再灌注损伤
炎症
补体系统
缺血
抗体
发病机制
血管通透性
免疫学
医学
经典补体途径
病理
内科学
作者
Martin R. Weiser,Julian P. Williams,Francis D. Moore,Lester Kobzik,Minghe Ma,Herbert B. Hechtman,Michael C. Carroll
标识
DOI:10.1084/jem.183.5.2343
摘要
Reperfusion of ischemic tissue induces an acute inflammatory response that can result in necrosis and irreversible cell injury to both local vascular endothelium and parenchyma. To examine the pathogenesis of ischemia/reperfusion injury, we have used mice deficient in complement components C3, C4, or serum immunoglobulin in a hindlimb model of ischemia. We found that mice homozygous deficient in C3 or C4 were equally protected against reperfusion injury based on a significant reduction in leakage of radiolabeled albumin out of the vasculature. This demonstrates that classical pathway complement is an important factor in the initiation of inflammation following reperfusion. Furthermore, mice deficient in serum immunoglobulin were equally protected and this protection could be reversed by reconstitution with serum from normal mice. Thus, this report describes a novel mechanism for reperfusion injury that involves antibody deposition and activation of complement leading to inflammation permeability.
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