cancer development and management: From colitis to colitis-associated dysplasia and carcinoma.},
journal = {Biochimica et biophysica acta. Reviews on cancer},
volume = {},
number = {},
pages = {189381},
doi = {10.1016/j.bbcan.2025.189381},
pmid = {40617308},
issn = {1879-2561},
abstract = {Colitis-associated colorectal cancer (CAC) develops as a result of prolonged colitis in patients with inflammatory bowel disease. In recent years, the role of the gut microbiota in colitis-associated colorectal carcinogenesis has begun to be recognized. Specific microbes, such as enterotoxigenic Bacteroides fragilis, Fusobacterium nucleatum, and pks[+]Escherichia coli, promote carcinogenesis by regulating oncogenic signaling, epithelial-mesenchymal transition, autophagy induction, and the immune microenvironment. Conversely, commensal fungi and probiotics exert tumor-suppressive effects by inhibiting inflammatory pathways and immune cell recruitment. Emerging microbiota-targeted strategies, including precision probiotics and fecal microbiota transplantation, can restore ecological homeostasis, attenuate inflammation, and enhance the efficacy of conventional therapies. This review summarizes the current understanding of the mechanisms underlying microbiota-driven CAC pathogenesis and assesses the potential applications of gut microbiota in the development of diagnostic tools and therapeutic interventions.},
}

@article {pmid40615821,
year = {2025},
author = {Upadhyay, P and Kumar, S and Tyagi, A and Tyagi, AR and Barbhuyan, T and Gupta, S},
title = {Gut Microbiome rewiring via fecal transplants: Uncovering therapeutic avenues in Alzheimer's disease models.},
journal = {BMC neuroscience},
volume = {26},
number = {1},
pages = {39},
pmid = {40615821},
issn = {1471-2202},
support = {File no.R.12014/20/2018//Department of Health Research, India/ ; DBT Core grant//National Institute of Immunology New Delhi India/ ; },
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Fecal Microbiota Transplantation/methods ; *Alzheimer Disease/therapy/microbiology/psychology ; Mice ; Disease Models, Animal ; Mice, Inbred C57BL ; Male ; Mice, Transgenic ; Oxidative Stress ; },
abstract = {BACKGROUND: Emerging evidence implicates the gut microbiome in Alzheimer's disease (AD) pathogenesis, yet the underlying mechanisms remain elusive. This study elucidates the bidirectional relationship between gut microbiota and AD using fecal microbiota transplantation (FMT) in a mouse model.

RESULT: Through meticulous experimentation, we conducted reciprocal FMT between AD (5xFAD) and healthy (C57BL/6) mice to unravel the impact of gut microbiome alterations on cognitive function and neuroinflammation. FMT from 5xFAD to C57BL/6 mice induced profound memory impairment and cognitive deficits, accompanied by elevated inflammatory cytokine levels, oxidative stress markers, and systemic inflammation, as evidenced by increased plasma cytokines. Conversely, transplanting healthy microbiota into 5xFAD mice yielded remarkable behavioral improvements, including enhanced spatial memory performance in the Morris water maze, directly correlating with cognitive recovery. Our findings underscore the pivotal role of the gut microbiome in AD pathogenesis and offer a promising therapeutic avenue.

CONCLUSION: Targeted modulation of the gut microbiome through strategies like FMT may offer potential benefits in Alzheimer's disease by influencing neuroinflammation, oxidative stress, and cognitive function. This comprehensive study provides novel insights into the gut-brain axis dynamics and paves the way for innovative microbiome-based interventions in AD management.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Fecal Microbiota Transplantation/methods
*Alzheimer Disease/therapy/microbiology/psychology
Mice
Disease Models, Animal
Mice, Inbred C57BL
Male
Mice, Transgenic
Oxidative Stress

@article {pmid40615512,
year = {2025},
author = {Ruan, S and Liu, J and Yuan, X and Ye, X and Zhang, Q},
title = {Aerobic exercise alleviates cognitive impairment in T2DM mice through gut microbiota.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {23917},
pmid = {40615512},
issn = {2045-2322},
mesh = {Animals ; *Gastrointestinal Microbiome/physiology ; *Cognitive Dysfunction/therapy/etiology/microbiology ; *Physical Conditioning, Animal ; *Diabetes Mellitus, Type 2/complications/microbiology ; Male ; Mice ; Mice, Inbred C57BL ; *Diabetes Mellitus, Experimental/complications/microbiology ; Fecal Microbiota Transplantation ; },
abstract = {The risk of cognitive impairment is markedly elevated in patients with type 2 diabetes mellitus (T2DM). While exercise has been shown to mitigate cognitive deficits associated with diabetes, the underlying mechanisms remain poorly understood. Recent studies suggest that exercise can modulate the composition of the gut microbiota, which, in turn, may influence the central nervous system via the microbiota-gut-brain axis. However, the specific role of gut microbiota in mediating exercise-induced improvements in cognitive function in T2DM remains unclear. In this study, we aimed to investigate whether exercise can alleviate cognitive impairment in T2DM mice by modulating the intestinal microbiota, and to elucidate the mechanisms underlying this effect. This study was conducted using male C57BL/6J mice. Mice fed a normal diet were assigned to the non-diabetic control group (NC), while those fed a high-fat diet were intraperitoneally injected with streptozotocin (STZ) and subsequently divided into the diabetic control group (DM), an exercise group (DM-EXE), and a fecal microbiota transplantation group (DM-FMT). The DM-EXE group underwent treadmill exercise for 8 weeks. During this period, the DM-FMT group received fecal microbiota transplants from the DM-EXE group for 2 consecutive days per week. Following the 8-week intervention, stool samples were collected for 16S rDNA high-throughput sequencing. The fear conditioning test was performed to assess cognitive function. Intestinal mucosa samples were collected to evaluate the expression of intestinal tight junction proteins. Additionally, the expression levels of synaptic proteins, glucose transporters, neurotrophic factors, and inflammatory markers were measured in the hippocampus. Our findings demonstrate that T2DM mice exhibit impaired cognitive function and significant alterations in their gut microbiota compared to non-diabetic controls. Exercise partially reversed these changes in the intestinal microbiota and alleviated cognitive impairment in T2DM mice. Additionally, transplantation of intestinal microbiota from exercised mice improved cognitive function in T2DM mice. Aerobic exercise may mitigate cognitive impairment in T2DM mice by modulating the gut microbiota. The underlying mechanisms appear to involve enhanced neural synaptic plasticity, reduced neuroinflammation, and improved neuronal glucose metabolism.},
}

Animals
*Gastrointestinal Microbiome/physiology
*Cognitive Dysfunction/therapy/etiology/microbiology
*Physical Conditioning, Animal
*Diabetes Mellitus, Type 2/complications/microbiology
Male
Mice
Mice, Inbred C57BL
*Diabetes Mellitus, Experimental/complications/microbiology
Fecal Microbiota Transplantation

@article {pmid40615289,
year = {2025},
author = {Chen, H},
title = {Mapping the clinical trial landscape of gut microbiota modulation in neurodegenerative diseases.},
journal = {European journal of internal medicine},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ejim.2025.06.032},
pmid = {40615289},
issn = {1879-0828},
}

@article {pmid40614920,
year = {2025},
author = {Yadav, S and Raj, RG},
title = {Parkinson's disease and the gut microbiota connection: unveiling dysbiosis and exploring therapeutic horizons.},
journal = {Neuroscience},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.neuroscience.2025.07.003},
pmid = {40614920},
issn = {1873-7544},
abstract = {Parkinson's disease (PD) is a progressive neurodegenerative disorder marked by dopaminergic neuronal loss, α-synuclein aggregation, and sustained neuroinflammation. Emerging evidence supports the gut-brain-microbiota axis as a pivotal player in the disease's pathogenesis. Dysbiosis, disruptions in the gut microbial composition, has been consistently observed in individuals with PD, with notable reductions in beneficial, short-chain fatty acid-producing bacteria and elevations in pro-inflammatory microbial species. These alterations contribute to increased intestinal permeability, systemic inflammation, and heightened neuroinflammatory responses that may drive α-synuclein misfolding and dopaminergic degeneration. In addition, microbial metabolites, including lipopolysaccharides and amyloid proteins such as curli, may promote neurodegeneration via immune and molecular mimicry pathways. Recent advances highlight the bidirectional influence of the microbiota-gut-brain axis on PD symptoms, ranging from motor deficits to non-motor features like constipation, depression, and cognitive decline. Several microbiota-modulating interventions, including probiotics, prebiotics, dietary strategies, antibiotics, and fecal microbiota transplantation, have demonstrated neuroprotective potential in both preclinical and clinical contexts. However, inter-individual variability, methodological heterogeneity, and the absence of longitudinal, multi-omics-integrated studies limit current understanding. The gut microbiome also holds promise as a non-invasive biomarker for early PD detection and prognosis, though standardization remains a challenge. Future research must clarify causal mechanisms, optimize therapeutic delivery, and integrate genetic, metabolic, and environmental data to advance precision medicine approaches. This review consolidates current knowledge on gut microbiota's role in PD pathophysiology and therapeutic innovation, providing a roadmap for future research directions.},
}

@article {pmid40614649,
year = {2025},
author = {Wang, Y and Ma, S and Wu, L and Zhao, R},
title = {Betaine promotes chicken growth through modulating gut microbiota and FXR-mediated activation of IGF genes.},
journal = {Poultry science},
volume = {104},
number = {9},
pages = {105455},
doi = {10.1016/j.psj.2025.105455},
pmid = {40614649},
issn = {1525-3171},
abstract = {Betaine is a growth-promoting additive used in both the animal production and microbial fermentation industries. The primary mechanisms by which betaine promotes animal growth are well known through its direct action on the host cells. However, it remains unclear whether betaine exerts its growth-promoting effects in chickens dependent on the gut microbiota. Here, we found that betaine promotes the growth of broiler chickens while enhancing the richness and diversity of the cecal microbiota and increasing beneficial bacteria, such as Lactobacillus, Limosilactobacillus, and Prevotella (P < 0.05). However, the growth-promoting effects of betaine were abolished in broilers treated with an antibiotic cocktail. Furthermore, fecal microbiota transplantation from betaine-supplemented chickens could recapitulate the promoting effect of betaine on body weight, breast muscle weight, and hepatic insulin-like growth factors (IGFs) synthesis (P < 0.05), indicating that the gut microbiota plays an indispensable role in betaine's growth-promoting action. Mechanistically, betaine promotes (P < 0.05) the synthesis of bile acids, and microbial function predictions suggest that betaine upregulates the biosynthetic pathways of primary and secondary bile acids. Notably, the expression of the bile acid receptor farnesoid X receptor (FXR) was upregulated (P < 0.05) in the liver, promoting FXR binding to the IGFs genes promoter regions and activating the transcription of IGFs gene. Taken together, our findings suggest that betaine promotes broiler growth via microbiota-dependent mechanisms, accompanied by FXR-mediated upregulation of IGFs gene expression in the liver, providing new perspectives and theoretical support for understanding the complexity of animal growth regulation.},
}

