Complement-induced granulocyte aggregation in vivo.
Previous studies from our laboratories have demonstrated that granulocytes (PMNs), when exposed to activated complement (C) (specifically C5a), will aggregate and be provoked to damage cultured endothelial cells in vitro; it was postulated that these phenomena might also occur in vivo, constituting a previously unsuspected mechanism of immune tissue damage. The studies here presented confirm by intravital microscopy that PMN aggregation and leukoembolization in fact occur in live animals when C is activated or C5a is infused, and that these are accompanied by extravasation of plasma proteins in a pattern suggesting endothelial damage. It is concluded that altered microvascular behavior of PMNs is a possible pathogenetic mechanism in disease states associated with C activation.
D000818:Animals; D001011:Aorta; D001160:Arterioles / Q000187:drug effects / Q000473:pathology; D002449:Cell Aggregation; D003167:Complement Activation; D003165:Complement System Proteins / Q000276:immunology*; D004617:Embolism / Q000209:etiology / Q000276:immunology; D004727:Endothelium / Q000473:pathology; D005260:Female; D006098:Granulocytes / Q000276:immunology*; D008775:Methylprednisolone / Q000494:pharmacology; D008856:Microscopy, Fluorescence / Q000379:methods; D009504:Neutrophils / Q000276:immunology; D051381:Rats; D014743:Videotape Recording
D003165:Complement System Proteins; D008775:Methylprednisolone