Interleukin-1 stimulates prostacyclin production by cultured human endothelial cells by increasing arachidonic acid mobilization and conversion

Interleukin-1 (IL-1) induced slow, lasting activation of human endothelial cells (EC) to release prostacyclin (PGl₂). This was accompanied by endogenous ³H-arachidonic acid (₃H-AA) release and by a time-dependent increase in the cells' ability to convert exogenous AA. The continuous presence of IL-1 was not required, but about a 1-hour stimulation with the cytokine was sufficient to trigger the cells to synthesize PGl₂ for several hours. The spectrum of ₃H-AA conversion shows that, in addition to 6-ketoprostaglandin F_1α, prostaglandin F_2αalso was raised after IL-1. The recovery of PGl₂ synthesis after aspirin was faster in IL-1-treated EC than in control cells. These data define some of the characteristics of IL-1 stimulation of PGl₂ and suggest that this process is mediated both by endogenous AA mobilization and by an increase in cyclooxygenase activity.