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Interleukin‐1 up‐regulates transcription of its own receptor in a human fibroblast cell line TIG‐1: role of endogenous PGE2 and cAMP

The regulation of interleukin‐1 receptor (IL‐1R) mRNA expression by IL‐1 in a human lung fibroblast cell line (TIG‐1) was investigated. After 2 h of stimulation with human recombinant IL‐1α or IL‐1β, the levels of T cell/fibroblast‐type IL‐1R mRNA increased, and the elevation was sustained for at least 72 h. IL‐1 also stimulated synthesis of prostaglandin E2 (PGE2) and secondary cAMP accumulation. Exogenously added PGE2 increased the levels of both IL‐1R mRNA and intracellular cAMP. Forskolin, cholera toxin and 8‐Bromo adenosine (8‐Br‐cAMP) all increased IL‐1R mRNA levels. Indomethacin blocked IL‐1 stimulation of IL‐1R mRNA expression, PGE2 production and cAMP. 125I‐labeled IL‐1α‐binding studies showed that this cell line expresses 2.6 × 104 IL‐1R per cell with a Kd of 5.1 × 10−10 M. After treatment of the cells with IL‐1, the level of IL‐1R increased over that of control cells. PGE2 also increased IL‐1R without alteration in its affinity. Cross‐linking experiments indicate that this cell line expresses the 80‐kDa receptor molecule before and after treatment with PGE2; the molecular mass corresponds to the T cell/fibroblast type IIL‐1R. These results indicate that IL‐1 does not directly stimulate expression of IL‐1R mRNA or cell surface IL‐1R, but only indirectly by stimulation of endogenous PGE2.