Gut MicrobesPub Date : 2025-12-01Epub Date: 2025-01-24DOI: 10.1080/19490976.2025.2456592
Xinyu Zhao, Ye Qiu, Lanfan Liang, Xiangsheng Fu
{"title":"Interkingdom signaling between gastrointestinal hormones and the gut microbiome.","authors":"Xinyu Zhao, Ye Qiu, Lanfan Liang, Xiangsheng Fu","doi":"10.1080/19490976.2025.2456592","DOIUrl":"10.1080/19490976.2025.2456592","url":null,"abstract":"<p><p>The interplay between the gut microbiota and gastrointestinal hormones plays a pivotal role in the health of the host and the development of diseases. As a vital component of the intestinal microecosystem, the gut microbiota influences the synthesis and release of many gastrointestinal hormones through mechanisms such as modulating the intestinal environment, producing metabolites, impacting mucosal barriers, generating immune and inflammatory responses, and releasing neurotransmitters. Conversely, gastrointestinal hormones exert feedback regulation on the gut microbiota by modulating the intestinal environment, nutrient absorption and utilization, and the bacterial biological behavior and composition. The distributions of the gut microbiota and gastrointestinal hormones are anatomically intertwined, and close interactions between the gut microbiota and gastrointestinal hormones are crucial for maintaining gastrointestinal homeostasis. Interventions leveraging the interplay between the gut microbiota and gastrointestinal hormones have been employed in the clinical management of metabolic diseases and inflammatory bowel diseases, such as bariatric surgery and fecal microbiota transplantation, offering promising targets for the treatment of dysbiosis-related diseases.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2456592"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143033089","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gut MicrobesPub Date : 2025-12-01Epub Date: 2025-01-27DOI: 10.1080/19490976.2025.2457499
Geoffrey A Preidis
{"title":"The neonatal gut microbiome in health and disease.","authors":"Geoffrey A Preidis","doi":"10.1080/19490976.2025.2457499","DOIUrl":"10.1080/19490976.2025.2457499","url":null,"abstract":"","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2457499"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11776465/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046573","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gut dysbiosis-induced vitamin B6 metabolic disorder contributes to chronic stress-related abnormal behaviors in a cortisol-independent manner.","authors":"Wenxiang Qing, Huimin Chen, Xin Ma, Jie Chen, Yuan Le, Hui Chen, Jianhua Tong, Kaiming Duan, Daqing Ma, Wen Ouyang, Jianbin Tong","doi":"10.1080/19490976.2024.2447824","DOIUrl":"10.1080/19490976.2024.2447824","url":null,"abstract":"<p><p>Chronic stress can result in various conditions, including psychological disorders, neurodegenerative diseases, and accelerated brain aging. Gut dysbiosis potentially contributes to stress-related brain disorders in individuals with chronic stress. However, the causal relationship and key factors between gut dysbiosis and brain disorders in chronic stress remain elusive, particularly under non-sterile conditions. Here, using a repeated restraint stress (RRS) rat model, we show that sequential transplantation of the cecal contents of different RRS stages to normal rats reproduced RRS-induced core phenotypes, including abnormal behaviors, increased peripheral blood corticosterone and inflammatory cytokines, and a unique gut microbial phenotype. This core phenotypic development was effectively inhibited with probiotic supplement. The RRS-induced unique gut microbial phenotypes at the genus level were positively or negatively associated with the levels of 20 plasma metabolites, including vitamin B6 metabolites 4-pyridoxic acid and 4-pyridoxate. Vitamin B6 supplement during RRS alleviated weight loss, abnormal behaviors, peripheral inflammation, and neuroinflammation, but did not affect the peripheral corticosterone levels in chronic stressed rats. Dampening inflammatory signaling via knocking out caspase 11 or caspase 1 inhibitor abolished RRS-induced abnormal behaviors and peripheral and neuroinflammation but did not decrease peripheral corticosterone in mice. These findings show that gut dysbiosis-induced vitamin B6 metabolism disorder is a new non-hypothalamic-pituitary-adrenal axis mechanism of chronic stress-related brain disorders. Both probiotics and vitamin B6 supplement have potential to be developed as therapeutic strategies for preventing and/or treating chronic stress-related illness.