@article {pmid40613778,
year = {2025},
author = {Wang, W and He, X and Liang, C and Wang, Y and Yu, Y and Zhang, F},
title = {Washed microbiota transplantation alleviates tyrosine kinase inhibitors associated gastrointestinal adverse effects.},
journal = {International journal of cancer},
volume = {},
number = {},
pages = {},
doi = {10.1002/ijc.70034},
pmid = {40613778},
issn = {1097-0215},
support = {2021YFA0717004//the National Key R&D Program of China/ ; 2023-3HIM//Nanjing Medical University Fan Daiming Research Funds for Holistic Integrative Medicine/ ; },
abstract = {Gut microbiota dysbiosis is implicated in tyrosine kinase inhibitor (TKI)-induced gastrointestinal adverse effects (GAEs), often necessitating medication adjustments or discontinuation in severe or persistent cases. This study aimed to evaluate the efficacy and safety of washed microbiota transplantation (WMT) in managing TKI-induced GAEs. This prospective study involved cancer patients presenting TKI-induced GAEs. The primary outcome was the clinical remission rate at Week 8 post-WMT, which was assessed by the common terminology criteria for adverse events grade. The secondary outcomes included the clinical asymptomatic rate, the onset time of clinical remission, and the variation of C-reactive protein (CRP) levels. Twenty-four patients undergoing 66 WMTs were analyzed. The overall clinical remission and asymptomatic rates were 75.00% (18/24) and 29.17% (7/24), respectively. GAEs, including diarrhea, abdominal pain, and abdominal distention, showed significant improvement post-WMT (all p < .05), while hematochezia exhibited a decreasing trend in severity. Median time to remission was 14.5 days (inter-quartile range, 7-24). Within 8 weeks post-WMT, three initially responsive patients experienced relapse. CRP levels significantly decreased (p < .05), and no severe adverse events were reported. This study proposes WMT as a potential treatment for TKI-induced GAEs, particularly for patients who do not respond adequately to conventional treatments.},
}

@article {pmid40613520,
year = {2025},
author = {Ramos Martínez, A and Gutiérrez-Villanueva, A and González-Haba Ruiz, M and Diego-Yagüe, I and Nieto-Fernández, A and Muñez, E and Fernández Cruz, A and Calderón Parra, J},
title = {Fecal microbiota transplantation for prevention of recurrent acute cholangitis. Review of four published cases.},
journal = {Revista espanola de enfermedades digestivas},
volume = {},
number = {},
pages = {},
doi = {10.17235/reed.2025.11404/2025},
pmid = {40613520},
issn = {1130-0108},
abstract = {INTRODUCTION: Recurrent acute cholangitis (RAC) constitutes a relevant clinical problem that may condition the prognosis of the patient. Chronic suppressive antibiotic therapy can be used for preventive purposes, but it is associated with adverse effects and can select resistant bacterial strains. Fecal microbiota transfer (FMT) has been shown to be effective in preventing recurrent Clostridioides difficile infection and could be a useful strategy in patients with RAC.

OBJECTIVE: To review the experience of the use of FMT in the prevention of episodes of RAC by reviewing published cases.

RESULT: Four cases were identified in which FMT significantly reduced RAC episodes. The patients were characterized by lack of efficacy of conventional treatments, had different predisposing factors for RAC and frequent colonization and infection by multidrug-resistant bacteria.

CONCLUSIONS: The four cases presented provide limited but encouraging evidence of the preventive effect of FMT on successive episodes in patients without biliary tract obstruction. Larger and more adequately designed studies will be necessary to deepen the knowledge of this possible preventive strategy.},
}

@article {pmid40613134,
year = {2025},
author = {Yao, Y and Ye, Y and Zheng, C},
title = {The Impact of Microbiota-Mediated Immune Regulation on Recurrent Pregnancy Loss and Intervention Strategies.},
journal = {American journal of reproductive immunology (New York, N.Y. : 1989)},
volume = {94},
number = {1},
pages = {e70121},
doi = {10.1111/aji.70121},
pmid = {40613134},
issn = {1600-0897},
support = {LHDMZ23H190002//Huadong Medicine Joint Funds of the Zhejiang Provincial Natural Science Foundation of China/ ; },
mesh = {Humans ; Female ; *Abortion, Habitual/immunology/microbiology/therapy ; Pregnancy ; *Gastrointestinal Microbiome/immunology ; *Dysbiosis/immunology ; *Microbiota/immunology ; *Endometrium/microbiology/immunology ; Probiotics/therapeutic use ; Fecal Microbiota Transplantation ; Animals ; Immune Tolerance ; },
abstract = {Recurrent pregnancy loss (RPL) significantly affects reproductive health in couples of childbearing age. Its pathogenesis is complex, with nearly 50% of cases remaining unexplained, and immune regulation plays a key role in its development. This review focuses on the relationship between human microbiota (gut, reproductive tract, and endometrial microbiota), immune regulation, and RPL, systematically summarizing related research progress. RPL patients exhibit characteristic changes in the gut, reproductive tract, and endometrial microbiota, such as reduced gut microbial diversity, decreased beneficial bacteria, increased harmful bacteria in the reproductive tract, and an imbalanced endometrial microbiota structure. Dysbiosis can lead to immune regulation abnormalities, increasing the risk of RPL by disrupting immune tolerance, triggering inflammatory responses, and interfering with metabolism. Although microbiota-based interventions, such as probiotics, prebiotics, and fecal microbiota transplantation, show potential, they face challenges related to strain selection, donor screening, and unclear mechanisms. Current research also faces limitations in detection technology and sample size, and the understanding of the microbiota-immune-RPL relationship requires further deepening. Future studies should clarify causal relationships using advanced technologies, develop more effective detection and intervention methods, and create personalized treatment plans based on individual patient characteristics to improve clinical diagnosis and treatment of RPL and safeguard women's reproductive health.},
}

Humans
Female
*Abortion, Habitual/immunology/microbiology/therapy
Pregnancy
*Gastrointestinal Microbiome/immunology
*Dysbiosis/immunology
*Microbiota/immunology
*Endometrium/microbiology/immunology
Probiotics/therapeutic use
Fecal Microbiota Transplantation
Animals
Immune Tolerance

@article {pmid40612747,
year = {2025},
author = {Wu, J and Jia, B and Gong, S and Li, Y and Wang, J and Huang, Y and Guo, J},
title = {Protective effects of Atractylodes macrocephala polysaccharides on acetaminophen-induced liver injury.},
journal = {Frontiers in pharmacology},
volume = {16},
number = {},
pages = {1583334},
pmid = {40612747},
issn = {1663-9812},
abstract = {BACKGROUND: Drug-induced liver injury (DILI) is a major clinical concern due to its unpredictable nature and lack of effective therapeutic options.

METHODS: This study investigated the hepatoprotective effects of Atractylodes macrocephala polysaccharides (AMPs) in a mouse model of acetaminophen (APAP)-induced liver injury. Mice were pretreated with AMPs for 7 days prior to APAP challenge, and liver injury was evaluated through histopathology, serum biochemistry, molecular assays, and gut microbiota analysis.

RESULTS: AMPs treatment significantly reduced serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels compared to the APAP group (p < 0.05). Hepatic oxidative stress was alleviated, as indicated by increased levels of glutathione (GSH, p < 0.05) and superoxide dismutase (SOD, p < 0.05), and reduced malondialdehyde (MDA, p < 0.05). AMPs also suppressed inflammatory cytokines, including Il-1β, Tnf-α, Il-6, and Nlrp3 (p < 0.05), and modulated apoptosis-related proteins by downregulating Bax and upregulating Bcl-2 and Bcl-xl expression (p < 0.05). Furthermore, AMPs improved gut microbiota diversity and enriched beneficial genera such as Roseburia, as revealed by 16S rDNA sequencing. Fecal microbiota transplantation from AMPs-treated mice replicated these hepatoprotective effects, highlighting the involvement of the gut-liver axis.

CONCLUSION: These findings support the therapeutic potential of AMPs as a multifaceted agent for DILI, exerting protective effects through modulation of oxidative stress, inflammation, apoptosis, and intestinal dysbiosis.},
}

@article {pmid40612440,
year = {2025},
author = {Wenjiao, D and Yurou, W and Jiaqi, X and Yan, H and Hongfang, J and Min, C and Jianjin, G},
title = {Animal studies on the modulation of differential efficacy of polyethylene glycol loxenatide by intestinal flora.},
journal = {Frontiers in endocrinology},
volume = {16},
number = {},
pages = {1508473},
pmid = {40612440},
issn = {1664-2392},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; *Fecal Microbiota Transplantation ; *Diabetes Mellitus, Experimental/microbiology/drug therapy/therapy ; *Polyethylene Glycols/pharmacology ; *Diabetes Mellitus, Type 2/microbiology/drug therapy ; *Hypoglycemic Agents/pharmacology/therapeutic use ; Diet, High-Fat/adverse effects ; Blood Glucose ; },
abstract = {BACKGROUND: Gut microbiota has demonstrated an increasingly important role in the onset and development of type 2 diabetes mellitus (T2DM), Further investigations have revealed the interactions between drugs and the gut microbiome. However, there are still gaps in research regarding the potential interactions between the gut microbiota and GLP-1 and their therapeutic response in people with T2DM. In addition, Fecal microbiota transplantation (FMT) has become a promising strategy for patients with T2DM.

50 healthy male C57BL/6 mice were fed a high-fat diet in combination with STZ to establish a T2DM mouse model. 40 mice were divided into the T2DM group (n=10) and the PEX168 group (n=30). the PEX168 group was divided into two subgroups of the IE group (HbA1c ≤6. 5%, n=12) and the SE group (HbA1c >6. 5%, n=12), 12 mice in each group. Using IE mice as fecal donors and SE mice as recipients, fecal microbiota transplantation was performed between the two groups, the FMT group (given fecal bacterial suspension, n=5) and the Sham group (given equal amounts of sterile saline, n=5). The intestinal microorganisms of mice in the IE group (donor) and SE group (recipient) were also analyzed for differences. To assess the protective effect of FMT on drug efficacy and T2DM, and to explore the underlying mechanisms.

RESULTS: After 10 weeks, compared with the control group, the HbA1c of the experimental group was significantly reduced, still, the level of HBA1c of the mice in the unsatisfactory group was significantly higher than that in the ideal group. Compared with the unsatisfactory group, fasting blood glucose, 2h postprandial blood glucose, blood glucose AUC and body weight were significantly reduced in the ideal group. 16srDNA sequencing showed that the levels of Bacteroidota, Akkermansia, Parabacteroides, Bifidobacteria and other bacteria in the ideal efficacy group were significantly higher than those in the non-ideal efficacy group (P<0.05). The levels of Firmicutes, Romboutsia, Clostridium, Turicibacter and other bacteria in the unsatisfactory group were significantly higher than those in the ideal group (P<0.05). The dominant flora of mice in the ideal drug efficacy group was negatively correlated with HbA1c and blood sugar, and the dominant flora of mice in the unsatisfactory drug efficacy group was positively correlated with pro-inflammatory factors such as blood sugar. Moreover, FMT treatment significantly improved the efficacy of PEX168 and liver steatosis in the group with unsatisfactory efficacy.

