Bradykinin synergistically potentiates interleukin-1 induced bone resorption and prostanoid biosynthesis in neonatal mouse calvarial bones.

Interleukin-1 (IL-1) alpha and beta dose-dependently stimulated the release of 45Ca and the formation of prostaglandin E2 (PGE2) and PGI2 in cultured mouse calvarial bones, with IL-1 beta being the most potent agonist. Bradykinin (BK; 10 nmol/l) synergistically potentiated the effect of IL-1 alpha (10 pg/ml) and IL-1 beta (5 pg/ml) both on 45Ca release and on biosynthesis of PGE2 and PGI2. The capacity of BK to potentiate IL-1 beta induced 45Ca release and PGE2 formation was seen at concentrations of BK from 1-1000 nmol/l. These data indicate that BK and IL-1, which are formed in inflammatory processes, may act in concert to stimulate bone resorption in the vicinity of inflammatory lesions.