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Research Article Free access | 10.1172/JCI109031

Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.

T Sacks, C F Moldow, P R Craddock, T K Bowers, and H S Jacob

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Published May 1, 1978 - More info

Published in Volume 61, Issue 5 on May 1, 1978
J Clin Invest. 1978;61(5):1161–1167. https://doi.org/10.1172/JCI109031.
© 1978 The American Society for Clinical Investigation
Published May 1, 1978 - Version history
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Abstract

During hemodialysis, alternative pathway complement activation leads to pulmonary sequestration of granulocytes, with loss of pulmonary vascular endothelial integrity and, at times, protein-rich pulmonary edema. An in vitro model of this phenomenon was constructed utilizing 51Cr-labeled human umbilical vein endothelial cell cultures. In this system, granulocytes, when exposed to activated complement (C), induce endothelial damage; this injury is mediated primarily by oxygen radicals produced by the granulocytes. C5a appears to be the C component responsible for granulocyte-induced cytotoxicity; studies with cytochalasin B-treated granulocytes suggest that close approximation of the granulocytes and endothelial cells is necessary for maximal cell injury.

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