Tohoku J. Exp. Med., 2005, 207(4)
Inflammatory Mediators Down-Regulate 11β-Hydroxysteroid Dehydrogenase Type 2 in a Human Lung Epithelial Cell Line BEAS-2B and the Rat Lung
SATOSHI SUZUKI, HIROYOSHI TSUBOCHI, HIRONORI ISHIBASHI, YASUSHI MATSUDA, TAKASHI SUZUKI,1 ZYGMUNT S. KROZOWSKI,2 HIRONOBU SASANO1 and TAKASHI KONDO
Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan, 1 Department of Pathology, Tohoku University School of Medicine, Sendai, Japan, and 2 Laboratory of Molecular Hypertension, Baker Medical Research Institute, Melbourne, Australia
In the lung, anti-inflammatory actions of glucocorticoids would be determined by 11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2), the microsomal enzyme responsible for the breakdown of bio-active glucocorticoids. However, regulation of 11β-HSD2 under inflammatory conditions such as acute lung injury is not well understood. In the present study, we examined whether inflammatory substances would influence the activity and mRNA expression of 11β-HSD2 in the lung. In a human bronchial epithelial cell line BEAS-2B, endotoxin inhibited 11β-HSD2 enzyme activity in a dose-dependent manner over 48 h with a significant decrease in the mRNA expression. Likewise, tumor necrosis factor (TNF)-
keywords —— 11β-hydroxysteroid dehydrogenase type 2; endotoxin; inflammation; acute lung injury; glucocorticoids
© 2005 Tohoku University Medical Press
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Tohoku J. Exp. Med., 2005, 207, 293-301
Correspondence: Satoshi Suzuki, M.D., Department of Thoracic Surgery, Institute of Development, Aging and Cancer, Tohoku University, 4-1 Seiryomachi, Aoba-ku, Sendai 980-8575, Japan.
e-mail: satoshisuzuki@idac.tohoku.ac.jp