Abstract
To study the contribution of polymorphonuclear (PMN) and mononuclear (MN) phagocytes to the development of acute lung injury, we studied lung injury after intratracheal instillation of lipopolysaccharide (0.02 mg/kg) in guinea pigs previously exposed to heat-killed Corynebacterium parvum. In on group, cyclophosphamide was given to deplete peripheral PMNs. In another group, gadolinium chloride (GdCl3) was injected to suppress the function of MNs. Four hours after instillation of lippoly soccharide, the animals were killed, bronchoalveolar lavage was done, and the lungs were examined histopathologically. 125I-labeled albumin was injected to estimate the endothelial damage, and 131I-labeled albumin was injected to correct for blood contamination in the samples. In the group given cyclophosphamide, lung injury was no less than in the control group. In contrast, lung injury was less sever in the group given GdCl3 than in the control group. These findings suggest that MN are important in the pathogenesis of lung injury, especially in individuals who are immunologically primed by infection.
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