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2447824"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730634/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947797","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gut MicrobesPub Date : 2025-12-01Epub Date: 2025-02-13DOI: 10.1080/19490976.2025.2464221
Grace A Maldarelli, Maeva Metz, Seun Oguntunmibi, Nancy Tran, Grace Xiang, Dana Lukin, Ellen J Scherl, Randy S Longman
{"title":"IgG-seq identifies immune-reactive enteric bacteria in Crohn's disease with spondyloarthritis.","authors":"Grace A Maldarelli, Maeva Metz, Seun Oguntunmibi, Nancy Tran, Grace Xiang, Dana Lukin, Ellen J Scherl, Randy S Longman","doi":"10.1080/19490976.2025.2464221","DOIUrl":"https://doi.org/10.1080/19490976.2025.2464221","url":null,"abstract":"<p><p>Joint inflammation is the most common extraintestinal manifestation of Crohn's disease (CD). Although alterations in the enteric microbiota are described in CD with spondyloarthritis (CD-SpA), it is not known whether distinct taxa serve as markers for clinical subtypes of axial (AxSpA) or peripheral SpA (pSpA) in CD. Moreover, it is not yet known whether these taxa generate a specific systemic IgG response. Here, we sequenced the fecal microbiome from 106 individuals (44 CD, 39 CD-SpA, 14 CD-AxSpA, and 9 healthy controls [HC]). This unique cohort revealed distinct taxonomic compositions of CD and CD-SpA compared to HC and demonstrates that the composition of the CD-AxSpA microbiome is distinct from that of CD-pSpA. Using autologous serum, we identified enteric bacteria recognized by serum IgG and demonstrate differences in the IgG coating index of specific bacterial genera associated with CD-SpA. The IgG coating index of <i>Mediterraneibacter gnavus</i> differentiated patients with CD-pSpA and is positively associated with joint disease activity. This work illustrates divergent microbiome compositions in CD-SpA subtypes, as well as the recognition of distinct enteric bacteria by serum IgG with the potential to serve as a marker of joint inflammation in CD.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2464221"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"PMA1-containing extracellular vesicles of <i>Candida albicans</i> triggers immune responses and colitis progression.","authors":"Zhen Xu, Shuping Qiao, Zelin Wang, Chen Peng, Yayi Hou, Baorui Liu, Guochun Cao, Tingting Wang","doi":"10.1080/19490976.2025.2455508","DOIUrl":"10.1080/19490976.2025.2455508","url":null,"abstract":"<p><p><i>Candida albicans</i> (<i>C. albicans</i>) exhibits aberrant changes in patients with colitis, and it has been reported to dominate the colonic mucosal immune response. Here, we found that PMA1 expression was significantly increased in <i>C. albicans</i> from patients with IBD compared to that in healthy controls. A Crispr-Cas9-based fungal strain editing system was then used to knock out PMA1 expression in <i>C. albicans</i>. Compared to <i>WT-C.a</i>, <i>ΔPMA1-C.a</i> could not aggravate colitis. Proteomic analysis showed that PMA1 was transported by extracellular vesicles (EVs) of <i>C. albicans</i>. PMA1-containing EVs aggravated colitis, modulated the migration of cDC2 from the lamina propria to mesenteric lymph nodes, and induced TH17 cell differentiation. Moreover, the adaptor protein CARD9 was critical in PMA1-containing EV-induced colitis, and CARD9-deficient DCs did not induce TH17 cell differentiation or IL-17A production. Mechanically, CARD9 combines with the glycolytic protein GAPDH (aa2-146 domain) through its CARD region. CARD9 deficiency led to decreased enzyme activity of GAPDH and decreased glycolysis of DCs. These findings indicate that PMA1 is a potential virulence factor responsible for the pathogenesis of <i>C. albicans</i> colitis.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2455508"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11792855/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gut MicrobesPub Date : 2025-12-01Epub Date: 2025-02-18DOI: 10.1080/19490976.2025.2463570
