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Am J Physiol Lung Cell Mol Physiol 278: L245-L252, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 2, L245-L252, February 2000

Effect of steroid on hyperoxia-induced ICAM-1 expression in pulmonary endothelial cells

Yukio Suzuki1, Kazumi Nishio1, Kei Takeshita2, Osamu Takeuchi3, Kenji Watanabe4, Nagato Sato2, Katsuhiko Naoki2, Hiroyasu Kudo2, Takuya Aoki2, and Kazuhiro Yamaguchi2

Departments of 1 Internal Medicine, 3 Biomedical Research, and 4 Oriental Medicine, Kitasato Institute Hospital, Tokyo 108-8642; and 2 Department of Medicine, School of Medicine, Keio University, Tokyo 160-8582, Japan

Intercellular adhesion molecule-1 (ICAM-1) of the vascular endothelium plays a key role in the development of pulmonary oxygen toxicity. We studied the effect of steroid on hyperoxia-induced ICAM-1 expression using cultured endothelial cells in vitro. Human pulmonary artery endothelial cells (HPAECs) were cultured to confluence, and then the monolayers were exposed to either control (21% O2-5% CO2) or hyperoxic (90% O2-5% CO2) conditions with and without a synthetic glucocorticoid, methylprednisolone (MP). MP reduced hyperoxia-induced ICAM-1 and ICAM-1 mRNA expression in a dose-dependent manner. Neutrophil adhesion to hyperoxia-exposed endothelial cells was also inhibited by MP treatment. In addition, MP attenuated hyperoxia-induced H2O2 production in HPAECs as assessed by flow cytometry. An electrophoretic mobility shift assay demonstrated that hyperoxia activated nuclear factor-kappa B (NF-kappa B) but not activator protein-1 (AP-1) and that MP attenuated hyperoxia-induced NF-kappa B activation dose dependently. With Western immunoblot analysis, Ikappa B-alpha expression was decreased by hyperoxia and increased by MP treatment. These results suggest that MP downregulates hyperoxia-induced ICAM-1 expression by inhibiting NF-kappa B activation via increased Ikappa B-alpha expression.

intercellular adhesion molecule-1; nuclear factor-kappa B; inhibitory protein Ikappa B-alpha ; glucocorticoid


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