{"title":"神经干细胞TSP50缺乏通过改变肠道微生物群加重小鼠结肠炎。","authors":"Xiaoli Li, Rong Jin, Zhaoxia Wang, Chunxue Niu, Zhenbo Song, Xiaoling Liu, Jian Huang, Huan Zhang, Xia Qian, Feng Gao, Shuyue Wang, Chunlei Yu, Luguo Sun, Yanxin Huang, Lihua Zheng, Guannan Wang, Ying Sun, Xiaoguang Yang, Yongli Bao, Jiawei Li","doi":"10.1038/s41522-025-00737-3","DOIUrl":null,"url":null,"abstract":"<p><p>Inflammatory bowel disease (IBD) is a complex disease characterized by persistent chronic inflammation of the gastrointestinal tract and periodic episodes. Despite the increasing number of related studies, the detailed pathogenesis of IBD has not been elucidated. In recent years, host-microbiota interactions in the pathogenesis of IBD have received extensive attention. Testes-specific protease 50 (TSP50) is a potential risk gene for IBD, but whether it can affect the susceptibility of colitis by regulating the gut microbiome is still unclear. Here, we showed that TSP50 deficiency in neural stem cells (NSCs) aggravated colitis in mice by altering intestinal microbiome. Mechanistically, TSP50 maintained the level of neurotransmitter acetylcholine (ACh) by degrading acetylcholinesterase (AChE), thereby maintaining intestinal mucosa and intestinal microecological homeostasis and reducing the susceptibility to colitis. These findings provide a new perspective on the interaction between host and commensal microbiota, which may be beneficial for developing potential therapeutic strategies for IBD.</p>","PeriodicalId":19370,"journal":{"name":"npj Biofilms and Microbiomes","volume":"11 1","pages":"93"},"PeriodicalIF":9.2000,"publicationDate":"2025-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134233/pdf/","citationCount":"0","resultStr":"{\"title\":\"TSP50 deficiency in neural stem cells aggravates colitis in mice by altering intestinal microbiome.\",\"authors\":\"Xiaoli Li, Rong Jin, Zhaoxia Wang, Chunxue Niu, Zhenbo Song, Xiaoling Liu, Jian Huang, Huan Zhang, Xia Qian, Feng Gao, Shuyue Wang, Chunlei Yu, Luguo Sun, Yanxin Huang, Lihua Zheng, Guannan Wang, Ying Sun, Xiaoguang Yang, Yongli Bao, Jiawei Li\",\"doi\":\"10.1038/s41522-025-00737-3\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Inflammatory bowel disease (IBD) is a complex disease characterized by persistent chronic inflammation of the gastrointestinal tract and periodic episodes. Despite the increasing number of related studies, the detailed pathogenesis of IBD has not been elucidated. In recent years, host-microbiota interactions in the pathogenesis of IBD have received extensive attention. Testes-specific protease 50 (TSP50) is a potential risk gene for IBD, but whether it can affect the susceptibility of colitis by regulating the gut microbiome is still unclear. Here, we showed that TSP50 deficiency in neural stem cells (NSCs) aggravated colitis in mice by altering intestinal microbiome. Mechanistically, TSP50 maintained the level of neurotransmitter acetylcholine (ACh) by degrading acetylcholinesterase (AChE), thereby maintaining intestinal mucosa and intestinal microecological homeostasis and reducing the susceptibility to colitis. These findings provide a new perspective on the interaction between host and commensal microbiota, which may be beneficial for developing potential therapeutic strategies for IBD.</p>\",\"PeriodicalId\":19370,\"journal\":{\"name\":\"npj Biofilms and Microbiomes\",\"volume\":\"11 1\",\"pages\":\"93\"},\"PeriodicalIF\":9.2000,\"publicationDate\":\"2025-06-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12134233/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"npj Biofilms and Microbiomes\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1038/s41522-025-00737-3\",\"RegionNum\":1,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOTECHNOLOGY & APPLIED MICROBIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"npj Biofilms and Microbiomes","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1038/s41522-025-00737-3","RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
TSP50 deficiency in neural stem cells aggravates colitis in mice by altering intestinal microbiome.
Inflammatory bowel disease (IBD) is a complex disease characterized by persistent chronic inflammation of the gastrointestinal tract and periodic episodes. Despite the increasing number of related studies, the detailed pathogenesis of IBD has not been elucidated. In recent years, host-microbiota interactions in the pathogenesis of IBD have received extensive attention. Testes-specific protease 50 (TSP50) is a potential risk gene for IBD, but whether it can affect the susceptibility of colitis by regulating the gut microbiome is still unclear. Here, we showed that TSP50 deficiency in neural stem cells (NSCs) aggravated colitis in mice by altering intestinal microbiome. Mechanistically, TSP50 maintained the level of neurotransmitter acetylcholine (ACh) by degrading acetylcholinesterase (AChE), thereby maintaining intestinal mucosa and intestinal microecological homeostasis and reducing the susceptibility to colitis. These findings provide a new perspective on the interaction between host and commensal microbiota, which may be beneficial for developing potential therapeutic strategies for IBD.
期刊介绍:
npj Biofilms and Microbiomes is a comprehensive platform that promotes research on biofilms and microbiomes across various scientific disciplines. The journal facilitates cross-disciplinary discussions to enhance our understanding of the biology, ecology, and communal functions of biofilms, populations, and communities. It also focuses on applications in the medical, environmental, and engineering domains. The scope of the journal encompasses all aspects of the field, ranging from cell-cell communication and single cell interactions to the microbiomes of humans, animals, plants, and natural and built environments. The journal also welcomes research on the virome, phageome, mycome, and fungome. It publishes both applied science and theoretical work. As an open access and interdisciplinary journal, its primary goal is to publish significant scientific advancements in microbial biofilms and microbiomes. The journal enables discussions that span multiple disciplines and contributes to our understanding of the social behavior of microbial biofilm populations and communities, and their impact on life, human health, and the environment.