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Title: Interleukin-32α expression in human colonic subepithelial myofibroblasts. Author: Yagi Y, Andoh A, Imaeda H, Aomatsu T, Ohsaki R, Inatomi O, Bamba S, Tsujikawa T, Shimizu T, Fujiyama Y. Journal: Int J Mol Med; 2011 Feb; 27(2):263-8. PubMed ID: 21152864. Abstract: Interleukin (IL)-32 is a recently described proinflammatory cytokine, characterized by induction of nuclear factor (NF)-κB activation. We studied IL-32α expression in human colonic subepithelial myofibroblasts (SEMFs). Colonic SEMFs were isolated from normal human colon tissue. IL-32α protein expression was evaluated by Western blot analyses, and IL-32α mRNA expression was analyzed by real-time PCR. IL-32α mRNA was weakly expressed without a stimulus, and its expression was markedly enhanced by IL-1ß and TNF-α. IL-1ß and TNF-α enhanced intracellular accumulation of IL-32α protein, but IL-32α was not detected in supernatants. Each cytokine dose- and time-dependently induced IL-32α mRNA expression. An inhibitor of phosphatidylinositol 3-kinase (LY294002) significantly suppressed IL-1ß- and TNF-α-induced IL-32α mRNA expression, although MAPK inhibitors had no effect. Akt activation in response to these cytokines was confirmed by Western blotting. Blockade of NF-κB activation by an adenovirus expressing a stable mutant form of IκBα markedly suppressed IL-1ß- and TNF-α-induced IL-32α mRNA expression. Human colonic SEMFs expressed IL-32α in response to IL-1ß and TNF-α. IL-32α mRNA expression depends on the phosphatidylinositol 3-kinase and the NF-κB system.[Abstract] [Full Text] [Related] [New Search]