# Role of Kinin B2 Receptor Signaling in Astrocyte-driven Neuroinflammation

## TL;DR

This study explores how the B2R receptor contributes to brain inflammation, showing it plays a key role in astrocyte-driven responses.

## Contribution

The study reveals cell type-specific roles of B2R in neuroinflammation, particularly in astrocytes.

## Key findings

- B2R mRNA expression increases in astrocytes and cortical tissue after LPS stimulation.
- Pharmacological B2R blockade suppresses proinflammatory gene expression in astrocytes.
- In vivo B2R antagonism only partially reduces neuroinflammation, suggesting cell-specific functions.

## Abstract

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.

B2R antagonism highlights cell type–specific roles in neuroinflammation. B2R pharmacological antagonism suppresses proinflammatory gene expression in astrocytes but shows limited in vivo efficacy, indicating differential functions across brain cell types.

The online version contains supplementary material available at 10.1007/s10571-026-01679-w.