Epithelial overexpression of interleukin-32α in inflammatory bowel disease

M. Shioya, A. Nishida, Y. Yagi, A. Ogawa, T. Tsujikawa, S. Kim-Mitsuyama, A. Takayanagi, N. Shimizu, Y. Fujiyama, A. Andoh

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172 Citations (Scopus)


Interleukin (IL)-32 is a recently described proinflammatory cytokine, characterized by induction of nuclear factor (NF)-κB activation. We studied IL-32α expression in the inflamed mucosa of inflammatory bowel disease (IBD). We also investigated mechanisms regulating IL-32α expression. Tissue samples were obtained endoscopically or surgically from patients with ulcerative colitis (UC) (n = 10), Crohn's disease (CD) (n = 10), ischaemic colitis (n = 4) and normal colorectal tissues (n = 10). IL-32α expression was evaluated by standard immunohistochemical procedure. IL-32 mRNA expression was analysed by Northern blot. IL-32α was expressed weakly by colonic epithelial cells from normal individuals and subjects with ischaemic colitis. In the inflamed mucosa of IBD patients, epithelial IL-32α expression was increased markedly. In UC and CD patients, IL-32α expression was enhanced in affected mucosa compared to non-affected mucosa. In intestinal epithelial cell lines, expression of IL-32α mRNA and protein was enhanced by IL-1β, interferon (IFN)-γ and tumour necrosis factor (TNF)-α. A combination of TNF-α plus IFN-γ exerted synergistic effects. IL-32α induction by IL-1β and/or TNF-α was mediated by NF-κB activation. Epithelial IL-32α expression was increased in IBD patients, and in CD patients in particular. IL-32α might be involved in the pathophysiology of IBD as a proinflammatory cytokine and a mediator of innate immune response.

Original languageEnglish
Pages (from-to)480-486
Number of pages7
JournalClinical and Experimental Immunology
Issue number3
Publication statusPublished - 2007 Sept
Externally publishedYes


  • Cytokine
  • IBD
  • NOD2

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology


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