Interleukin-1β and tumor necrosis factor-α upregulate interleukin-23 subunit p19 gene expression in human colonic subepithelial myofibroblasts
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- Published online on: January 1, 2005 https://doi.org/10.3892/ijmm.15.1.79
- Pages: 79-83
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Abstract
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.
