Journal of Gastroenterology

, Volume 45, Issue 10, pp 999–1007

Interleukin-33 expression is specifically enhanced in inflamed mucosa of ulcerative colitis

Authors

  • Ayako Kobori
    • Department of MedicineShiga University of Medical Science
  • Yuhki Yagi
    • Department of MedicineShiga University of Medical Science
  • Hirotsugu Imaeda
    • Department of MedicineShiga University of Medical Science
  • Hiromitsu Ban
    • Department of MedicineShiga University of Medical Science
  • Shigeki Bamba
    • Department of MedicineShiga University of Medical Science
  • Tomoyuki Tsujikawa
    • Department of MedicineShiga University of Medical Science
  • Yasuharu Saito
    • Department of MedicineShiga University of Medical Science
  • Yoshihide Fujiyama
    • Department of MedicineShiga University of Medical Science
    • Division of Mucosal Immunology, Graduate School of MedicineShiga University of Medical Science
Original Article—Alimentary Tract

DOI: 10.1007/s00535-010-0245-1

Cite this article as:
Kobori, A., Yagi, Y., Imaeda, H. et al. J Gastroenterol (2010) 45: 999. doi:10.1007/s00535-010-0245-1

Abstract

Background

Interleukin (IL)-33 is a cytokine belonging to the IL-1 family. IL-33 has been shown to elicit a Th2-like cytokine response in immune cells. In this study, we investigated IL-33 expression in the inflamed mucosa of patients with inflammatory bowel disease (IBD), and characterized the molecular mechanisms responsible for IL-33 expression in human colonic subepithelial myofibroblasts (SEMFs).

Methods

IL-33 mRNA expression was determined by real-time polymerase chain reaction (PCR). IL-33 expression in the IBD mucosa was evaluated by immunohistochemical methods.

Results

IL-33 mRNA expression was significantly elevated in active lesions from patients with ulcerative colitis (UC), but was not detected in inactive lesions from UC patients or in lesions from patients with either active or inactive Crohn’s disease. Colonic SEMFs were identified as a major source of IL-33 in the mucosa. IL-1β and tumor necrosis factor-α (TNF-α) significantly enhanced IL-33 mRNA and protein expression in isolated colonic SEMFs. IL-1β and TNF-α did not affect IL-33 expression in intestinal epithelial cell lines (HT-29 and Caco-2 cells). This IL-1β- and TNF-α-induced IL-33 mRNA expression was mediated by p42/44 mitogen activated protein kinase (MAPK) pathway-dependent activation of nuclear factor (NF)-κB and activator protein (AP)-1.

Conclusions

IL-33, derived from colonic SEMFs, may play an important role in the pathophysiology of UC.

Keywords

IBDCytokineBiomarker

Copyright information

© Springer 2010