CONCLUSION: In summary, we used the combined method of 16S rDNA and metabolomics to systematically elucidate the efficacy of microflora on PEX168 and the possible mechanism of FMT in treating T2DM by PEX168. The difference in intestinal flora between individuals can affect the therapeutic effect of drugs. Moreover, FMT therapy can affect multiple metabolic pathways and colonization of beneficial bacteria to maintain the drug's therapeutic effect on T2DM mice.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Male
Mice
Mice, Inbred C57BL
*Fecal Microbiota Transplantation
*Diabetes Mellitus, Experimental/microbiology/drug therapy/therapy
*Polyethylene Glycols/pharmacology
*Diabetes Mellitus, Type 2/microbiology/drug therapy
*Hypoglycemic Agents/pharmacology/therapeutic use
Diet, High-Fat/adverse effects
Blood Glucose

@article {pmid40611525,
year = {2025},
author = {Wang, D and Wang, H and Li, Y and Lu, J and Tang, X and Yang, D and Wang, M and Zhao, D and Liu, F and Zhang, S and Sun, L},
title = {Alistipes senegalensis is Critically Involved in Gut Barrier Repair Mediated by Panax Ginseng Neutral Polysaccharides in Aged Mice.},
journal = {Advanced science (Weinheim, Baden-Wurttemberg, Germany)},
volume = {},
number = {},
pages = {e16427},
doi = {10.1002/advs.202416427},
pmid = {40611525},
issn = {2198-3844},
support = {U24A20795//National Natural Science Foundation of China/ ; 82204709//National Natural Science Foundation of China/ ; 82004099//National Natural Science Foundation of China/ ; JJKH20230991KJ//Jilin Provincial Department of Education Project/ ; 20240404018ZP//Jilin Provincial Scientific and Technological Development Program/ ; },
abstract = {Ginseng polysaccharides (GPs) are known to have beneficial effects on the gut epithelium and age-related systemic-inflammation through regulation of gut microbiota. However, the underlying pathways and key members of the microbial community involved in this process are poorly understood. In this study, administration of ginseng neutral polysaccharide (GPN) is found to alleviate gut leak and low-grade inflammation, concomitantly with improving the physiological function aged mice. Fecal microbiota transplantation and fecal conditioned medium are used to assess the specific involvement of gut bacterial metabolites in the effects of GPNs. Comprehensive multi-omics analyses showed that GPN significantly enriched the abundance of Alistipes senegalensis, an indole-producing commensal bacterium. Increased expression of tight junction-associated proteins, as well as activation of gut stem cells, are found to be mediated by the AhR pathway, indicating the causal mechanism by which GPN reduced increases in gut permeability. The results are verified in Caco-2/THP-1 cells, Caenorhabditis elegans, and enteroids. To the knowledge, this is the first identification of an integral functional axis through which GPN and functional metabolites of A. senegalensis influence the gut barrier and reduce systemic inflammation, providing clues for the potential development of innovative plant polysaccharide treatment strategies to promote healthy aging.},
}

@article {pmid40611207,
year = {2025},
author = {Wang, Q and Zhang, M and Meng, M and Luo, Z and Pan, Z and Deng, L and Qin, J and Guo, B and Zhu, D and Zhang, Y and Guo, H and Liang, Y and Su, Z},
title = {Integration bile acid metabolomics and gut microbiome to study the anti-liver fibrosis effects of total alkaloids of Corydalis saxicola Bunting.},
journal = {Chinese medicine},
volume = {20},
number = {1},
pages = {106},
pmid = {40611207},
issn = {1749-8546},
support = {82060763//National Natural Science Foundation of China/ ; GXFCDP-PS-2022//Guangxi First-class Discipline Project for Pharmaceutical Sciences/ ; GXQH202409//Guangxi Youth Qihuang Scholars Training Project/ ; },
abstract = {BACKGROUND: Bile acids and gut microbiota participate in the pathogenesis of liver fibrosis (LF). The total alkaloids of Corydalis saxicola Bunting (TACS) is a traditional Chinese medicine extract that has been used to treat LF, but the underlying mechanisms are not clear. This study performed integrated metabolomics and gut microbiome analysis to study the anti-LF mechanism of TACS using a rat model.

METHODS: Ultra-performance liquid chromatography quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS) was used to identify the chemical compounds in TACS. Biochemical and histopathological analysis were performed to determine the efficacy of TACS. Bile acid-targeted metabolomics was used to assess changes in the bile acid (BA) profiles in TACS-treated LF rats. 16S rRNA gene sequencing and metagenomics were used to assess changes in the gut microbiota of the TACS-treated LF rats. Antibiotic cocktail treatment and fecal microbiota transplantation (FMT) were used to determine the relationship between the gut microbiota and the anti-LF effects of TACS. Metagenomics was used to identify significantly enriched gut microbiota after TACS treatment and its correlation with the anti-LF effects was verified by in vivo experiments.

RESULTS: TACS treatment significantly reduced the levels of serum liver enzymes, fibrosis and pro-inflammatory cytokines in the liver. TACS significantly increased the levels of chenodeoxycholic acid (CDCA) and taurochenodeoxycholic acid (TCDCA) in the cecum and decreased the levels of cholic acid (CA) and deoxycholic acid (DCA) in the liver of the LF rats. TACS significantly increased the abundances of Lactobacillus and Akkermansia in the LF rats. Antibiotic cocktail treatment and FMT have shown that the effect of TACS cure liver fibrosis depends on the gut microbiota. The abundance of Lactobacillus reuteri was significantly increased by TACS. Administration of Lactobacillus reuteri via gavage ameliorated LF.

CONCLUSIONS: TACS exerted anti-LF effects in rats by modulating bile acid metabolism and gut microbiome.},
}

@article {pmid40609706,
year = {2025},
author = {Daneri, L and Urbano, A and Escudero-Sánchez, R and Halperin, AV and Moreno-Blanco, A and Corbacho, MD and Suárez-Carantoña, C and Rodríguez-Jiménez, C and Serrano-Villar, S and Campo, RD and Cobo, J},
title = {Lyophilised fecal microbiota transfer in capsules for recurrent Clostridioides difficile infection.},
journal = {International journal of antimicrobial agents},
volume = {},
number = {},
pages = {107561},
doi = {10.1016/j.ijantimicag.2025.107561},
pmid = {40609706},
issn = {1872-7913},
abstract = {BACKGROUND: Recent guidelines recommend fecal microbiota transplantation (FMT) for patients who experience multiple episodes of Clostridioides difficile infection (CDI). The availability of lyophilised and encapsulated FMT in recent years has greatly improved patient comfort and convenience. While the effectiveness of FMT in oral capsules seems comparable to that achieved through other routes, further experience is needed, particularly in Europe, where there is currently limited published experience. The objective of this study was to present our experience with this therapeutic modality.

METHODS: A retrospective cohort study on patients with recurrent CDI treated by lyophilised, encapsulated FMT. All patients were followed for a minimum of 12 weeks. The primary outcome was recurrence at three months.

RESULTS: A total of 36 patients received 38 FMTs. The median age of the cohort was 78.5 years, with a median of four previous episodes. At the three-month follow-up, 27 of the 36 patients (75.0%) were free of CDI. One patient exhibited recurrence before the six-month mark. Two of the ten patients with FMT failure were successfully rescued with a second FMT. Of the nine patients who underwent rescue attempts, seven did not experience recurrence, resulting in a cure rate of 91.7% for the 36 patients. We did not detect severe adverse effects related to the FMT.

CONCLUSION: We confirm an acceptable effectiveness of lyophilised capsulated oral FMT. Interestingly, most patients with FMT failure can be cured with a new treatment, which need not necessarily be a new FMT.},
}

@article {pmid40607920,
year = {2025},
author = {Pan, Y and Shen, L and Wu, Z and Wang, X and Liu, X and Zhang, Y and Luo, Q and Liu, S and Fang, X and Shu, Q and Chen, Q},
title = {Hepcidin sustains Kupffer cell immune defense against bloodstream bacterial infection via gut-derived metabolites in mice.},
journal = {The Journal of clinical investigation},
volume = {},
number = {},
pages = {},
doi = {10.1172/JCI189607},
pmid = {40607920},
issn = {1558-8238},
abstract = {Bloodstream bacterial infections cause one-third of deaths from bacterial infections, and eradication of circulating bacteria is essential to prevent disseminated infections. We here found that hepcidin, the master regulator of systemic iron homeostasis, affected Kupffer cell (KC) immune defense against bloodstream bacterial infections by modulating the gut commensal bacteria-derived tryptophan derivative indole-3-propionic acid (IPA). Hepcidin deficiency impaired bacterial capture by KCs and exacerbated systemic bacterial dissemination through morphological changes in KCs. Gut microbiota depletion and fecal microbiota transplantation revealed that the gut microbiota mediated the alteration of KCs volume. Mechanistically, hepcidin deficiency led to a decreased abundance of the IPA-producing commensal Lactobacillus intestinalis and a concomitant reduction in the gut-to-liver shuttling of its metabolite IPA. IPA supplementation or Lactobacillus intestinalis colonization restored the KC volume and hepatic immune defense against bloodstream bacterial infection in hepcidin-deficient mice. Moreover, hepcidin levels in patients with bacteremia were associated with days of antibiotic usage and hospitalization. Collectively, our findings described a previously unappreciated role of hepcidin in sustaining KC-mediated hepatic defense against bloodstream bacterial infections through the gut commensal Lactobacillus intestinalis and its tryptophan derivative IPA. More importantly, restoring the crosstalk between the gut microbiota and liver through IPA-inspired therapies may offer a promising strategy for enhancing the host defense against bloodstream bacterial infections in those with low hepcidin levels and a high risk for bacterial infections.},
}

