Lipopolysaccharide induces functional ICAM-1 expression in rat alveolar epithelial cells in vitro

Lipopolysaccharide (LPS)-induced lung inflammation is known to increase pul monary intercellular adhesion molecule-1 (ICAM-1) expression. In the presen t study, L2 cells, a cell line of alveolar epithelial cells, were stimulate d with LPS, and ICAM-1 expression was studied. ICAM-1 protein on L2 cells p eaked at 6 (38% increase; P < 0.01) and 10 (48% increase; P < 0.001) h afte r stimulation with Escherichia coli and Pseudomonas aeruginosa LPS, respect ively. ICAM-1 mRNA expression was markedly increased, with a peak at 2-4 (E . coli) and 4-6 (P. aeruginosa) h. Adherence assays of neutrophils to LPS-s timulated L2 cells showed a threefold increase in adherence (P < 0.001). Pr etreatment of the neutrophils with antilymphocyte function-associated antig en-1 and anti-Mac-1 antibodies reduced adherence by 54% (P < 0.001). Analys is of immunofluorescence staining for ICAM-1 showed an exclusive apical exp ression of ICAM-1. These results indicate that LPS upregulates functional a ctive ICAM-1 on the apical part of the membrane in rat pneumocytes.