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Am J Physiol Lung Cell Mol Physiol 278: L572-L579, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 3, L572-L579, March 2000

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

Caveh Madjdpour1,2, Beat Oertli2, Urs Ziegler3, John M. Bonvini2, Thomas Pasch1, and Beatrice Beck-Schimmer1,2

1 Institute of Anesthesiology, 2 Institute of Physiology, and 3 Institute of Anatomy, University of Zurich, 8091 Zurich, Switzerland

Lipopolysaccharide (LPS)-induced lung inflammation is known to increase pulmonary intercellular adhesion molecule-1 (ICAM-1) expression. In the present study, L2 cells, a cell line of alveolar epithelial cells, were stimulated with LPS, and ICAM-1 expression was studied. ICAM-1 protein on L2 cells peaked at 6 (38% increase; P < 0.01) and 10 (48% increase; P < 0.001) h after stimulation with Escherichia coli and Pseudomonas aeruginosa LPS, respectively. 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-stimulated L2 cells showed a threefold increase in adherence (P < 0.001). Pretreatment of the neutrophils with anti-lymphocyte function-associated antigen-1 and anti-Mac-1 antibodies reduced adherence by 54% (P < 0.001). Analysis of immunofluorescence staining for ICAM-1 showed an exclusive apical expression of ICAM-1. These results indicate that LPS upregulates functional active ICAM-1 on the apical part of the membrane in rat pneumocytes.

intercellular adhesion molecule-1; alveolar epithelium; endotoxin; neutrophil adherence


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