Citrullination of CAMP exacerbating mucosal inflammation in inflammatory bowel disease.

ABSTRACT:

Background

Cathelicidin (CAMP), plays important roles in pathogen defense, immune regulation, and epithelial barrier maintenance. While previous studies have highlighted its protective function, the post-translational modifications and downstream immune-metabolic effects of CAMP in the pathogenesis of inflammatory bowel disease remain unclear.

Methods

A dextran sodium sulfate (DSS)-induced colitis mouse model was employed to assess the role of CAMP and its citrullination mediated by peptidyl arginine deiminase 4 (PAD4). Proteomic and metaproteomic analyses were performed to investigate microbiota composition and functional shifts. We generated gene-deficient mouse models, CAMP knockout (KO) and PAD4-KO mice, to dissect molecular mechanisms. Epithelial integrity, inflammatory

SUBMITTER: Chang X 

PROVIDER: S-EPMC12624863 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature