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.
Reperfusion injury of ischemic skeletal muscle is mediated by natural antibody and complement
Martin R. Weiser,J. Williams,F. Moore,L. Kobzik,Minghe Ma,H. Hechtman,M. Carroll
Published 1996 in Journal of Experimental Medicine
ABSTRACT
PUBLICATION RECORD
- Publication year
1996
- Venue
Journal of Experimental Medicine
- Publication date
1996-05-01
- Fields of study
Biology, Medicine
- Identifiers
- External record
- Source metadata
Semantic Scholar, PubMed
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