Role of Kinin B2 Receptor Signaling in Astrocyte-driven Neuroinflammation

The kallikrein-kinin system (KKS) plays a key role in inflammatory responses, but its specific contribution to neuroinflammation remains to be fully elucidated. The bradykinin B₂ receptor (B₂R), 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 B₂R to neuroinflammation using complementary in vitro and in vivo models. Lipopolysaccharide (LPS) stimulation significantly upregulated B₂R mRNA expression in primary astrocyte cultures and in the cortical tissue of wild-type mice. Pharmacological blockade of B₂R in astrocytes markedly suppressed the LPS-induced proinflammatory gene expression. In contrast, B₂R antagonism in vivo resulted in only partial attenuation of the neuroinflammatory response. Together, these findings suggest cell type-specific roles for B₂R and underscore its key contribution to astrocyte-mediated neuroinflammation.