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Am J Physiol Lung Cell Mol Physiol 278: L560-L571, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 3, L560-L571, March 2000

Effects of dexamethasone on rhinovirus infection in cultured human tracheal epithelial cells

Tomoko Suzuki, Mutsuo Yamaya, Kiyohisa Sekizawa, Norihiro Yamada, Katsutoshi Nakayama, Satoshi Ishizuka, Masahito Kamanaka, Tetsushi Morimoto, Yoshio Numazaki, and Hidetada Sasaki

Departments of Geriatric and Respiratory Medicine and Pediatrics, Tohoku University School of Medicine, Sendai 980-8574; Virus Center, Clinical Research Division, Sendai National Hospital, Sendai 983-0045; and Department of Respiratory Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba 305-8575, Japan

To examine the effects of glucocorticoid on rhinovirus (RV) infection, primary cultures of human tracheal epithelial cells were infected with either RV2 or RV14. Viral infection was confirmed by demonstrating that viral RNA in infected cells and viral titers of supernatants and lysates from infected cells increased with time. RV14 infection upregulated the expression of mRNA and protein of intercellular adhesion molecule-1 (ICAM-1), the major RV receptor, on epithelial cells, and it increased the production of interleukin (IL)-1beta , IL-6, IL-8, and tumor necrosis factor-alpha in supernatants. Dexamethasone reduced the viral titers of supernatants and cell lysates, viral RNA of infected cells, and susceptibility of RV14 infection in association with inhibition of cytokine production and ICAM-1 induction. In contrast to RV14 infection, dexamethasone did not alter RV2 infection, a minor group of RVs. These results suggest that dexamethasone may inhibit RV14 infection by reducing the surface expression of ICAM-1 in cultured human tracheal epithelial cells. Glucocorticoid may modulate airway inflammation via reducing the production of proinflammatory cytokines and ICAM-1 induced by rhinovirus infection.

asthma; common cold; airway inflammation; intercellular adhesion molecule-1


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