@article {pmid40607758,
year = {2025},
author = {Wei, Y and Mao, J and Tang, W and Ma, Y and Li, J and Su, S and Ni, Z and Wu, J and Liu, D and Wang, H},
title = {Targeting Catenibacterium mitsuokai with icariin modulates gut microbiota and improves hepatic lipid metabolism in intrauterine growth restriction.},
journal = {The ISME journal},
volume = {},
number = {},
pages = {},
doi = {10.1093/ismejo/wraf141},
pmid = {40607758},
issn = {1751-7370},
abstract = {Male offspring with intrauterine growth restriction exhibit more pronounced hepatic lipid metabolism abnormalities than females, necessitating earlier intervention. Icariin has been shown to effectively modulate hepatic lipid metabolism in male piglets with intrauterine growth restriction. However, the role of gut microbiota in this process remains to be elucidated. This study aimed to explore the influence of gut microbiota on icariin-induced enhancement of hepatic lipid metabolism. By examining changes in microbiota composition and hepatic lipid metabolism following icariin intervention, the study demonstrated an association between microbial alterations and hepatic lipid regulation through fecal microbiota transplantation. The impact of Catenibacterium on gut microbiota structure and hepatic lipid metabolism was assessed in vivo, and the direct effect of icariin on Catenibacterium was explored in vitro. Results revealed that icariin intervention modified fecal, ileal, and colonic microbiota in male piglets with intrauterine growth restriction, enhanced gut morphology and barrier function, and normalized the expression of hepatic peroxisome proliferator-activated receptor (PPAR) signaling pathway-related genes. Fecal microbiota transplantation from piglets with intrauterine growth restriction impaired intestinal barrier function and led to hepatic lipid deposition, whereas transplantation from icariin-treated donors showed no pathological changes, an outcome associated with reduced abundance of Catenibacterium. Mechanistically, icariin inhibits adenosine triphosphate synthesis to suppress Catenibacterium, remodels gut microbiota, reduces lipopolysaccharide production and translocation, and activates the hepatic PPARα/CD36 axis. In conclusion, icariin intervention alleviates hepatic lipid metabolic disorders in male offspring with intrauterine growth restriction by suppressing Catenibacterium, restoring gut microbial balance, and enhancing intestinal barrier integrity to limit lipopolysaccharide translocation.},
}

@article {pmid40606926,
year = {2025},
author = {Pandey, H and Goel, P and Srinivasan, VM and Tang, DWT and Wong, SH and Lal, D},
title = {Gut microbiota in non-alcoholic fatty liver disease: Pathophysiology, diagnosis, and therapeutics.},
journal = {World journal of hepatology},
volume = {17},
number = {6},
pages = {106849},
pmid = {40606926},
issn = {1948-5182},
abstract = {Non-alcoholic fatty liver disease (NAFLD), also referred to as metabolic-associated fatty liver disease, is among the most prevalent chronic liver conditions. In some cases, NAFLD may lead to liver inflammation and non-alcoholic steatohepatitis, which can eventually progress to liver cirrhosis and hepatocellular carcinoma. The pathophysiology of NAFLD is complex, involving both genetic and environmental factors. NAFLD is a multisystem disease linked to a higher likelihood of developing metabolic disorders such as type 2 diabetes, obesity, and cardiovascular and chronic kidney diseases. The gut-liver axis represents a key connection between the gut microbiota and the liver, and its disruption has been linked to NAFLD. Growing evidence underscores the significant role of gut microbiota in the onset and progression of NAFLD, with alterations in the gut microbiome and impaired gut barrier function. Studies have identified key microbiota signatures and metabolites linked to NAFLD, implicating oxidative stress, endotoxemia, and inflammatory pathways that further strengthen the connection between gut microbiota and NAFLD. Modulation of gut microbiota through diet and microbiota-centered therapies, such as next-generation probiotics and fecal microbiota transplantation, holds promise for treating NAFLD. In this review, we explore the key link between gut microbiota and the development and progression of NAFLD, as well as its potential applications in the diagnosis and treatment of the disease.},
}

@article {pmid40606817,
year = {2025},
author = {Li, X and Lei, Q and Xie, J and Li, F and Liu, J and Chen, Y and Mao, Q},
title = {Research on functional constipation with anxiety or depression: a bibliometric analysis.},
journal = {Frontiers in psychiatry},
volume = {16},
number = {},
pages = {1607297},
pmid = {40606817},
issn = {1664-0640},
abstract = {BACKGROUND: Although the phenomenon of functional constipation (FC) that accompanies anxiety or depression has been extensively investigated worldwide, no bibliometric studies are available in this regard. This study therefore aimed to analyze the current status and extent of research and areas of interest in the study of FC with anxiety or depression.

METHODS: Data from studies on FC with anxiety or depression, that were performed between 2003 and 2024, were retrieved from the Web of Science Core Collection database. Data regarding the annual number of publications, authors, countries, and references were assessed using CiteSpace v6.3.R1 (64-bit) and Microsoft Excel, and those pertaining to keywords and cited authors were evaluated using VOSviewer 1.6.20. The co-occurrence and clustering functions were then used to generate visual knowledge maps.

RESULTS: The overall annual publication volume demonstrated an upward trend between 2003 and 2024; this was indicative of promising research prospects. The 427 publications identified included 6 types of papers, among which original research articles represented the highest proportion (357 [83.61%] articles published across 200 journals). Neurogastroenterology and Motility had the highest publication volume (30 articles, 7.02%). The United States of America had published most of the papers (135 articles, 31.61%) on the topic. Harvard University was the research institution with the most published papers (21 articles, 4.92%), and Michel Bouchoucha had authored the highest number of articles (13 articles, 3.04%).

CONCLUSION: Future studies in the field of basic medicine need to determine the etiology and pathogenesis of FC with anxiety or depression; in particular, they need to evaluate the role of opioid drugs as a key etiological factor. The role played by the brain-gut axis also warrants investigation. From the clinical perspective, studies need to focus on evidence-based medicine; particular emphasis needs to be placed on randomized double-blind controlled trials with stringent quality control, high-quality meta-analyses, and evaluation of questionnaires and scales. Treatment techniques need to be explored in greater detail; in this context, it is recommended that fecal microbiota transplantation and biofeedback therapy are adopted in the clinic. Furthermore, Patients with FC, especially those with a history of anxiety or depression, tend to have overlapping dyspepsia symptoms.},
}

@article {pmid40606527,
year = {2025},
author = {Paaske, SE and Baunwall, SMD and Rubak, T and Rågård, N and Kelsen, J and Hansen, MM and Lødrup, AB and Erikstrup, LT and Mikkelsen, S and Erikstrup, C and Dahlerup, JF and Hvas, CL},
title = {Clinical management of Clostridioides difficile infection with faecal microbiota transplantation: a real-world cohort study.},
journal = {EClinicalMedicine},
volume = {85},
number = {},
pages = {103302},
pmid = {40606527},
issn = {2589-5370},
abstract = {BACKGROUND: Clostridioides difficile infection (CDI) causes high morbidity and mortality. Faecal microbiota transplantation (FMT) is well-established for CDI, but therapeutic strategies may be optimised. We aimed to evaluate clinical outcomes by analysing therapeutic strategies in a real-life cohort of patients with CDI treated with FMT.

METHODS: We conducted a multi-site cohort study, including 1170 patients with CDI, treated with FMT through capsules, colonoscopy, or nasojejunal tube between May 2016 and December 2023. The primary outcome was cure of C. difficile-associated diarrhea (CDAD) eight weeks after treatment. We investigated antibiotic pretreatment type and length, FMT dosing and administration, and post-FMT prophylactic vancomycin during non-CDI antibiotic use, applying multivariable mixed-effect regression analysis including the patient as a random effect. The study was preregistered at ClinicalTrials.gov, NCT03712722.

FINDINGS: The 1170 patients received 1643 FMT treatments. Patients' median age was 71 years (interquartile range 56-80 years). Following their first FMT treatment, 699 patients (60% (95% confidence interval: 57-63%)) were cured of CDAD. After repeated FMT treatments, 944 patients (81% (78-83%)) were cured. Prolonged antibiotic pretreatment was associated with higher cure rates (65% (59-70%), odds ratio (OR): 1.22 (1.10-1.36), p < 0.001). FMT administration through oral, multi-dose capsules (69% (63-74%), OR: 1.19 (1.11-1.27), p < 0.001) or colonoscopy (69% (61-76%), OR: 1.14 (1.04-1.24), p = 0.01) resulted in the highest cure rates. Neither antibiotic pretreatment type nor prophylactic vancomycin during non-CDI antibiotics affected cure rates. In patients for whom FMT was initially unsuccessful, repeated FMT was more effective than antibiotic treatment alone.

INTERPRETATION: CDI outcomes could be improved by optimising antibiotic pretreatment duration, selecting appropriate FMT delivery methods, and repeating FMT.

FUNDING: Innovation Fund Denmark (j.no. 8056-00006B).},
}

@article {pmid40605266,
year = {2025},
author = {Herman, C and Barker, BM and Bartelli, TF and Chandra, V and Krajmalnik-Brown, R and Jewell, M and Li, L and Liao, C and McAllister, F and Nirmalkar, K and Xavier, JB and Caporaso, JG},
title = {A review of engraftment assessments following fecal microbiota transplant.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2525478},
doi = {10.1080/19490976.2025.2525478},
pmid = {40605266},
issn = {1949-0984},
mesh = {*Fecal Microbiota Transplantation ; Humans ; *Gastrointestinal Microbiome ; *Clostridium Infections/therapy/microbiology ; Clostridioides difficile/physiology ; Animals ; Feces/microbiology ; Bacteria/classification/genetics/isolation & purification ; },
abstract = {Fecal Microbiota Transplant (FMT) is a treatment for recurrent Clostridium difficile infections and is being explored for other clinical applications, from alleviating digestive and neurological disorders, to restoring microbiomes impacted by cancer treatment. Quantifying the extent of engraftment following an FMT is important in understanding a recipient's response to treatment. Engraftment and clinical response need to be investigated independently to evaluate an FMT's role (or lack thereof) in achieving a clinical response. Standardized bioinformatics methodologies for quantifying engraftment extent would not only improve assessment and understanding of FMT outcomes, but also facilitate comparison of FMT results and protocols across studies. Here we review FMT studies, integrating three concepts from microbial ecology as framework to discuss how these studies approached assessing engraftment extent: 1) Community Coalescence investigates microbiome shifts following FMT engraftment, 2) Indicator Features tracks specific microbiome features as a signal of engraftment, and 3) Resilience examines how resistant post-FMT recipients' microbiomes are to reverting back to baseline. These concepts explore subtly different questions about the microbiome following FMT. Taken together, they provide holistic insight into how an FMT alters a recipient's microbiome composition and provide a clear framework for quantifying and communicating about microbiome engraftment.},
}

*Fecal Microbiota Transplantation
Humans
*Gastrointestinal Microbiome
*Clostridium Infections/therapy/microbiology
Clostridioides difficile/physiology
Animals
Feces/microbiology
Bacteria/classification/genetics/isolation & purification

@article {pmid40604869,
year = {2025},
author = {Rychlik, A and Kaczmar, E and Mikulska, I and Makowska, K},
title = {Assessment of the effect of prokinetic drugs on transit time and gastrointestinal cleanliness in capsule endoscopy.},
journal = {BMC veterinary research},
volume = {21},
number = {1},
pages = {417},
pmid = {40604869},
issn = {1746-6148},
mesh = {Animals ; *Metoclopramide/pharmacology ; *Capsule Endoscopy/veterinary/methods ; Dogs ; *Gastrointestinal Transit/drug effects ; *Gastrointestinal Agents/pharmacology ; *Cisapride/pharmacology ; Male ; Female ; *Gastrointestinal Tract/drug effects ; },
abstract = {BACKGROUND: Endoscopic examinations are increasingly used in veterinary medicine. Examination using flexible endoscopes is limited to the anterior gastrointestinal tract (panendoscopy) and colon (colonoscopy), while a significant part of the small intestine remains unexamined. Capsular endoscopy is increasingly used, allowing macroscopic assessment of the entire digestive tract. The current study assessed the effect of prokinetic drugs on transit time and cleanliness of the tested part of the digestive tract in capsule endoscopy.

