Interleukin 1‐induced lymphocyte binding to endothelial cells. Role of cAMP as a second messenger

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Abstract
Interleukin 1 (IL 1) is a potent protein mediator of inflammation. Among other things it increases the number of lymphocytes adhering to endothelial cell monolayers. We analyzed the signal transduction during IL 1‐induced lymphocyte binding. Dibutyryl cyclic AMP, which is a cAMP analog able to penetrate into the cytosol, increased lymphocyte binding to the same extent as IL 1. Direct activation of adenylate cyclase by forskolin enhanced also lymphocyte binding. IL 1 increased the level of cytosolic cAMP in a time‐ and dose‐dependent manner measured with radioimmunoassay. 2′, 5′‐Dideoxyadenosine, which is an inhibitor of adenylate cyclase, decreased both the IL 1‐induced lymphocyte binding to endothelial cells and elevation in cytosolic cAMP levels. Lymphocyte binding increased with cytosolic cAMP levels in accordance with elevation of IL 1 concentration. These results suggest that cAMP is essential in signal transduction during IL 1‐induced lymphocyte binding to cultured endothelial cell monol‐layers.