Lipopolysaccharide induces functional ICAM-1 expression in rat alveolar epithelial cells in vitro.
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.
Madjdpour
C
C
Institute of Anesthesiology, University of Zurich, 8091 Zurich, Switzerland.
Oertli
B
B
Ziegler
U
U
Bonvini
J M
JM
Pasch
T
T
Beck-Schimmer
B
B
D000818:Animals; D002448:Cell Adhesion / Q000187:drug effects; D002460:Cell Line; D004847:Epithelial Cells / Q000378:metabolism; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009504:Neutrophils / Q000502:physiology; D011650:Pulmonary Alveoli / Q000166:cytology / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D014018:Tissue Distribution
D008070:Lipopolysaccharides; D012333:RNA, Messenger; D018799:Intercellular Adhesion Molecule-1