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Role of bradykinin B2 and B1 receptors in the local, remote, and systemic inflammatory responses that follow intestinal ischemia and reperfusion injury

Item Type:Article
Title:Role of bradykinin B2 and B1 receptors in the local, remote, and systemic inflammatory responses that follow intestinal ischemia and reperfusion injury
Creators Name:Souza, D.G. and Lomez, E.S.L. and Pinho, V. and Pesquero, J.B. and Bader, M. and Pesquero, J.L. and Teixeira, M.M.
Abstract:The administration of bradykinin may attenuate ischemia and reperfusion (I/R) injury by acting on B2Rs. Blockade of B2R has also been shown to ameliorate lesions associated with I/R injury. In an attempt to explain these contradictory results, the objective of the present work was to investigate the role of and interaction between B1 and B2 receptors in a model of intestinal I/R injury in mice. The bradykinin B 2R antagonist (HOE 140) inhibited reperfusion-induced inflammatory tissue injury and delayed lethality. After I/R, there was an increase in the expression of B1R mRNA that was prevented by HOE 140. In mice that were deficient in B1Rs (B1R-/- mice), inflammatory tissue injury was abrogated, and lethality was delayed and partially prevented. Pretreatment with HOE 140 reversed the protective anti-inflammatory and antilethality effects provided by the B1R -/- phenotype. Thus, B2Rs are a major driving force for B1R activation and consequent induction of inflammatory injury and lethality. In contrast, activation of B2Rs may prevent exacerbated tissue injury and lethality, an effect unmasked in B1R-/- mice and likely dependent on the vasodilatory actions of B2Rs. Blockade of B1Rs could be a more effective strategy than B 2 or B1/B2 receptor blockade for the treatment of the inflammatory injuries that follow I/R.
Keywords:Bradykinin, Bradykinin B1 Receptor, Bradykinin B2 Receptor, Chemokine CCL2, Cytokines, Inbred C57BL Mice, Inflammation Mediators, Interleukin-1, Interleukin-18, Intestines, Knockout Mice, Lung, Messenger RNA, Receptor Cross-Talk, Reperfusion Injury, Animals, Mice
Source:Journal of Immunology
ISSN:0022-1767
Publisher:American Association of Immunologists (U.S.A.)
Volume:172
Number:4
Page Range:2542-2548
Date:1 January 2004
Official Publication:https://doi.org/10.4049/jimmunol.172.4.2542
PubMed:View item in PubMed

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