L13a-dependent translational control in macrophages limits the pathogenesis of colitis.

ABSTRACT: Sustained inflammation from infiltrated immune cells plays a pivotal role in the pathogenesis of ulcerative colitis (UC). Previously, we established the role of ribosomal protein L13a in the regulation of an inflammation-responsive post-transcriptional operon in myeloid cells. However, the role of this protein as a molecular cue to control the severity of colitis is not known. Here, we examined whether L13a-dependent translational control in macrophages could serve as an endogenous defense against colitis. The administration of dextran sodium sulfate induced experimental colitis in myeloid-specific L13a-knockout (KO) and control mice. Pathological scoring and injury to the colon mucosa evaluated the severity of colitis. The steady-state levels of several pro-inflammatory cytokines and chem

SUBMITTER: Poddar D 

PROVIDER: S-EPMC5101439 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature