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

J Clin Invest. 1978 May;61(5):1161-7. doi: 10.1172/JCI109031.


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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Blood Vessels / pathology*
  • Cells, Cultured
  • Complement System Proteins / metabolism*
  • Endothelium / pathology
  • Free Radicals
  • Granulocytes / physiology*
  • Humans
  • Leukocytes / physiology*
  • Lysosomes / enzymology
  • Neutrophils / physiology
  • Oxygen*
  • Peroxidase / metabolism
  • Renal Dialysis / adverse effects
  • Superoxides


  • Free Radicals
  • Superoxides
  • Complement System Proteins
  • Peroxidase
  • Oxygen