Journal
CIRCULATION
Volume 101, Issue 9, Pages 1019-1026Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.CIR.101.9.1019
Keywords
reperfusion; interleukins; nitric oxide; cell adhesion molecules
Funding
- NHLBI NIH HHS [R01-HL-59266] Funding Source: Medline
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Background-The anti-inflammatory cytokine interleukin-10 (IL-10) has been detected in the plasma of patients with myocardial ischemia/reperfusion. The aim of our study was to investigate the role of endogenously produced IL-10 in myocardial ischemia/reperfusion. Methods and Results-In the present study, we used wild-type and IL-10-deficient mice subjected to myocardial ischemia/reperfusion. Significant levels of IL-10 were produced in wild-type mice at 2 to 6 hours after myocardial reperfusion, The genetic deletion of IL-10 enhanced neutrophil infiltration into the reperfused tissues at 6 hours after reperfusion and increased infarct size and myocardial necrosis. Furthermore, in the absence of IL-10, an enhancement of the inflammatory response was seen, as demonstrated by increased plasma levels of tumor necrosis factor-alpha, nitrite/nitrate (breakdown products of NO), and increased tissue expression of intercellular adhesion molecule-1. Reperfusion for 24 hours was associated with a 75% mortality rate in IL-10- deficient mice, whereas no deaths occurred in the wild-type animals. Conclusions-The present findings provide the first direct evidence that endogenous IL-10 inhibits the production of tumor necrosis factor-ct and NO and serves to protect the isehemic and reperfused myocardium through the suppression of neutrophil recruitment.
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