Bradykinin B1 and B2 receptor agonists synergistically potentiate interleukin-1-induced prostaglandin biosynthesis in human gingival fibroblasts.

The interactions between bradykinin (BK) and interleukin-1 (IL-1) on prostaglandin formation in human gingival fibroblasts have been studied. IL-1 alpha and IL-1 beta stimulated prostaglandin E2 (PGE2) formation in the gingival fibroblasts with IL-1 beta being the most potent agonist. The effects of both IL-1 alpha and IL-1 beta on PGE2 biosynthesis was synergistically potentiated by BK, in a dose-related manner. The synergistic interaction between IL-1 beta and BK on PGE2 production was seen both with B1 (des-Arg9-BK) and B2 (BK, Lys-BK) BK receptor agonists. No synergistic interaction between BK and IL-1 beta was seen on arachidonic acid release. These data suggest that BK and IL-1 act in concert to enhance prostanoid formation in inflammatory lesions and that the level of interaction is distal to phospholipase activity.