METHODS: The study aimed to evaluate the usefulness of two prokinetic drugs (metoclopramide and cisapride) in capsule endoscopy studies while assessing the quality of the macroscopic image. Each animal included into the study had endoscopic examination three times - without the administration of prokinetic drugs, after receiving metoclopramide and after receiving cisapride.

RESULTS: The total passage time of the capsule through the gastrointestinal tract was the longest in the group receiving metoclopramide (691.33 min) and the shortest in the group receiving cisapride (584.17 min). The best quality images were observed in the control group.

CONCLUSION: This research has confirmed the hypothesis that administration of prokinetic drugs increases the probability of recording the entire macroscopic image of the gastrointestinal tract during endoscopy in dogs. A negative feature of their administration is significantly reduced recording quality because of the level of cleanliness of the tested gastrointestinal section.},
}

Animals
*Metoclopramide/pharmacology
*Capsule Endoscopy/veterinary/methods
Dogs
*Gastrointestinal Transit/drug effects
*Gastrointestinal Agents/pharmacology
*Cisapride/pharmacology
Male
Female
*Gastrointestinal Tract/drug effects

@article {pmid40602277,
year = {2025},
author = {Wu, H and Li, YL and Wang, Y and Wang, YG and Hong, JH and Pang, MM and Liu, PM and Yang, JJ},
title = {Anemoside B4 alleviates ulcerative colitis by attenuating intestinal oxidative stress and NLRP3 inflammasome via activating aryl hydrocarbon receptor through remodeling the gut microbiome and metabolites.},
journal = {Redox biology},
volume = {85},
number = {},
pages = {103746},
doi = {10.1016/j.redox.2025.103746},
pmid = {40602277},
issn = {2213-2317},
abstract = {Ulcerative colitis (UC) is a chronic, non-specific inflammatory disease of the intestines with a significant increase in global incidence in recent years. Oxidative stress and inflammation are two hallmarks of UC pathogenesis. Anemoside B4 (AB4), a pentacyclic triterpenoid saponin, exhibits significant antioxidant and anti-inflammatory properties and shows potential for preventing UC. Here, an animal model induced by dextran sodium sulfate (DSS) was used to investigate the effect of AB4 on UC. The results demonstrated that AB4 significantly reduces intestinal oxidative stress and inflammation in UC mice, while also protecting intestinal barrier function. Furthermore, AB4 helps restore intestinal microbial balance primarily by modulating the abundance of Lactobacillus, which enhances the metabolism of short-chain fatty acids and upregulates the production of butyric acid (BA). Pseudogerm-free mice and fecal microbiota transplantation (FMT) demonstrated that AB4 significantly mitigated UC in a gut microbe-dependent manner. Both AB4 and BA markedly activate the aromatic hydrocarbon receptor (AhR). The intestinal organoid results suggest BA may activate the AhR to inhibit ROS production and activation of NLRP3 inflammasome, thereby protecting intestinal integrity. Administration of AhR antagonists abolished the protective effects, thus confirming the involvement of AhR in the underlying mechanism. Overall, these results indicate that AB4 is an effective agent against UC mainly by activating the AhR through gut microbial short-chain fatty acid metabolites to inhibit intestinal oxidative stress and inflammation.},
}

@article {pmid40601184,
year = {2025},
author = {Rico-Caballero, V and Romero-Rivera, M and Moreno-Blanco, A and Aira, A and Casals-Pascual, C and Rodríguez-Jiménez, C and Quereda, C and Soriano, A and Del Campo, R},
title = {Fecal microbiota transplant as treatment for recurrent urinary tract infections: a proof-of-concept study.},
journal = {European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology},
volume = {},
number = {},
pages = {},
pmid = {40601184},
issn = {1435-4373},
}

@article {pmid40600295,
year = {2025},
author = {Shao, H and Min, F and Bai, T and Liu, Y and Zheng, S and Wu, Y and Di, C and Lin, M and Li, X and Chen, H},
title = {Bifidobacterium breve M-16V alleviates cow's milk allergy by regulating the gut microbiota and metabolites in human microbiota-associated mice.},
journal = {Food & function},
volume = {},
number = {},
pages = {},
doi = {10.1039/d5fo02012c},
pmid = {40600295},
issn = {2042-650X},
abstract = {Cow's milk allergy (CMA) is one of the most common food allergies, especially in infants and young children. Growing evidence from animal studies has shown that some specific probiotics can alleviate CMA, but clinical evidence remains insufficient due to certain limitations. In the present study, we transplanted fecal material from three CMA children into antibiotic-pretreated mice (hum-CMA mice) to mimic the intestinal microecology of allergic individuals, followed by allergen sensitization and Bifidobacterium breve (B. breve) M-16V intervention. Our results showed that B. breve M-16V effectively ameliorated CMA symptoms and allergy-related indicators in hum-CMA mice. Moreover, B. breve M-16V differentially affected the composition of intestinal microbes, but the abundance of beneficial bacteria, such as short-chain fatty acid-producing bacteria, was consistently elevated in all three groups of hum-CMA mice. Subsequent untargeted metabolomics analyses revealed that B. breve M-16V improved the pattern of serum metabolites, and these differential metabolites were mainly involved in glutathione metabolism, glycerophospholipid metabolism, and tryptophan metabolism. All the findings indicate that B. breve M-16V can alleviate the anaphylactic reaction in hum-CMA mice by regulating the intestinal microbiota and metabolites, providing a valuable scientific basis for the clinical application of probiotics in food allergy.},
}

@article {pmid40600174,
year = {2025},
author = {Ebrahimi, R and Shahrokhi Nejad, S and Fekri, M and Nejadghaderi, SA},
title = {Advancing prostate cancer treatment: the role of fecal microbiota transplantation as an adjuvant therapy.},
journal = {Current research in microbial sciences},
volume = {9},
number = {},
pages = {100420},
pmid = {40600174},
issn = {2666-5174},
abstract = {Prostate cancer (PCa) is a major cause of cancer-related deaths worldwide. While current treatments such as surveillance, surgery, and radiation are effective, they have their limitations. These can include patient incompliance due to side effects or resistance to hormonal changes, highlighting the need for alternative approaches. Human microbiota, a complex and dynamic host, plays a significant role in the homeostasis and is associated with several diseases or cancers in cases of dysregulation and dysbiosis. Research on fecal microbiota profiling and its association with certain cancers has opened new possibilities for preventing and managing tumor progression. One such possibility is fecal microbial transplantation (FMT). Studies show that different composition of urinary microbiota is found in various urinary tract diseases. Gut microbiota can regulate immune response against tumors; therefore, FMT may help modulate gut microbiota in a way that potentially enhances responses to immune checkpoint inhibitors, as suggested by emerging evidence in other cancers, though this needs further validation in PCa. Nevertheless, long-term complications and the safety of FMT are still questioned. We reviewed the roles of gut microbiota in PCa and suggested FMT as a potential tool in the treatment of PCa, which needs further investigations.},
}

@article {pmid40599506,
year = {2025},
author = {Alnahwi, HH and AlGhawi, RJ and Alsahaf, HAA and Ahmed, E},
title = {Recurrent Clostridioides difficile Infection (CDI) in Patients Treated With Vancomycin at Johns Hopkins Aramco Healthcare (JHAH), Dhahran, Saudi Arabia.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e85116},
pmid = {40599506},
issn = {2168-8184},
abstract = {Introduction Clostridioides difficile infection (CDI) is a leading cause of healthcare-associated diarrhea with a significant risk of recurrence, posing challenges for patient management and infection control. Identifying risk factors for recurrence is essential to improve outcomes and prevent relapses. Methods This retrospective cohort study included 860 adult patients (≥18 years) treated with vancomycin for CDI at Johns Hopkins Aramco Healthcare (JHAH) in Dhahran, Saudi Arabia, between January 2015 and December 2020. Patients with confirmed CDI based on stool polymerase chain reaction (PCR) or toxin assays, complete medical records, and adequate follow-up data were included. The study excluded those not treated with vancomycin, under 18 years of age, with incomplete records, those who received fecal microbiota transplantation or experimental treatments, and those lacking follow-up data. Data on demographics, comorbidities, hospitalization, medication use, and recurrence were analyzed using univariate and multivariate logistic regression models. Results Univariate analysis showed that age 40-65 years (OR = 1.53; 95% CI: 1.024-2.285; p = 0.038), age >65 years (OR = 1.894; 95% CI: 1.282-2.799; p = 0.001), cirrhosis (OR = 9.104; 95% CI: 1.233-67.192; p = 0.03), hospitalization (OR = 1.974; 95% CI: 1.417-2.749; p < 0.0001), and type 2 diabetes mellitus (OR = 1.65; 95% CI: 1.106-2.462; p = 0.014) were significantly associated with CDI recurrence. After adjusting for confounders, only hospitalization remained a statistically significant independent predictor (OR = 1.597; 95% CI: 1.098-2.325; p = 0.014). Conclusion Hospitalization was identified as the most significant independent risk factor for CDI recurrence. These findings highlight the need for enhanced infection control practices and close monitoring of hospitalized patients with CDI. Future prospective and multicenter studies are recommended to validate these results and explore additional modifiable risk factors to reduce recurrence rates.},
}

@article {pmid40599494,
year = {2025},
author = {Boton, N and Patel, PK and Beekmann, SE and Polgreen, PM and Buckel, WR and Mahoney, MV and Mehrotra, P and Lee, MSL},
title = {Clinician Management Preferences for Clostridioides difficile Infection in Adults: A 2024 Emerging Infections Network Survey.},
journal = {Open forum infectious diseases},
volume = {12},
number = {7},
pages = {ofaf335},
pmid = {40599494},
issn = {2328-8957},
abstract = {BACKGROUND: The 2021 Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA) guidelines for Clostridioides difficile infection (CDI) introduced new recommendations for managing initial and recurrent CDI. Since then, new microbiome-based therapies for preventing recurrent CDI have become available. We surveyed infectious diseases (ID) clinicians to understand their experiences, practices, and challenges in CDI management.

METHODS: An electronic survey was distributed to members of the IDSA Emerging Infections Network in May 2024, targeting ID physicians and healthcare professionals in the United States who manage adult CDI. The survey assessed treatment preferences, clinical practices, and barriers to accessing and prescribing CDI therapies.

RESULTS: Of the 500 respondents who reported treating CDI in the past year, 83% (417/500) indicated that vancomycin was their most frequently prescribed agent for initial, nonfulminant CDI. Additionally, 72% (357/498) reported that their institutional guidelines recommended vancomycin as the first-line agent. The most common barrier to fidaxomicin use was challenges with outpatient insurance coverage (82% [408/496]). Bezlotoxumab was available to 74% (370/500) of respondents, though 33% (165/497) indicated they do not use bezlotoxumab routinely. Most clinicians (87% [437/500]) had previously recommended fecal microbiota transplantation (FMT) for recurrent CDI, though only 48% (239/500) had current access to FMT using donor stool. Fecal microbiota live-jslm was available to 36% (179/500), and fecal microbiota spores live-brpk was available to 30% (150/500).