Hayleigh K Ast, Matthew Hammer, Shiqi Zhang, Alisha Bruton, Irene E Hatsu, Brenda Leung, Ryan McClure, Priya Srikanth, Yuliya Farris, Lydia Norby-Adams, Lisa M Robinette, L Eugene Arnold, Jonathan R Swann, Jiangjiang Zhu, Lisa Karstens, Jeanette M Johnstone
{"title":"Gut microbiome changes with micronutrient supplementation in children with attention-deficit/hyperactivity disorder: the MADDY study.","authors":"Hayleigh K Ast, Matthew Hammer, Shiqi Zhang, Alisha Bruton, Irene E Hatsu, Brenda Leung, Ryan McClure, Priya Srikanth, Yuliya Farris, Lydia Norby-Adams, Lisa M Robinette, L Eugene Arnold, Jonathan R Swann, Jiangjiang Zhu, Lisa Karstens, Jeanette M Johnstone","doi":"10.1080/19490976.2025.2463570","DOIUrl":"https://doi.org/10.1080/19490976.2025.2463570","url":null,"abstract":"<p><p>Micronutrients have demonstrated promise in managing inattention and emotional dysregulation in children with attention-deficit/hyperactivity disorder (ADHD). One plausible pathway by which micronutrients improve symptoms is the gut microbiome. This study examines changes in fecal microbial composition and diversity after micronutrient supplementation in children with ADHD (<i>N</i> = 44) and highlights potential mechanisms responsible for the behavioral improvement, as determined by blinded clinician-rated global improvement response to micronutrients. Participants represent a sub-group of the Micronutrients for ADHD in Youth (MADDY) study, a double blind randomized controlled trial in which participants received micronutrients or placebo for 8 weeks, followed by an 8-week open extension. Stool samples collected at baseline, week 8, and week 16 were analyzed using 16S rRNA amplicon sequencing targeting the V4 hypervariable region. Pairwise compositional analyses investigated changes in fecal microbial composition between micronutrients versus placebo and responders versus non-responders. A significant change in microbial evenness, as measured by alpha diversity, and beta-diversity, as measured by Bray-Curtis, was observed following micronutrients supplementation. The phylum <i>Actinobacteriota</i> decreased in the micronutrients group compared to placebo. Two butyrate-producing bacterial families: <i>Rikenellaceae</i> and <i>Oscillospiraceae</i>, exhibited a significant increase in change following micronutrients between responders versus non-responders. These findings suggest that micronutrients modulated the composition of the fecal microbiota and identified specific bacterial changes associated with micronutrient responders.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2463570"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Maternal-infant probiotic transmission mitigates early-life stress-induced autism in mice.","authors":"Li Qing, Xin Qian, Huiyue Zhu, Jingyu Wang, Jingge Sun, Zhiying Jin, Xinyu Tang, Yingqi Zhao, Gang Wang, Jianxin Zhao, Wei Chen, Peijun Tian","doi":"10.1080/19490976.2025.2456584","DOIUrl":"10.1080/19490976.2025.2456584","url":null,"abstract":"<p><p>Autism, a disorder influenced by both genetic and environmental factors, presents significant challenges for prevention and treatment. While maternal-infant gut microbiota has been a focus in autism research, preventive strategies targeting maternal gut microbiota remain underexplored. This study demonstrates that prenatal probiotic intake can effectively prevent maternal separation-induced autistic-like behaviors in offspring without altering the embryonic neurodevelopment in mice. Using specific PCR primers and cross-fostering experiments, we traced the vertical transmission of probiotics, primarily