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

Tomoko Suzuki, Mutsuo Yamaya, Kiyohisa Sekizawa, Masayoshi Hosoda, Norihiro Yamada, Satoshi Ishizuka, Katsutoshi Nakayama, Masaru Yanai, Yoshio Numazaki, Hidetada Sasaki

Research output: Contribution to journalArticlepeer-review

61 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)L1115-L1127
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume280
Issue number6 24-6
DOIs
Publication statusPublished - 2001

Keywords

  • Air-way inflammation
  • Asthma
  • Common cold
  • Intercellular adhesion molecule-1
  • Vacuolar adenosine 5′-triphosphatase

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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