IL-18 maintains the homeostasis of mucosal immune system via inflammasome-independent but microbiota-dependent manner
IL-18通过共生菌依赖但炎症小体非依赖的方式维持肠道免疫稳态作者机构:Hefei National Laboratory for Physical Sciences at MicroscaleThe CAS Key Laboratory of Innate Immunity and Chronic DiseaseSchool of Basic Medical SciencesDivision of Life Sciences and MedicineUniversity of Science and Technology of ChinaHefei 230027China The Center for MicrobesDevelopment and HealthKey Laboratory of Molecular Virology and ImmunologyInstitut Pasteur of ShanghaiChinese Academy of SciencesShanghai 200031China CAS Center for Excellence in Cell and Molecular BiologyUniversity of Science and Technology of ChinaHefei 230027China
出 版 物:《Science Bulletin》 (科学通报(英文版))
年 卷 期:2021年第66卷第20期
页 面:2115-2123,M0004页
核心收录:
学科分类:1001[医学-基础医学(可授医学、理学学位)] 100102[医学-免疫学] 10[医学]
基 金:supported by the National Key Research and Development Program of China(2020YFA0509101) the National Natural Science Foundation of China(91742202,81722022,and 81821001) the Young Talent Support Program and Fundamental Research Funds for the Central Universities and the University Synergy Innovation Program of Anhui Province(GXXT-2019-026)
主 题:Dysbiosis Immune system IL-18 Inflammasome
摘 要:Inflammasomes and their product interleukin 18(IL-18)play important roles in gut microbiota monitoring and homeostasis,and their loss of function could lead to microbiota dysbiosis and accelerate disease ***,the impacts of the resulting microbiota dysbiosis on the mucosal immune system are largely ***,we show that dysbiotic microbiota from Il18^(-/-)mice induced immune cell loss in the small intestine(SI)in an inflammasome-independent *** experiments revealed that the immunotoxic phenotype of these microbiota was transferable to wild type(WT)mice and induced immune cell death through the receptor-interacting protein kinase 3(RIP3)-mixed lineage kinase domain like pseudokinase(MLKL)*** of microbiota composition identified two types of bacteria at the genus level,Ureaplasma and Parasutterella,that accumulated in Il18^(-/-)mice and negatively mediated changes in immune cells in the ***,dysbiosis in Il18^(-/-)mice also contributed to increased susceptibility to Listeria ***,our results demonstrate that IL-18 is essential to microbiota homeostasis and that dysbiotic microbiota could significantly shape the landscape of the immune system.