TY - JOUR
T1 - Bafilomycin A1 inhibits rhinovirus infection in human airway epithelium
T2 - Effects on endosome and ICAM-1
AU - Suzuki, Tomoko
AU - Yamaya, Mutsuo
AU - Sekizawa, Kiyohisa
AU - Hosoda, Masayoshi
AU - Yamada, Norihiro
AU - Ishizuka, Satoshi
AU - Nakayama, Katsutoshi
AU - Yanai, Masaru
AU - Numazaki, Yoshio
AU - Sasaki, Hidetada
N1 - Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2001
Y1 - 2001
N2 - 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-κB in the cells, and bafilomycin A1 reduced the activated nuclear factor-κB. 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.
AB - 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-κB in the cells, and bafilomycin A1 reduced the activated nuclear factor-κB. 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.
KW - Air-way inflammation
KW - Asthma
KW - Common cold
KW - Intercellular adhesion molecule-1
KW - Vacuolar adenosine 5′-triphosphatase
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U2 - 10.1152/ajplung.2001.280.6.l1115
DO - 10.1152/ajplung.2001.280.6.l1115
M3 - Article
C2 - 11350790
AN - SCOPUS:0034979290
VL - 280
SP - L1115-L1127
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 1040-0605
IS - 6 24-6
ER -