via fecal/vaginal contamination. Early probiotic colonization conferred resilience against stress-induced gut pathogenic microbes and Th17-mediated peripheral inflammation while significantly inhibiting hypermyelination and neuroinflammation linked to systemic inflammation. Microbial metabolites like tyrosol and xanthurenic acid alleviated neuroinflammation and hypermyelination in vitro, though the causal relationship among neuroinflammation, hypermyelination, and autism in vivo requires further validation. These findings underscore the importance of the maternal-infant microbiota transmission window in autism prevention and highlight the clinical potential of prenatal probiotic interventions.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2456584"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143390682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gut MicrobesPub Date : 2025-12-01Epub Date: 2024-12-22DOI: 10.1080/19490976.2024.2442037
Fangfang Chen, Songhe Guo, Yiqiu Li, Yongfan Lu, Le Liu, Shengxin Chen, Jun An, Ge Zhang
{"title":"<i>Fusobacterium nucleatum</i>-driven CX3CR1<sup>+</sup> PD-L1<sup>+</sup> phagocytes route to tumor tissues and reshape tumor microenvironment.","authors":"Fangfang Chen, Songhe Guo, Yiqiu Li, Yongfan Lu, Le Liu, Shengxin Chen, Jun An, Ge Zhang","doi":"10.1080/19490976.2024.2442037","DOIUrl":"https://doi.org/10.1080/19490976.2024.2442037","url":null,"abstract":"<p><p>The intracellular bacterium <i>Fusobacterium nucleatum</i> (Fn) mediates tumorigenesis and progression in colorectal cancer (CRC). However, the origin of intratumoral Fn and the role of Fn-infected immunocytes in the tumor microenvironment remain unclear. Here, we observed that Fn-infected neutrophils/macrophages (PMNs/MΦs), especially PMNs, accumulate in tumor tissues and fecal Fn abundance correlates positively with an abundance of blood PD-L1<sup>+</sup> PMNs in CRC patients. Moreover, Fn accumulates in tumor tissues of tumor-bearing mice <i>via</i> intragingival infection and intravenous injection. Mechanistically, Fn can survive inside PMNs by reducing intracellular ROS levels and producing H<sub>2</sub>S. Specifically, the lysozyme inhibitor Fn1792 as a novel virulence factor of Fn suppressed apoptosis of phagocytes by inducing CX3CR1 expression. Furthermore, Fn-driven CX3CR1<sup>+</sup>PD-L1<sup>+</sup> phagocytes transfer intracellular Fn to tumor cells, which recruit PMNs/MΦs through the CXCL2/8-CXCR2 and CCL5/CCR5 axes. Consequently, CX3CR1<sup>+</sup>PD-L1<sup>+</sup> PMNs infiltration promotes CRC metastasis and weakens the efficacy of immunotherapy. Treatment with the doxycycline eradicated intracellular Fn, thereby reducing the CX3CR1<sup>+</sup>PD-L1<sup>+</sup> PMNs populations and slowing Fn-promoted tumor growth and metastasis in mice. These results suggest phagocytes as Fn-presenting cells use mutualistic strategies to home to tumor tissues and induce immunosuppression, and treatment with ROS-enhanced antibiotics can inhibit Fn-positive tumor progression.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2442037"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142876869","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The regulatory effect of chitooligosaccharides on islet inflammation in T2D individuals after islet cell transplantation: the mechanism behind <i>Candida albicans</i> abundance and macrophage polarization.","authors":"Yayu Zhang, Xiaoguo Ji, Kunlin Chang, Hao Yin, Mengyao Zhao, Liming Zhao","doi":"10.1080/19490976.2024.2442051","DOIUrl":"10.1080/19490976.2024.2442051","url":null,"abstract":"<p><p>Islet cell transplantation (ICT) represents a promising therapeutic approach for addressing diabetes mellitus. However, the islet inflammation during transplantation significantly reduces the surgical outcome rate, which is related to the polarization of macrophages. Chitooligosaccharides (COS) was previously reported which could modulate the immune system, alleviate inflammation, regulate gut microecology, and repair the intestinal barrier. Therefore, we hypothesized COS could relieve