Pulmonary microvascular alterations and injury induced by complement fragments: synergistic effect of complement activation, neutrophil sequestration, and prostaglandins.
Fragments of C5 that are generated at, or administered to, extravascular sites in the pulmonary parenchyma induced neutrophil infiltration, edema, tissue damage, and a complete inflammatory response. Generation of C5 fragments within the vascular system induced leukocyte sequestration in the pulmonary vasculature, but without detectable increased vascular permeability or neutrophil migration. By contrast, the combination of short episode of hypoxemia with the intravascular C5 activation led significant increases in pulmonary vascular permeability, mild endothelial alterations, and emigration of neutrophils. Infusion of 10 micrograms PGE2 into animals in which intravascular complement had been activated produced changes in the lungs that were similar to, though less severe than, the combination of hypoxia and complement activation.
D000818:Animals; D003167:Complement Activation; D003182:Complement C5 / Q000276:immunology; D015232:Dinoprostone; D008168:Lung / Q000276:immunology; D008833:Microcirculation / Q000276:immunology; D009504:Neutrophils / Q000276:immunology*; D011014:Pneumonia / Q000276:immunology; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000276:immunology; D011817:Rabbits
D003182:Complement C5; D011453:Prostaglandins; D011458:Prostaglandins E; D015232:Dinoprostone