Histone demethylase JMJD2D protects against enteric bacterial infection via up-regulating colonic IL-17F to induce β-defensin expression

• DOI: 10.1371/journal.ppat.1012316
• Publication Date: 2024-06-21T17:56:34Z
• Authors: Yong Zhang; Bei Li; Yilin Hong; Ping Luo; Zaifa Hong; Xiaochun Xia; Pingli Mo; Chundong Yu; Wenbo Chen
• Keywords: Citrobacter rodentium; Chromatin immunoprecipitation

Histone demethylase JMJD2D (also known as KDM4D) can specifically demethylate H3K9me2/3 to activate its target gene expression. Our previous study has demonstrated that protect intestine from dextran sulfate sodium (DSS)-induced colitis by activating Hedgehog signaling; however, involvement in host defense against enteric attaching and effacing bacterial infection remains unclear. The present was aimed investigate the role of bacteria underlying mechanisms. pathogen Citrobacter rodentium ( C . ) model used mimic clinical colonic infection. responses wild-type -/- mice oral were investigated. Bone marrow chimeric infected with expression knocked down CMT93 cells using small hairpin RNAs, Western blot real-time PCR assays performed these cells. relationship between STAT3 studied co-immunoprecipitation chromatin immunoprecipitation. significantly up-regulated epithelial response displayed an impaired clearance , more body weight loss, severe tissue pathology compared mice. exhibited IL-17F cells, which restricts inducing antimicrobial peptides. Accordingly, showed a decreased β-defensin-1, β-defensin-3, β-defensin-4 Mechanistically, activated signaling phosphorylation cooperated induce interacting been recruited promoter H3K9me3. demonstrates contributes through up-regulating β-defensin