cAMP mediates IL-1-induced lymphocyte penetration through endothelial monolayers.
 Endothelial cell incubated with IL-1 have been shown adhere more lymphocytes than nontreated endothelial cells.
 Here we demonstrate that IL-1 can also increase lymphocyte penetration through endothelial monolayers in vitro.
 IL-1 induced a transient increase in the number of lymphocytes penetrated through the endothelial monolayer into a filter in a time- and dose-dependent manner.
 This effect could be mimicked by increasing the cytosolic cAMP levels in the endothelial cells either by forskolin or dibutyryl-cAMP.
 Concomitantly we were able to show that IL-1 increased the cytosolic cAMP levels in endothelial cells.
 An inhibitor of adenylate cyclase, ddAdo, decreased both the IL-1-induced cAMP elevation and lymphocyte penetration.
 A protein kinase A inhibitor HA 1004 could inhibit the IL-1-induced lymphocyte penetration, where as protein kinase C (N-(2-guamidino-ethyl)-5-isoquinolinesyl foamide hydrocloride) and calcium-calmodulin (N-(6-aminohexyl)-5-chloro-1-naphthalensulfanamide) inhibitors had no effect.
 Adding dibutyryl-cGMP or calcium ionophore to the endothelial cells could not mimic IL-1-induced penetration and finally IL-1 did not induce PKC translocation in endothelial cells.
 These data support the view that IL-1 acts via cAMP as a second messenger in regard to lymphocyte penetration through endothelial cells.
 The above data demonstrate that IL-1-induced lymphocyte penetration through endothelial cells and that this IL-1-induced signal is transduced via cAMP in endothelial cells.
