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.