Effect of circulating neutrophil depletion on lung injury induced by inhaled silica particles

into the alveolar region during inflammation may injure the lung parenchyma by releasing cytotoxic oxygen radi-cals and proteases. Because brief exposures to crystalline silica elicit recruitment of PMNs into the alveolar region, which is strongly correlated with parameters of cytotoxic-ity, increased alveolar epithelial permeability, and lysosomal enzyme release, we sought to evaluate the potential role of PMNs in silica-induced lung injury. Rats were depleted of PMNs by administration of an anti-rat PMN antiserum prior to exposure to siica Pul-monary inflammatory responses to silica in this group were compared to responses in normal silica-exposed rats as well as sham-exposed normal or PMN-depleted rats. Bronchoalveolar lavage fluids from normal, silica-exposed rats contained 9.7 x 106 PMNs immediately af-ter exposurc’for 3 days, compared to 0.01 x 106 PMNs for both normal or PMN-depleted, sham-exposed rats. Bron-choalveolar lavage fluids from successfully PMN-depleted, exposed rats contained significantly fewer (0.7 x 106) PMNs compared to normal silica-exposed rats. In both groups of silica-exposed rats, a variety of bio-chemical indicators of lung injury were increased significantly compared to measurements from both sham-exposed groups, but there were no differences between PMN-depleted and normal silica-exposed groups. The results suggest that recruitment of PMNs into the alveolar region is not a necessary prerequisite for the observed in-creases in biochemical indicators of silica-induced acut