Butyrate ameliorates ulcerative colitis through targeting STING-dependent ER stress signaling and limiting CD4⁺ TRM T cells accumulation.

ABSTRACT: This study aimed to investigate the role of butyrate in regulating STING-induced endoplasmic reticulum stress (ERS) and CD4⁺ tissue-resident memory (TRM) T cells responses during the progression of ulcerative colitis (UC). Our results demonstrated that butyrate significantly alleviated dextran sulfate sodium (DSS)-induced colitis, as evidenced by restored intestinal epithelial architecture, reduced inflammatory cytokine, and decreased CD4⁺ TRM T cells. These protective effects were likely mediated through modulation of the STING-ERS pathway. Using a CT26 cell model, we further confirmed that STING activation promotes ERS, leading to enhanced secretion of inflammatory factors and subsequent induction of CD4⁺ TRM T cells. Importantly, butyrate effectively sup

SUBMITTER: Xiao T 

PROVIDER: S-EPMC12642100 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature