Macrolide antibiotics inhibit respiratory syncytial virus infection in human airway epithelial cells

Masanori Asada, Motoki Yoshida, Tomoko Suzuki, Yukimasa Hatachi, Takahiko Sasaki, Hiroyasu Yasuda, Katsutoshi Nakayama, Hidekazu Nishimura, Ryoichi Nagatomi, Hiroshi Kubo, Mutsuo Yamaya

Research output: Contribution to journalArticlepeer-review

35 Citations (Scopus)

Abstract

To examine the effects of macrolide antibiotics on RS virus infection in airways, human tracheal epithelial cells were pre-treated with bafilomycin A1 and clarithromycin, and infected with RS virus. Viral titers in supernatant fluids and RNA of RS virus, and concentrations of cytokines in supernatant fluids, including interleukin-6 increased with time after infection. Bafilomycin A1 and clarithromycin reduced viral titers in supernatant fluids of RS virus, RNA of RS virus, the susceptibility to RS virus infection, and concentrations of cytokines induced by virus infection. N-acetyl-S-geranylgeranyl-l-cysteine, an inhibitor for a small GTP binding protein of RhoA, isoform A of the Ras-homologus (Rho) family, an active form of which is associated with RS virus infection via binding to its fusion protein (F protein), reduced viral titers in supernatant fluids and RNA of RS virus. Bafilomycin A1 and clarithromycin inhibited RhoA activation induced by lysophosphatidic acid in the cells. Fasudil, an inhibitor of Rho kinase, also reduced viral titers in supernatant fluids and RNA of RS virus. These findings suggest that macrolide antibiotics may inhibit RS virus infection, partly through the reduced expression of F protein receptor, activated RhoA, and the inhibition of subsequent Rho kinase activation in human airway epithelial cells.

Original languageEnglish
Pages (from-to)191-200
Number of pages10
JournalAntiviral Research
Volume83
Issue number2
DOIs
Publication statusPublished - 2009 Aug

Keywords

  • Bronchial asthma
  • COPD
  • Macrolide
  • Respiratory syncytial virus
  • RhoA

ASJC Scopus subject areas

  • Pharmacology
  • Virology

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