Levels of immunoreactive ICAM-1 in rat lung were followed during the k
inetic development of acute oleic acid-induced lung injury in the rat
by the ELISA assay. Significant increases in ICAM-1 immunoreactivity w
ere 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 war also observed on cr
yostat sections of lungs from oleic acid-treated rats. No direct effec
t of oleic acid on ICAM-1 levels of cultured human umbilical vein endo
thelial cells or rat lung microvascular endothelial cells was observed
. This suggests that either oleic acid raises rat lung ICAM-1 levels o
n endothelial cells by an indirect mechanism or that oleic acid increa
ses ICAM-1 levels on other cell types, such as fibroblasts or lung epi
thelial cells, by direct or indirect mechanisms. Some of the increased
ICAM-1 may also be due to the accumulation of ICAM-1 containing circu
lating leukocytes in the lung. The role of ICAM-1 in the pathophysiolo
gy of oleic acid-induced lung injury and the mechanism by which oleic
acid increases ICAM-1 expression in the lung therefore remain to be de
fined by future experimentation.