Oxygen radicals mediate endothelial cell damage by complement-stimulated granulocytes. An in vitro model of immune vascular damage.
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.
D001808:Blood Vessels / Q000473:pathology*; D002478:Cells, Cultured; D003165:Complement System Proteins / Q000378:metabolism*; D004727:Endothelium / Q000473:pathology; D005609:Free Radicals; D006098:Granulocytes / Q000502:physiology*; D006801:Humans; D007962:Leukocytes / Q000502:physiology*; D008247:Lysosomes / Q000201:enzymology; D009504:Neutrophils / Q000502:physiology; D010100:Oxygen; D009195:Peroxidase / Q000378:metabolism; D006435:Renal Dialysis / Q000009:adverse effects; D013481:Superoxides
D005609:Free Radicals; D013481:Superoxides; D003165:Complement System Proteins; D009195:Peroxidase; D010100:Oxygen