Kinins and neuroinflammation: Dual effect on prostaglandin synthesis

The role of kinins, well known as peripheral inflammatory mediators, in the modulation of brain inflammation is unclear. The present data show that bradykinin, a bradykinin B2 receptor agonist, enhanced both basal and lipopolysaccharide-induced prostaglandin E2 synthesis in rat neonatal glial cells in culture. By contrast, Lys-des-Arg9-bradykinin, which is a kinin breakdown product and a selective bradykinin B1 receptor agonist, attenuated both basal and lipopolysaccharide-induced production of prostaglandin E2 in glia. These results suggest a feedback regulatory mechanism of kinins on glial cells, in which prostaglandin synthesis is initially enhanced by bradykinin (B2) and eventually blocked by the effect of the kinin breakdown product, acting on bradykinin B1 receptors.