Increased immunoreactive rat lung ICAM-1 in oleic acid-induced lung injury.

Levels of immunoreactive ICAM-1 in rat lung were followed during the kinetic development of acute oleic acid-induced lung injury in the rat by the ELISA assay. Significant increases in ICAM-1 immunoreactivity were found on rat lung membranes within 30 min of oleic acid injection. The increased immunoreactive ICAM-1 persisted for the duration of the study (4 h) and paralleled lung injury as measured by decreased lung compliance. Enhanced ICAM-1 immunofluorescence was also observed on cryostat sections of lungs from oleic acid-treated rats. No direct effect of oleic acid on ICAM-1 levels of cultured human umbilical vein endothelial cells or rat lung microvascular endothelial cells was observed. This suggests that either oleic acid raises rat lung ICAM-1 levels on endothelial cells by an indirect mechanism or that oleic acid increases ICAM-1 levels on other cell types, such as fibroblasts or lung epithelial cells, by direct or indirect mechanisms. Some of the increased ICAM-1 may also be due to the accumulation of ICAM-1 containing circulating leukocytes in the lung. The role of ICAM-1 in the pathophysiology of oleic acid-induced lung injury and the mechanism by which oleic acid increases ICAM-1 expression in the lung therefore remain to be defined by future experimentation.