作者: Jinfeng Lu , Zhenshan Liu , Junjie Zhao , Hongxiang Sun , Ningbo Wu
关键词: Epithelium 、 Intestinal epithelium 、 Microbiology 、 Biology 、 Population 、 Antimicrobial peptides 、 Dysbiosis 、 Kinase 、 Colitis 、 Bacteria
摘要: Dysregulation of the immune barrier function intestinal epithelium can often result in dysbiosis. In this study we report a novel role epithelial cell (IEC)-derived liver kinase B1 (LKB1) suppressing colitogenic microbiota. IEC-specific deletion LKB1 (LKB1ΔIEC) resulted an increased susceptibility to dextran sodium sulfate (DSS)-induced colitis and definitive shift composition microbial population mouse intestine. Importantly, transfer microbiota from LKB1ΔIEC mice was sufficient confer DSS-induced wild-type recipient mice. Collectively, data indicate that deficiency cells nurtures outgrowth bacteria commensal community. addition, reduced production IL-18 antimicrobial peptides colon. Administration exogenous restored expression peptides, corrected several bacterial genera, rescued sensitivity DSS challenge. Taken together, our reveals important IECs for by expression.