pancreatic inflammation by regulating macrophage polarization and gut microbiota. First, 18S rDNA gene sequencing was performed on fecal samples from the ICT population, showing abnormally increased amount of <i>Candida albicans</i>, possibly causing pancreatic inflammation. Functional oligosaccharides responsible for regulating macrophage polarization and inhibiting the growth of <i>Candida albicans</i> were screened. Afterwards, human flora-associated T2D (HMA-T2D) mouse models of gut microbiota were established, and the ability of the selected oligosaccharides were validated <i>in vivo</i> to alleviate inflammation and regulate gut microbiota. The results indicated that ICT significantly decreased the alpha diversity of gut fungal, altered fungal community structures, and increased <i>Candida albicans</i> abundance. Moreover, <i>Candida albicans</i> promoted M1 macrophage polarization, leading to islet inflammation. COS inhibited <i>Candida albicans</i> growth, suppressed the MyD88-NF-κB pathway, activated STAT6, inhibited M1, and promoted M2 macrophage polarization. Furthermore, COS-treated HMA-T2D mice displayed lower M1 macrophage differentiation and higher M2 macrophage numbers. Additionally, COS also enhanced <i>ZO-1</i> and <i>Occludin</i> mRNA expression, reduced <i>Candida albicans</i> abundance, and balanced gut microecology. This study illustrated that COS modulated macrophage polarization via the MyD88/NF-κB and STAT6 pathways, repaired the intestinal barrier, and reduced <i>Candida albicans</i> abundance to alleviate islet inflammation.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2442051"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11660412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142853997","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Gut MicrobesPub Date : 2025-12-01Epub Date: 2025-01-08DOI: 10.1080/19490976.2024.2446378
Levi M Teigen, Austin Hoeg, Hijab Zehra, Priyali Shah, Remy Johnson, Kristen Hutchison, Megan Kocher, Annie W Lin, Abigail J Johnson, Byron P Vaughn
{"title":"Nutritional optimization of fecal microbiota transplantation in humans: a scoping review.","authors":"Levi M Teigen, Austin Hoeg, Hijab Zehra, Priyali Shah, Remy Johnson, Kristen Hutchison, Megan Kocher, Annie W Lin, Abigail J Johnson, Byron P Vaughn","doi":"10.1080/19490976.2024.2446378","DOIUrl":"10.1080/19490976.2024.2446378","url":null,"abstract":"<p><p>Diet constitutes a major source of nutrient flow to the gut microbes. As such, it can be used to help shape the gut microbiome. Fecal microbiota transplantation (FMT) is an increasingly promising therapy in disease states beyond recurrent <i>Clostridioides difficile</i> infection, but diet is largely overlooked for its potential to help optimize this therapy. Therefore, the aim of this scoping review is to present the literature landscape that captures pre- and post-FMT dietary intake in humans, identify research gaps, and provide recommendations for future research. A comprehensive search strategy was developed and searches were run in five databases. Studies were included if they discussed adults who underwent FMT for any recognized treatment indication and had dietary intake as a study objective, this search encompassed studies with interventions that included foods and dietary supplements. The initial screening identified a total of 7721 articles, of which 18 met the inclusion criteria for this review. Studies were heterogeneous, but taken together, they introduce a framework that defines important nutritional considerations for both donors and FMT recipients in the period around FMT dosing. This framework is summarized with this review and highlights the opportunities available to develop FMT-based precision nutrition strategies to optimize its clinical efficacy.</p>","PeriodicalId":12909,"journal":{"name":"Gut Microbes","volume":"17 1","pages":"2446378"},"PeriodicalIF":12.2,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11730610/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142947808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}