CONCLUSIONS: Significant barriers, including high costs, insurance challenges, and limited availability of CDI therapies, impact clinical decision-making and adherence to guideline recommendations.},
}

@article {pmid40597484,
year = {2025},
author = {Zhang, C and Zhang, X and Qiu, H and Song, Q and Wang, Y and Zhang, C and Zhang, Q},
title = {Fermented Gastrodia elata Bl. Intervenes gut microbiota and amino acid metabolism in zebrafish to promote 5-HT homeostasis against sleep disturbances.},
journal = {Food research international (Ottawa, Ont.)},
volume = {217},
number = {},
pages = {116757},
doi = {10.1016/j.foodres.2025.116757},
pmid = {40597484},
issn = {1873-7145},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Zebrafish ; *Amino Acids/metabolism ; *Serotonin/metabolism ; *Gastrodia/chemistry ; Homeostasis/drug effects ; *Fermented Foods ; Fermentation ; *Sleep Wake Disorders/prevention & control ; Sleep Initiation and Maintenance Disorders/chemically induced ; Fecal Microbiota Transplantation ; },
abstract = {Sleep disturbances (SD) is a prevalent health issue in modern society. Consequences involve negative impacts on numerous aspects of physical, psychological, and daily life. This study aimed to elucidate the protective effects of Fermented Gastrodia elata Bl. (FGE) against pentylenetetrazole (PTZ)-induced SD and uncover the underlying molecular mechanisms. Our findings revealed that FGE significantly attenuated PTZ-induced insomnia behavior, circadian rhythm disturbances, and compromised gut barrier functions. Mechanistically, gut microbiota and 5-HT within the microbiota-gut-brain axis are the key regulators in short-term SD. Fecal microbiota transplantation (FMT) experiment identified gut microbiota as a key mediator and potential therapeutic target for FGE. The comprehensive analysis of 16S rRNA sequencing and metabolomic analysis showed that amino acid metabolism-related pathways as key factors of FGE intervention. Notably, omics joint analysis demonstrated a strong association between the variations of the intestinal microbiota among different groups and the notable alterations in the brain metabolomic landscape. Meanwhile, the remodeling of intestinal microbial structure and metabolites drove the homeostasis of 5-HT levels in different tissues. Importantly, exogenous keystone bacteria supplementation to sleep-deprived zebrafish restored insomnia responses and amino acid metabolism. Targeted amino acid metabolism further confirmed amino acid metabolism as the central mechanistic pathway through which FGE exerts its protective function. Collectively, Collectively, these findings suggested that FGE showed a significant preventative action on short-term SD by intervening gut microbiota and amino acid metabolism in zebrafish to promote 5-HT homeostasis, which offers perspectives into new preventive strategies of traditional Chinese medicine dietary supplements for transient insomnia.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Zebrafish
*Amino Acids/metabolism
*Serotonin/metabolism
*Gastrodia/chemistry
Homeostasis/drug effects
*Fermented Foods
Fermentation
*Sleep Wake Disorders/prevention & control
Sleep Initiation and Maintenance Disorders/chemically induced
Fecal Microbiota Transplantation

@article {pmid40596796,
year = {2025},
author = {Liu, K and Wang, Y and Zhou, J and van der Meij, JJ and van der Laan, LJW and Li, P and Pan, Q},
title = {Decoding the role of the intestinal epithelium in hepatitis E virus infection using a human organoid prototype of "gut-liver" axis.},
journal = {Virology},
volume = {610},
number = {},
pages = {110615},
doi = {10.1016/j.virol.2025.110615},
pmid = {40596796},
issn = {1096-0341},
abstract = {Hepatitis E virus (HEV), a leading cause of acute viral hepatitis worldwide, is primarily transmitted via the fecal-oral route. A clinical study has reported that the intestine of a chronic hepatitis E patient is positive for HEV. However, whether the intestinal epithelium acts as a barrier for HEV transmission or whether productive enteric infection enhances transfer of the virus to the liver remains unclear. The advent of organoid technology provides a valuable platform for advancing the study of HEV-host interactions in a more physiologically relevant context. In this study, we demonstrate that primary human intestinal organoids (HIOs) efficiently support HEV replication. The infection was sustained in differentiated HIOs with specific phenotypes of intestinal cell types, namely enterocyte, goblet cell, and enteroendocrine cell lineages. Next, we constructed a gut-liver axis model using a transwell system by co-culturing HIOs with human liver-derived organoids. Importantly, infectious viral particles produced in HIOs were capable of transmission to human liver-derived organoids in this model. Bile acids are essential mediators of gut-liver crosstalk. We found that supplementing human bile or the primary bile acid chenodeoxycholic acid inhibited HEV replication in organoids via the farnesoid X receptor (FXR) signaling pathway. The effects of the secondary bile acid, ursodeoxycholic acid, were opposite and promoted viral replication. In conclusion, this model provides a novel approach to study the gut-liver axis in HEV transmission and the impact of bile acids in modulating HEV infection.},
}

@article {pmid40596758,
year = {2025},
author = {Wang, J and Tan, H and Ye, Z and Weng, S and Shi, Y and Xu, J and Liu, H and Li, J and Huang, L and Zhai, L and Luo, H and Lin, Z and Zhong, C and Tang, J and Wang, Z and Zhang, H and Zhang, B and Huang, C},
title = {Gut microbial Nordihydroguaiaretic acid suppresses macrophage pyroptosis to regulate epithelial homeostasis and inflammation.},
journal = {Gut microbes},
volume = {17},
number = {1},
pages = {2518338},
doi = {10.1080/19490976.2025.2518338},
pmid = {40596758},
issn = {1949-0984},
mesh = {Animals ; *Gastrointestinal Microbiome/drug effects ; Mice ; Fecal Microbiota Transplantation ; *Colitis/microbiology/chemically induced ; Homeostasis/drug effects ; *Macrophages/drug effects ; *Masoprocol/pharmacology/metabolism ; *Pyroptosis/drug effects ; Mice, Inbred C57BL ; Dysbiosis/microbiology ; Male ; Dextran Sulfate ; Disease Models, Animal ; Intestinal Mucosa/drug effects ; Aging ; Inflammatory Bowel Diseases/microbiology ; Bacteria/classification/genetics/isolation & purification/metabolism ; Humans ; },
abstract = {BACKGROUND: Aging is associated with increased severity of inflammatory bowel disease (IBD). Gut senescence and altered environmental factors contribute to changes in the intestinal metabolome, particularly in frail older individuals. However, the role of age-associated dysbiosis, characterized by a decline in beneficial gut microbiota and their metabolites, in exacerbating IBD remains unclear.

METHODS: To investigate the impact of aging-associated dysbiosis on colitis development, we employed fecal microbiota transplantation (FMT) in wild-type and IL-10-deficient mice. Aged mice were treated with gut microbiota from either young or aged mice and then subjected to dextran sulfate sodium (DSS) to induce experimental colitis. 16S rDNA sequencing and metabolomics were used to analyze microbial and metabolite profiles. Single-cell RNA sequencing (scRNA-seq) was performed to characterize lamina propria CD45[+] immune cell composition.

RESULTS: Aged mice receiving microbiota from young mice exhibited less severe colitis than those receiving microbiota from aged mice, as evidenced by reduced disease activity, weight loss, and colonic shortening. Besides, aged mice displayed a significant decrease in the Lactobacillus population, accompanied by a reduction in Nordihydroguaiaretic acid (NDGA) levels. Decreased fecal NDGA levels were also observed in both IBD patients and elderly individuals. Administration of NDGA alleviated experimental colitis by downregulating the GSDMD/NR4A1/NLRP3 axis-mediated macrophage pyroptosis. Deletion of GSDMD in macrophages significantly diminished the protective effect of NDGA on colitis.

CONCLUSIONS: Our findings demonstrate that aging is associated with dysbiosis and reduced NDGA production, which increases susceptibility to intestinal inflammation. Gut microbial NDGA exhibits potential anti-inflammatory activity in colitis, suggesting a promising therapeutic target for aged-related IBD.},
}

Animals
*Gastrointestinal Microbiome/drug effects
Mice
Fecal Microbiota Transplantation
*Colitis/microbiology/chemically induced
Homeostasis/drug effects
*Macrophages/drug effects
*Masoprocol/pharmacology/metabolism
*Pyroptosis/drug effects
Mice, Inbred C57BL
Dysbiosis/microbiology
Male
Dextran Sulfate
Disease Models, Animal
Intestinal Mucosa/drug effects
Aging
Inflammatory Bowel Diseases/microbiology
Bacteria/classification/genetics/isolation & purification/metabolism
Humans

@article {pmid40593111,
year = {2025},
author = {Zhou, X and Wei, C and Liu, J and Xia, X and Wang, L and Li, X},
title = {Cold environment regulates ischemic stroke through modulation of gut microbiota.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {21558},
pmid = {40593111},
issn = {2045-2322},
support = {42275197//National Natural Science Foundation of China/ ; TJYXZDXK-065B//Tianjin Key Medical Discipline (Specialty) Construction Project/ ; TJWJ2023XK007//the Key Projects of Tianjin Municipal Health Commission/ ; },
mesh = {*Gastrointestinal Microbiome/physiology ; *Cold Temperature/adverse effects ; Animals ; Fecal Microbiota Transplantation ; Mice ; Male ; Mice, Inbred C57BL ; Humans ; Dysbiosis/microbiology ; *Ischemic Stroke/microbiology/etiology ; Female ; Middle Aged ; Platelet Aggregation ; Aged ; Methylamines ; },
abstract = {Many diseases are influenced by environmental temperature, and recent studies have confirmed that cold exposure increases the risk of conditions such as ischemic stroke (IS). However, direct evidence supporting this hypothesis is lacking, and the molecular mechanisms through which cold exposure affects IS remain unclear. In this study, we found that chronic cold exposure increased platelet aggregation and the levels of certain inflammatory factors in high-risk stroke patients (HR), thereby increasing the risk of IS. Furthermore, before and after a cold wave, we observed gut microbiota dysbiosis in the HR group, including reduced relative abundance differences in Lachnospiraceae and Ruminococcaceae. The relative abundances of the Prevotella_9 and Catenibacterium genera increased, whereas that of Anaerostipes decreased. Notably, the results of fecal microbiota transplantation (FMT) indicated that cold-adapted microbiota transplantation partially replicated the microbiota characteristics of each donor subject and replicated the effects of cold exposure in C57BL/6J mice. Cold exposure impaired intestinal barrier function and interfered with microbial functions, such as increased lipid metabolism and LPS production, particularly by increasing the levels of TMAO derived from the gut microbiota. Our findings identify the significant role of abnormal gut microbiota-derived metabolites in cold exposure-related IS and highlight the potential opportunity to prevent or treat cold-related IS through the modulation of the gut microbiota.},
}

