New insights into mechanisms of oxyradical and neutrophil mediated lung injury.
Acute lung injury in rats developing after systemic complement activation or deposition of IgG immune complexes is complement-dependent and oxygen radical-mediated. Recent findings have shown that a soluble complement receptor (sCR1) is capable of attenuating injury. Additional studies have also demonstrated requirements for the cytokines, TNF alpha, and for L-arginine derived products in lung injury that follows deposition of IgG immune complexes.
Ward
P A
PA
Department of Pathology, University of Michigan Medical School, Ann Arbor.
Mulligan
M S
MS
D000818:Animals; D001120:Arginine / Q000502:physiology; D004730:Endothelium, Vascular / Q000276:immunology; D006878:Hydroxides / Q000378:metabolism; D017665:Hydroxyl Radical; D007105:Immune Complex Diseases / Q000276:immunology*; D009504:Neutrophils / Q000276:immunology*; D010100:Oxygen / Q000502:physiology*; D011650:Pulmonary Alveoli / Q000276:immunology; D051381:Rats; D011951:Receptors, Complement / Q000502:physiology; D012128:Respiratory Distress Syndrome / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D006878:Hydroxides; D011951:Receptors, Complement; D014409:Tumor Necrosis Factor-alpha; D017665:Hydroxyl Radical; D001120:Arginine; D010100:Oxygen