Role of kinin B(2) receptor signaling in astrocyte-driven neuroinflammation

The kallikrein–kinin system (KKS) plays a key role in inflammatory responses, but its specific contribution to neuroinf lammation remains to be fully elucidated. The bradykinin B(2) receptor (B(2)R), a principal effector of the KKS, is widely expressed in both neuronal and glial cells in the rodent and human brain. In this study, we investigated the molecular contribution of B(2)R to neuroinflammation using complementary in vitro and in vivo models. Lipopolysaccharide (LPS) stimulation significantly upregulated B(2)R mRNA expression in primary astrocyte cultures and in the cortical tissue of wild-type mice. Pharmacological blockade of B(2)R in astrocytes markedly suppressed the LPS-induced proinflammatory gene expression. In contrast, B(2)R antagonism in vivo resulted in only partial attenuation of the neuroinflammatory response. Together, these findings suggest cell type–specific roles for B(2)R and underscore its key contribution to astrocytemediated neuroinflammation.