What question did this study set out to answer?

This study aims to investigate how oxygen radicals from granulocytes contribute to endothelial cell damage during complement activation.

May 1, 1978Journal of Clinical Investigation1,114 citationsOpen Access

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

TST Sacks CMCharles F. Moldow PCP R Craddock

Key Points

This study aims to investigate how oxygen radicals from granulocytes contribute to endothelial cell damage during complement activation.
Developed an in vitro model using 51Cr-labeled human umbilical vein endothelial cell cultures.
Exposed endothelial cells to activated complement to study the effects of granulocytes on cell integrity.
Utilized cytochalasin B to assess the necessity of granulocyte-endothelial cell proximity for injury.
Granulocytes induce endothelial damage primarily through the action of oxygen radicals.
C5a is identified as the complement component responsible for granulocyte-mediated cytotoxicity.
Close proximity of granulocytes and endothelial cells enhances the extent of cell injury.

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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