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Am J Physiol Lung Cell Mol Physiol 280: L1115-L1127, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 6, L1115-L1127, June 2001

Bafilomycin A1 inhibits rhinovirus infection in human airway epithelium: effects on endosome and ICAM-1

Tomoko Suzuki1, Mutsuo Yamaya1, Kiyohisa Sekizawa2, Masayoshi Hosoda1, Norihiro Yamada1, Satoshi Ishizuka1, Katsutoshi Nakayama1, Masaru Yanai1, Yoshio Numazaki3, and Hidetada Sasaki1

1 Department of Geriatric and Respiratory Medicine, Tohoku University School of Medicine, Sendai 980-8574; 3 Virus Center, Clinical Research Division, Sendai National Hospital, Sendai 983-0045; and 2 Department of Pulmonary Medicine, Institute of Clinical Medicine, University of Tsukuba, Tsukuba 305-8575, Japan

To examine the effects of bafilomycin A1, a blocker of vacuolar H+-ATPase, on rhinovirus (RV) infection in the airway epithelium, primary cultures of human tracheal epithelial cells were infected with RV14. Viral infection was confirmed by showing that viral RNA in the infected cells and the viral titers in the supernatants of infected cells increased with time. RV14 infection upregulated the production of cytokines and mRNA of intercellular adhesion molecule (ICAM)-1 in epithelial cells. Bafilomycin A1 reduced the viral titers of RV14 and inhibited the production of cytokines and ICAM-1 before and after RV14 infection. Bafilomycin A1 reduced susceptibility of epithelial cells to RV14 infection. RV14 increased activated nuclear factor-kappa B in the cells, and bafilomycin A1 reduced the activated nuclear factor-kappa B. Bafilomycin A1 decreased the number of acidic endosomes in the epithelial cells. These results suggest that bafilomycin A1 may inhibit infection by RV14 by not only blocking RV RNA entry into the endosomes but also reducing ICAM-1 expression in the epithelial cells. Bafilomycin A1 may therefore modulate airway inflammation after RV infection.

intercellular adhesion molecule-1; asthma; common cold; airway inflammation; vacuolar adenosine 5'-triphosphatase


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