*Gastrointestinal Microbiome/physiology
*Cold Temperature/adverse effects
Animals
Fecal Microbiota Transplantation
Mice
Male
Mice, Inbred C57BL
Humans
Dysbiosis/microbiology
*Ischemic Stroke/microbiology/etiology
Female
Middle Aged
Platelet Aggregation
Aged
Methylamines

@article {pmid40593020,
year = {2025},
author = {Yue, Y and Yao, B and Liao, F and He, Z and Sangsawad, P and Yang, S},
title = {Fecal microbiota transplantation improves Sansui duck growth performance by balancing the cecal microbiome.},
journal = {Scientific reports},
volume = {15},
number = {1},
pages = {22403},
pmid = {40593020},
issn = {2045-2322},
support = {31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; 31960682//The National Nature Science Foundation of China/ ; },
abstract = {Improving growth performance is vital in poultry production. Although several studies have established associations between gut microbiota and growth, the direct impacts remain unclear. A total of 120 1-day-old Sansui ducks were randomly assigned to the FMT and CON groups. From the 1st day, ducks in the FMT group were orally administrated with 0.5 mL fecal microbiota suspension for three consecutive days, while sterile PBS solution was used as a substitute in the CON group. The results revealed that FMT improved average daily gain (ADG) (P < 0.001) and body weight (BW) (P < 0.001), with a tendency for a better feed conversion rate (FCR) (P = 0.062). LEfSe analysis indicated a significant increase in the abundance of the Lactobacillus (P < 0.001), Bifidobacterium (P = 0.006), Megamonas (P = 0.008), and Subdoligranulum (P = 0.005) in the FMT group. Similarly, the phyla Firmicutes/Bacteroidetes ratio was higher in the FMT group compared to the CON group. Additionally, the ACE, Chao, and Shannon indices were also significantly higher in the FMT group (P < 0.001). To sum up, FMT enhanced growth performance, which could be associated with reducing proinflammatory pathogen colonization in the duck cecum. This modulating effect likely results from increased microbial diversity and the enrichment of beneficial bacteria.},
}

@article {pmid40592776,
year = {2025},
author = {Zhang, X and Ishikawa, D and Nagahara, A},
title = {Fecal Microbiota Transplantation for Immune Regulation: Improving Ulcerative Colitis and Enhancing Cancer Immunotherapy.},
journal = {International immunology},
volume = {},
number = {},
pages = {},
doi = {10.1093/intimm/dxaf038},
pmid = {40592776},
issn = {1460-2377},
abstract = {The gut microbiota plays an integral role in maintaining health and regulating various host functions, including immune responses. Fecal microbiota transplantation (FMT) has emerged as a promising therapeutic approach to restore gut microbial balance. Although widely recognized for its efficacy in treating ulcerative colitis (UC), FMT is now being investigated as an adjuvant therapy to enhance the efficacy of immune checkpoint inhibitors (ICIs) in cancer treatment. This review summarizes the clinical applications of FMT in UC treatment and its potential role in cancer immunotherapy. FMT exhibits varying degrees of efficacy in the treatment of UC, with differences in outcomes attributed to variations in administration methods and donor selection. In cancer therapy, FMT has demonstrated the potential to improve ICI responses, particularly in patients with melanoma. However, its effects on other cancers remain unclear. Although FMT holds promise for UC and cancer immunotherapy, challenges such as inconsistent clinical outcomes and methodological variations persist. Standardized protocols and mechanistic studies are crucial to optimize FMT-based therapeutic strategies, and further research is required to establish its efficacy under diverse clinical conditions.},
}

@article {pmid40592615,
year = {2025},
author = {Sasaki, K and Takeshima, Y and Fujino, A},
title = {Reproducing in vitro artificial gut microbiota using glycerol stocks of fecal cultures combined with different prebiotic additives.},
journal = {Journal of bioscience and bioengineering},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.jbiosc.2025.06.002},
pmid = {40592615},
issn = {1347-4421},
abstract = {Artificial human microbiota can be produced in gut simulators from cryopreserved stocks. They are used for in vitro fermentation models and as alternative material for fecal microbiota transplantation therapy. However, current methods have limited information on microbial structure at the genus level and present challenges during cryopreservation. In this study, we used an edible glycerol stock of fecal batch culture instead of fresh feces to create artificial gut microbiota. Three glycerol stocks, generated through in vitro fecal fermentation with different prebiotic additives (such as fructooligosaccharide, xylan, pectin, and guar gum), were combined. Profiling via 16S rRNA gene amplicon sequencing revealed that the artificial gut microbiota derived from the combined glycerol stocks showed more amplicon sequence variants than those from a single glycerol stock. In the artificial microbiota, relative abundance values of common genera such as Bifidobacterium, Bacteroides, Prevotella, Faecalibacterium, and Escherichia were more than 10 % of those found in the original feces. Other commensal genera such as Collinsella, Anaerobutyricum hallii (formerly Eubacterium hallii) group, Anaerostipes, Blautia, Dorea, Lachnospiraceae UCG-004, and Oscillospiraceae UCG-003 were similarly maintained. Our data indicated that combining glycerol stocks of fecal cultures with different additives in a batch-type gut simulator is a useful option for producing artificial gut microbiota, the taxonomic compositions of which are comparable to those of the original feces.},
}

@article {pmid40592538,
year = {2025},
author = {Cymbal, M and Chatterjee, A and Baggott, B},
title = {Fecal microbiota transplantation: Current evidence and future directions.},
journal = {Cleveland Clinic journal of medicine},
volume = {92},
number = {7},
pages = {421-428},
doi = {10.3949/ccjm.92a.24107},
pmid = {40592538},
issn = {1939-2869},
mesh = {Humans ; *Fecal Microbiota Transplantation/methods/trends ; *Clostridium Infections/therapy ; *Gastrointestinal Microbiome ; Clostridioides difficile ; Dysbiosis/therapy ; },
abstract = {As we advance our understanding of the gut microbiota, the implications of dysbiosis are becoming increasingly apparent. Fecal microbiota transplantation (FMT), a well-established procedure, is recognized for effectively treating recurrent Clostridioides difficile infection, prompting further investigation into its other possible clinical applications. Donor selection and screening are essential to ensure safety and efficacy. Product development and standardization, such as the US Food and Drug Administration-approved live biotherapeutic products Rebyota and Vowst, are helping efforts to evaluate FMT for other gastrointestinal and extraintestinal diseases. However, additional clinical trials are needed to support its use beyond recurrent C difficile infection.},
}

Humans
*Fecal Microbiota Transplantation/methods/trends
*Clostridium Infections/therapy
*Gastrointestinal Microbiome
Clostridioides difficile
Dysbiosis/therapy

@article {pmid40591032,
year = {2025},
author = {Abebaw, D and Akelew, Y and Adugna, A and Tegegne, BA and Teffera, ZH and Belayneh, M and Fenta, A and Selabat, B and Kindie, Y and Baylie, T and Mekuriaw, MG and Jemal, M and Atnaf, A},
title = {Immunomodulatory properties of the gut microbiome: diagnostic and therapeutic potential for rheumatoid arthritis.},
journal = {Clinical and experimental medicine},
volume = {25},
number = {1},
pages = {226},
pmid = {40591032},
issn = {1591-9528},
mesh = {Humans ; *Arthritis, Rheumatoid/therapy/diagnosis/immunology/microbiology ; *Gastrointestinal Microbiome/immunology ; Dysbiosis/immunology ; Probiotics/therapeutic use ; *Immunomodulation ; Fecal Microbiota Transplantation ; Biomarkers ; Animals ; },
abstract = {Rheumatoid arthritis (RA) is a chronic autoimmune disorder characterized by persistent joint inflammation, synovial hyperplasia, and progressive joint destruction. Despite advancements in biologic disease-modifying antirheumatic drugs (bDMARDs) and TNF-α blockers, many RA patients still require more effective treatment options. Although genetic and environmental factors play a role in RA development, recent studies have emphasized the influence of the gut microbiota on disease onset and progression. Dysbiosis, or an imbalance in the gut microbial composition, has been linked to immune dysregulation, increased intestinal permeability, and systemic inflammation, all contributing to RA development. Research has revealed changes in the gut microbiome of RA patients, including an increased prevalence of Prevotella copri and a decreased presence of beneficial microbes such as Bifidobacterium, Bacteroides, and Lactobacillus. RA patients exhibit altered metabolite profiles, with reduced levels of short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, which are linked to immune regulation and intestinal barrier function. Specific metabolites, such as L-arginine, phosphorylcholine, and arachidonic acid, have potential as RA biomarkers, with predictive value for diagnosis. Therapeutic approaches focusing on the microbiome, including probiotics, fecal microbiota transplantation, and traditional medicines, show promise in alleviating RA symptoms and regulating immune function. This review provides an updated overview of the immunomodulatory effects of the gut microbiome and explores its potential applications in the diagnosis and treatment of RA.},
}

Humans
*Arthritis, Rheumatoid/therapy/diagnosis/immunology/microbiology
*Gastrointestinal Microbiome/immunology
Dysbiosis/immunology
Probiotics/therapeutic use
*Immunomodulation
Fecal Microbiota Transplantation
Biomarkers
Animals

@article {pmid40589476,
year = {2025},
author = {Olajide, TS and Ijomone, OM},
title = {Targeting gut microbiota as a therapeutic approach for neurodegenerative diseases.},
journal = {Neuroprotection},
volume = {3},
number = {2},
pages = {120-130},
pmid = {40589476},
issn = {2770-730X},
abstract = {Recent evidence suggests a more important role of the gut microbiota in neurodegenerative diseases (NDDs) given its relationship through the microbiota-gut-brain as an active communication system aiding in maintaining homeostasis between the brain and the gut. This review focuses on how modulation of gut microbiota can serves as a therapeutic strategy for NDDs, emphasizing the neuroprotective effects of probiotics. Probiotics are live microorganisms that confer health benefits, and their interaction with gut-microbiota influences neurogenesis, neurotransmitter regulation, and neuroinflammation. Recent advancements, including germ-free animal models, fecal microbiota transplantation (FMT), and diverse probiotic strains, have revealed the underlying mechanisms linking gut health to brain function. Notably, several Lactobacillus and Bifidobacterium species have been shown to exert neuroprotective effects via the upregulation of neurotrophic factors such as brain-derived neurotrophic factor and enhancing mitochondrial function through reducing the impacts of oxidative stress. Interestingly, FMT has exhibited a degree of success in overcoming cognitive impairment and motor deficits in preclinical studies and clinical trials. However, further research is warranted to explore its therapeutic potential in humans. Overall, this review highlights the significant role of gut microbiota in NDDs and advocates for gut-targeted interventions as innovative approaches to mitigate these diseases.},
}

