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Published on: June 8, 2012
Lipopolysaccharide induces functional ICAM-1 expression in rat alveolar epithelial cells in vitro
C Madjdpour1, B Oertli, U Ziegler
1Institute of Anesthesiology, University of Zurich, 8091 Zurich, Switzerland.
Insights
Lipopolysaccharide (LPS) increases lung inflammation by upregulating intercellular adhesion molecule-1 (ICAM-1) on alveolar cells. This enhances neutrophil adherence, crucial for immune response in the lungs.
Area of Science:
- Pulmonary immunology
- Cellular biology
- Inflammation research
Background:
- Lipopolysaccharide (LPS) is a potent inducer of inflammation.
- Increased pulmonary intercellular adhesion molecule-1 (ICAM-1) is associated with LPS-induced lung inflammation.
- Alveolar epithelial cells play a role in the inflammatory response.
Purpose of the Study:
- To investigate the effect of LPS on ICAM-1 expression in rat alveolar epithelial cells (L2 cells).
- To determine the functional consequence of LPS-induced ICAM-1 upregulation on neutrophil adherence.
- To characterize the localization of ICAM-1 on LPS-stimulated alveolar cells.
Main Methods:
- L2 cells were stimulated with Escherichia coli and Pseudomonas aeruginosa LPS.
- ICAM-1 protein and mRNA expression levels were quantified over time.
- Neutrophil adherence assays were performed on LPS-stimulated L2 cells.
- Immunofluorescence staining was used to determine ICAM-1 localization.
Main Results:
- LPS significantly increased ICAM-1 protein expression in L2 cells, peaking at 6-10 hours.
- ICAM-1 mRNA levels also increased markedly, with peaks at 2-6 hours depending on LPS source.
- Neutrophil adherence to LPS-stimulated L2 cells increased threefold and was partially inhibited by anti-LFA-1 and anti-Mac-1 antibodies.
- ICAM-1 was found exclusively on the apical surface of LPS-stimulated rat pneumocytes.
Conclusions:
- LPS upregulates functional ICAM-1 on the apical membrane of rat alveolar epithelial cells.
- This upregulation enhances neutrophil adherence, contributing to lung inflammation.
- The findings highlight the role of alveolar epithelial ICAM-1 in LPS-induced pulmonary inflammation.
Abstract:
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.
