Open AccessRab32‐related antimicrobial pathway is involved in the progression of dextran sodium sulfate‐induced colitis
Author(s) -
Xie Xiaodong,
Ni Qingshan,
Zhou Daxue,
Wan Ying
Publication year - 2018
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1002/2211-5463.12514
Subject(s) - colitis , pathogenesis , cxcl1 , immunology , immune system , chemokine , inflammatory bowel disease , cd11c , inflammation , innate immune system , medicine , biology , disease , pathology , phenotype , biochemistry , gene
Inflammatory bowel disease ( IBD ) is a multifactorial disease involving defective immune responses against invasive microbiota. Genes associated with innate immune responses to microbes have been highlighted in the pathogenesis of IBD . To determine the role of Rab32 in the pathogenesis of IBD , we administered dextran sodium sulfate ( DSS ) to CD 11c + cell‐specific Rab32 knockout ( CD 11c ‐Cre + Rab32 f/f ) mice to induce colitis. Rab32 deficiency in CD 11c + cells resulted in more severe disease progression and increased mortality. Histopathological analysis showed extensive damage to the colon mucosa in DSS ‐treated CD 11c ‐Cre + Rab32 f/f mice, including more severe damage to the epithelial layer and crypts, as well as more inflammatory cell infiltration. The pro‐inflammatory cytokines IL 1A, IL 1B, IL 6, and CSF 3 and chemokines CXCL 1 and CXCL 2 were significantly increased, and the frequency of CD 11b + Ly6G + neutrophils was higher in CD 11c ‐Cre + Rab32 f/f colitis mice. Furthermore, CD 11c + cells deficient for Rab32 exhibited a significant increase in bacterial translocation in inflamed colon tissue. The present data demonstrate that Rab32 knockout in CD 11c + cells aggravates the development of DSS ‐induced colitis and suggest that the Rab32‐related antimicrobial pathway is involved in the pathogenesis of IBD .