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Published on: July 26, 2017
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Kinin B1 receptor and TLR4 interaction in inflammatory response
Carolina Batista1,2, João Victor Roza Cruz1, Joice Stipursky1
1Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rua César Pernetta, S/N, Prédio do ICB (Anexo ao Bloco F do CCS), 3º andar, sala LJ.03.01, Cidade Universitária, Rio de Janeiro, RJ, CEP: 21941-902, Brazil.
Summary
This study reveals a connection between Bradykinin B1 receptor (B1R) and Toll-like receptor 4 (TLR4) signaling. Their interaction in endothelial cells suggests potential therapeutic targets for inflammatory conditions.
Area of Science:
- Biochemistry
- Immunology
- Physiology
Background:
- Bradykinin B1 receptor (B1R) and Toll-like receptor 4 (TLR4) are implicated in inflammatory processes.
- Previous research suggests lipopolysaccharide (LPS) may stimulate B1R.
Purpose of the Study:
- To investigate the potential interaction between B1R and TLR4.
- To understand the functional consequences of this interaction on vascular tone.
Main Methods:
- Assessed the impact of agonists (DBK, LPS) on thoracic aorta membrane potential in wild-type and knockout mice (B1R, TLR4).
- Examined receptor expression and localization using staining and proximity ligation assays in endothelial cells.
Main Results:
- LPS induced hyperpolarization in wild-type and B1R knockout mice, involving potassium channels.
- DBK caused hyperpolarization in B1R and TLR4 knockout mice, mediated by B2R and potassium channels, respectively.
- Agonist treatment increased B1R staining and altered B1R/TLR4 co-localization in endothelial cells, suggesting receptor interaction.
Conclusions:
- Findings support a link between B1R and TLR4 signaling pathways.
- The interplay of these receptors in inflammation highlights them as potential targets for novel therapeutic strategies.
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