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Regulation of levels of IL‐1 mRNA in human fibroblasts

Interleukin‐1 (IL‐1) has a crucial role in host defenses, inflammatory processes, and tissue homeostasis. A wide variety of cells produce this protein in response to a number of extracellular stimuli including microorganisms, antigenic stimuli, and products from other cells. Regulation of IL‐1 production at the molecular level is poorly understood. We studied expression, intracellular signals, and posttranscriptional regulation of IL‐1 mRNA in human mesenchymal cells by using Northern blot analysis. Tumor necrosis factor alpha (TNFα) and activators of protein kinase C including 12‐O‐tetradecanoylphorbol‐13‐acetate (TPA) and teleocidin induced the accumulation of IL‐1β mRNA in human fibroblasts (WI‐38). Effect of TNFα was not blocked by inhibitors of either protein synthesis (cycloheximide) or protein kinase C activity. Accumulation of IL‐1β mRNA was also increased by a calcium ionophore (A23187) and an inhibitor of the Na+/K+ pump (ouabain); both compounds are known to increase cytoplasmic levels of Ca++. Stability of IL‐1β mRNA in fibroblasts exposed to TPA was more than fourfold greater than after fibroblasts were exposed to either TNFα or cycloheximide. This suggests that posttranscriptional stabilization of IL‐1β mRNA is a major mechanism leading to accumulation of IL‐1β mRNA after activation of PKC in fibroblasts. Fibroblasts did not express IL‐1α mRNA after exposure to stimuli which induced the accumulation of IL‐1β mRNA. In summary, several different pathways regulate levels of IL‐1β mRNA in human mesenchymal cells.