@article {pmid40589142,
year = {2025},
author = {Tiwari, R and Paswan, A and Tiwari, G and Reddy, VJS and Posa, MK},
title = {Perspectives on Fecal Microbiota Transplantation: Uses and Modes of Administration.},
journal = {Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology},
volume = {41},
number = {},
pages = {e20250014},
doi = {10.62958/j.cjap.2025.014},
pmid = {40589142},
issn = {1000-6834},
mesh = {*Fecal Microbiota Transplantation/methods ; Humans ; *Gastrointestinal Microbiome ; Feces/microbiology ; *Nervous System Diseases/therapy ; },
abstract = {Fecal microbiota Transplantation (FMT), often referred to as stool transplantation, fecal transfusion, and fecal bacteria therapy, is considered one of the most medical innovations of the 20th century. Fecal microbiota Transplantation entails filtering and dilution of a healthy donor's feces before injecting it into the recipient's digestive system. In China, it was first administered orally in the fourth century for diarrhea and food poisoning under the name "Yellow Soup." It has recently been widely employed in a variety of clinical settings, including cases of Clostridium difficile infection that are recurring and resistant. By replacing the unhealthy intestinal microbiota with a healthy bacterial community, the FMT treatment aims to enhance the intestinal flora. It also looks at neurological conditions where alterations in gut microbiota are prevalent. We have discussed FMT in the context of its use in conditions affecting the nerve system, such as neurological and other conditions (multiple sclerosis, Parkinson's disease, Alzheimer's disease, stroke, epilepsy, Amyotrophic lateral sclerosis, Tourette syndrome, neuropathic pain, Huntington's diseases, etc.), as well as the role of gut microbiota in many neurological disorders.},
}

*Fecal Microbiota Transplantation/methods
Humans
*Gastrointestinal Microbiome
Feces/microbiology
*Nervous System Diseases/therapy

@article {pmid40589086,
year = {2025},
author = {Yadav, M and Gupta, A and Mathew, B and Tripathi, G and Dalal, N and Sharma, N and Yadav, P and Yadav, G and Singh, R and Bindal, V and Saif, R and Yadav, S and Sharma, N and Pandey, S and Bhat, SH and Singh, R and Kumar, J and Kushwaha, M and Khan, T and Sharma, NK and Bhaskar, A and Dwivedi, VP and Kumar, A and Kumar, N and Tripathi, DM and Trehanpati, N and Anupama Kumara, and Sharma, S and Sarin, SK and Maras, JS},
title = {Circulating urobilinogen contributes to Inflammation, Intestinal Permeability and corticosteroid non-response in Severe Alcohol-associated Hepatitis.},
journal = {Molecular therapy : the journal of the American Society of Gene Therapy},
volume = {},
number = {},
pages = {},
doi = {10.1016/j.ymthe.2025.06.041},
pmid = {40589086},
issn = {1525-0024},
abstract = {Severe alcohol-associated hepatitis (SAH) is a life-threatening condition with high mortality rates and poor response to prednisolone therapy. Identifying reliable early predictors of therapy response and survival is critical. Plasma metabolomics was conducted on 70 SAH patients (50 responders, 20 non-responders) to identify biomarkers for non-response and early mortality. These findings were validated in a cohort of 153 patients and an independent cohort of 245 using high resolution mass spectrometry, machine learning, and severity indices. Temporal metabolic changes indicated interactions between the host and microbiome, with a focus on inflammation and intestinal permeability. Plasma metabolomics revealed that non-responders had significantly higher urobilinogen levels (3.6-fold change). Additionally, a decrease in alpha/beta diversity and temporal metabolic inactivity characterized non-responders. Plasma urobilinogen levels predicted non-response (AUC>0.97) and identified non-survivors (AUC=0.94) with a threshold of >0.07 mg/ml. Urobilinogen levels correlated with bacterial peptides belonging to Firmicutes and Proteobacteria, neutrophil activation, oxidative stress, and pro-inflammatory cytokine production. These changes contributed to non-response by increasing glucocorticoid receptor β expression and compromising intestinal permeability. Fecal microbiota transplantation decreased urobilinogen levels by reducing bilirubin reductase gene-containing microbiota. Plasma urobilinogen >0.07 mg/ml could predict early mortality, and modulation of the gut microbiome may improve outcomes in SAH patients.},
}

@article {pmid40588803,
year = {2025},
author = {Hu, J and Feng, T and Zhang, L and Zhou, Q and Zhu, L},
title = {Leveraging gut microbiota for enhanced immune checkpoint blockade in solid tumor therapy.},
journal = {Chinese medical journal},
volume = {},
number = {},
pages = {},
pmid = {40588803},
issn = {2542-5641},
abstract = {Gut microbiota can modulate antitumor immunity and influence immune checkpoint blockade (ICB) therapy efficacy and treatment-associated toxicity. Variations in the therapeutic effect of ICB among individuals are partially attributed to microbiota. This review summarizes current knowledge on how specific bacterial species enhance or hinder ICB outcomes by regulating immune cell activation, antigen presentation, and systemic inflammation. The review further outlines translational strategies to optimize ICB, including microbiota-targeted interventions (e.g., prebiotics, fecal microbiota transplantation, and metabolite therapies) to overcome resistance and mitigate treatment-related toxicities, focusing on immune-related colitis. Additionally, emerging microbial biomarkers in melanoma, lung cancer, and hepatobiliary cancers that predict ICB response are discussed, highlighting the gut microbiome as a potential target for personalized cancer immunotherapy. By integrating mechanistic insights with clinical evidence, this review underscores the potential of microbiota-centered approaches to improve patient outcomes in ICB-based treatments, emphasizing the pivotal role of the gut microbiota in modulating both therapeutic efficacy and immune-related adverse events.},
}

@article {pmid40586386,
year = {2025},
author = {Li, K and Arbab, S and Du, Q and Zhou, J and Chen, Y and Tian, Y and Qijie, L and Ullah, H and Zhang, B},
title = {Regulatory and Influencing Factors of Digestive Function in Elderly People: Roles of the Gut Microbiota and Nutritional Interventions.},
journal = {Aging and disease},
volume = {},
number = {},
pages = {},
doi = {10.14336/AD.2025.0565},
pmid = {40586386},
issn = {2152-5250},
abstract = {Aging is a natural and gradual biological process through which living organisms undergo physical, physiological, and sometimes psychological changes over time. Aging is commonly associated with a decline in gastrointestinal function, leading to various digestive disorders that impact the quality of life of older adults. The gut microbiota is a highly complex ecosystem that plays crucial roles in digestion, metabolic processes, immune functions, and overall health. However, emerging evidence indicates that many elderly individuals maintain relatively stable digestive health, suggesting the influence of modifiable regulatory factors. In this review, we describe the key physiological, microbial, and nutritional factors that regulate and influence digestive function in an aging population. Additionally, we explored the impact of age-associated alterations in the gut microbiota on digestive health challenges in older adults and emphasized the therapeutic potential of targeted nutritional intervention approaches, such as dietary modifications, prebiotics, probiotics, and symbiotic and fecal microbiota transplantation, which have shown promise in rebalancing the gut microbiome and reducing inflammation.},
}

@article {pmid40585700,
year = {2025},
author = {Hamza Saeed, M and Qamar, S and Ishtiaq, A and Umaira Khan, Q and Atta, A and Atta, M and Ishtiaq, H and Khan, M and Saeed, MR and Iqbal, A},
title = {Fecal Microbiota Transplantation (FMT) in Clostridium difficile Infection: A Paradigm Shift in Gastrointestinal Microbiome Modulation.},
journal = {Cureus},
volume = {17},
number = {5},
pages = {e85054},
doi = {10.7759/cureus.85054},
pmid = {40585700},
issn = {2168-8184},
abstract = {Clostridium difficile (C. difficile) infection (CDI) poses a tremendous clinical challenge, especially in patients with recurrent disease and antibiotic resistance. Fecal microbiota transplantation (FMT) has become a new therapeutic strategy for restoring gut microbiota and decreasing CDI recurrence. The study aims to assess the clinical effectiveness of FMT in adult subjects with recurrent or refractory CDI, determine its effect on gut microbiome diversity, and track safety outcomes and rates of recurrence post-treatment. FMT was compared against standard antibiotic treatments to establish its efficacy in decreasing infection persistence and improving patients' quality of life. This study examines the efficacy, safety, and modulation of microbiota by FMT in an ensemble of 250 patients diagnosed with CDI, with equal gender distribution and a mean age of 55.61. Among the study participants, 131 (52.4%) underwent FMT by various routes of administration, including 66 (25.2%) through colonoscopy, 73 (29.2%) via a nasogastric tube, 60 (24.0%) via enema, and 54 (21.6%) through oral capsule administration. The success rate for FMT was reported as 88 (35.2%), partial success at 74 (29.6%), and treatment failure at 88 (35.2%). CDI recurrence was reported in 130 (52.0%) of patients after FMT. The gut microbiome enhanced diversity, measured in terms of the Shannon Diversity Index, increased significantly from 3.96 before FMT to 5.88 after FMT, thus indicating a favorable impact on gut microbial composition. Furthermore, 132 (52.8%) converted from C. difficile polymerase chain reaction (PCR) toxin positive to negative, corroborating successful pathogen clearance. On secondary outcomes, the quality of life in patients improved in 90 (36%), antibiotic dependence was reduced in 88 (35.2%), and hospitalization was lessened in 72 (28.8%). Inflammatory markers, such as white blood cell (WBC) counts and C-reactive protein (CRP), went downward but did not reach statistical significance. Logistic regression analysis identified age, severity of CDI, and prior exposure to antibiotics as the main predictors for the efficacy of FMT (p < 0.05). It is concluded that FMT is a promising alternative treatment for recurrent CDI through modulation of gut microbiota and decreasing the severity of infection. Future work is, however, required to establish treatment protocols with optimized results for long-term effectiveness and minimized recurrence risks.},
}

@article {pmid40585508,
year = {2025},
author = {Zhu, B and Wu, H and Zhang, H and Song, Q and Xiao, Y and Yu, B},
title = {Gut microbiota from voluntary exercised mice protects the intestinal barrier by inhibiting neutrophil extracellular trap formation.},
journal = {iScience},
volume = {28},
number = {6},
pages = {112763},
doi = {10.1016/j.isci.2025.112763},
pmid = {40585508},
issn = {2589-0042},
abstract = {Ulcerative colitis is an inflammatory bowel disease characterized by impaired intestinal barrier function, dysregulated immune responses, and alterations in the gut microbiota. Excessive formation of neutrophil extracellular traps (NETs), driven by peptidyl arginine deiminase 4 (PAD4) activity, contributes to inflammation modulated by the gut microbiota. In this study, we used a mouse model of dextran sulfate sodium-induced colitis to investigate the effects of voluntary exercise and its underlying mechanisms. Exercise preconditioning attenuated colitis severity, maintained intestinal barrier integrity, normalized gut microbiota composition, and suppressed NET formation. PAD4 inhibition further enhanced these effects. By contrast, the depletion of the gut microbiota by antibiotics largely abolished the benefits of exercise. Additionally, fecal microbiota transplantation from exercised mice recapitulated these protective effects. These findings elucidate the interplay among exercise, gut microbiota, and PAD4-mediated NET formation. Targeting these pathways may offer promising therapeutic strategies for colitis.},
}