Epithelial expression of interleukin-37b in inflammatory bowel disease.

Abstract

Interleukin (IL)-37 is a member of the IL-1 cytokine family. We investigated IL-37b expression in the inflamed mucosa of inflammatory bowel disease (IBD) patients. Furthermore, we analysed IL-37b expression in human colonic epithelial cells. The human colonic epithelial cell line T84 and human colonic subepithelial myofibroblasts (SEMFs) were used. IL-37b expression in the IBD mucosa was evaluated by immunohistochemistry. IL-37b mRNA and protein expression were determined by real time-polymerase chain reaction (PCR) and Western blotting, respectively. IL-37b was not detected in the normal colonic mucosa. In the inflamed mucosa of IBD patients, epithelial IL-37b expression was increased markedly. In ulcerative colitis (UC) and Crohn's disease (CD) patients, IL-37b expression was enhanced in the affected mucosa. In the intestinal epithelial cell line T84, the expression of IL-37b mRNA and protein was enhanced by tumour necrosis factor (TNF)-α. This IL-37b induction by TNF-α was mediated by nuclear factor (NF)-κB and activator protein (AP)-1 activation. Furthermore, IL-37b inhibited TNF-α-induced interferon-γ-inducible protein (IP)-10 expression significantly in human colonic SEMFs. Epithelial IL-37b expression was increased in IBD patients, especially UC patients. IL-37b may be involved in the pathophysiology of IBD as an anti-inflammatory cytokine and an inhibitor of both innate and acquired immune responses.

• Authors: H Imaeda, K Takahashi, T Fujimoto, E Kasumi, H Ban, S Bamba, H Sonoda, T Shimizu, Y Fujiyama, A Andoh
• Journal: Clinical and experimental immunology (Clin Exp Immunol) Vol. 172 Issue 3 Pg. 410-6 (Jun 2013) ISSN: 1365-2249 [Electronic] England
• PMID: 23600829 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: © 2013 British Society for Immunology.

Chemical References

• CXCL10 protein, human
• Chemokine CXCL10
• IL37 protein, human
• Interleukin-1
• NF-kappa B
• RNA, Messenger
• Transcription Factor AP-1
• Tumor Necrosis Factor-alpha
• Phosphatidylinositol 3-Kinases

Topics

• Adaptive Immunity
• Caco-2 Cells
• Case-Control Studies
• Cells, Cultured
• Chemokine CXCL10 (genetics, metabolism)
• Colitis, Ulcerative (genetics, immunology, metabolism, pathology)
• Crohn Disease (genetics, immunology, metabolism, pathology)
• Gene Expression (drug effects)
• Humans
• Immunity, Innate
• Inflammatory Bowel Diseases (genetics, immunology, metabolism, pathology)
• Interleukin-1 (genetics, metabolism)
• Intestinal Mucosa (drug effects, immunology, metabolism, pathology)
• MAP Kinase Signaling System
• Myofibroblasts (drug effects, immunology, metabolism, pathology)
• NF-kappa B (metabolism)
• Phosphatidylinositol 3-Kinases (metabolism)
• RNA, Messenger (genetics, metabolism)
• Transcription Factor AP-1 (metabolism)
• Tumor Necrosis Factor-alpha (pharmacology)