The pulmonary response of C5 sufficient and deficient mice to immune complexes.

Evidence based on inhibitor studies has been presented showing that immune complex-induced alveolitis is complement dependent. This study was undertaken to define the contribution to this inflammatory process by the C5 molecule or its fragments. Congenic C5 sufficient (B10.D2/nSn) and C5 deficient (B10.D2/oSn) mice were challenged by intrapulmonary administration of antigen-antibody complexes of bovine serum albumin/rabbit antibovine serum albumin prepared at equivalence. Injury was assessed at 6 and 48 h time points by histologic examination, analysis of cells from pulmonary lavage, and determination of wet/dry weight ratios of both treated and untreated lungs. Histologic findings at both time points revealed a more generalized and severe inflammatory infiltrate in C5 sufficient animals with neutrophil accumulation, edema, and hemorrhage. The differences in neutrophil accumulation were confirmed by pulmonary lavage where C5 sufficient animals had a significantly greater number and percentage of neutrophils at both time points. Wet/dry weight ratios of lung also reflected more severe damage in the C5 sufficient animals. We concluded that the C5 molecule and its phlogistic fragments are important mediators of acute inflammation in immune complex lung injury, and, quantitatively, may be the most important stimuli for neutrophil accumulation in this model.