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<p>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 B<sub>2</sub> receptor (B<sub>2</sub>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<sub>2</sub>R to neuroinflammation using complementary in vitro and in vivo models. Lipopolysaccharide (LPS) stimulation significantly upregulated B<sub>2</sub>R mRNA expression in primary astrocyte cultures and in the cortical tissue of wild-type mice. Pharmacological blockade of B<sub>2</sub>R in astrocytes markedly suppressed the LPS-induced proinflammatory gene expression. In contrast, B<sub>2</sub>R antagonism in vivo resulted in only partial attenuation of the neuroinflammatory response. Together, these findings suggest cell type–specific roles for B<sub>2</sub>R and underscore its key contribution to astrocyte-mediated neuroinflammation.</p> Graphical Abstract <p>B<sub>2</sub>R antagonism highlights cell type–specific roles in neuroinflammation. B<sub>2</sub>R pharmacological antagonism suppresses proinflammatory gene expression in astrocytes but shows limited in vivo efficacy, indicating differential functions across brain cell types.</p> <p></p>

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Role of Kinin B2 Receptor Signaling in Astrocyte-driven Neuroinflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月29日

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  • Mariana R. Tavares,
  • Gabriel R. Estrela,
  • Luana Lavezo,
  • Juliene L. S. Silva,
  • Ronaldo C. Araujo,
  • Michael Bader,
  • Frederick Wasinski

摘要

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.

Graphical Abstract

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.