Interleukin-1β and tumor necrosis factor-α upregulate interleukin-23 subunit p19 gene expression in human colonic subepithelial myofibroblasts
The recently identified cytokine interleukin-23 (IL-23) consists of p19 and p40 subunits. The major cellular source of IL-23 is dendritic cells and/or macrophages. We investigated the expression of IL-23 p19 mRNA in human colonic subepithelial myofibroblasts (SEMFs). p19 mRNA was not expressed in unstimulated SEMFs, but IL-1β and TNF-α strongly induced p19 mRNA expression in these cells. The effects of IL-1β were much stronger than those of TNF-α. These responses were observed in both a dose- and time-dependent manner. Furthermore, these cytokines acted synergistically when used in combination. A blockade of NF-κB activation by the overexpression of a stable form of IκBα completely blocked these responses, indicating that the induction of p19 mRNA expression by IL-1β and TNF-α was mediated by the NF-κB activation pathway. In conclusion, this is the first report demonstrating that IL-23 p19 mRNA is inducible in colonic myofibroblasts by IL-1β and TNF-α. The p19 expression in these cells might play a role in mucosal immune responses.
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Document Type: Research Article
Affiliations: Department of Internal Medicine, Shiga University of Medical Science, Otsu 520-2192, Japan
Publication date: January 1, 2005
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- The International Journal of Molecular Medicine is a monthly, peer-reviewed journal devoted to the publication of high quality studies related to the molecular mechanisms of human disease. The journal welcomes research on all aspects of molecular and clinical research, ranging from biochemistry to immunology, pathology, genetics, human genomics, microbiology, molecular pathogenesis, molecular cardiology, molecular surgery and molecular psychology.
The International Journal of Molecular Medicine aims to provide an insight for researchers within the community in regard to developing molecular tools and identifying molecular targets for the diagnosis and treatment of a diverse number of human diseases.
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