L-carbocisteine inhibits respiratory syncytial virus infection in human tracheal epithelial cells

Masanori Asada, Motoki Yoshida, Yukimasa Hatachi, Takahiko Sasaki, Hiroyasu Yasuda, Xue Deng, Hidekazu Nishimura, Hiroshi Kubo, Ryoichi Nagatomi, Mutsuo Yamaya

Research output: Contribution to journalArticlepeer-review

13 Citations (Scopus)


To examine the effects of l-carbocisteine on airway infection with respiratory syncytial (RS) virus, human tracheal epithelial cells were pretreated with l-carbocisteine and infected with RS virus. Viral titer, virus RNA, and pro-inflammatory cytokine secretion, including interleukin (IL)-1 and IL-6, increased with time after infection. l-carbocisteine reduced the viral titer in the supernatant fluids, the amount of RS virus RNA, RS virus infection susceptibility, and the concentration of pro-inflammatory cytokines induced by virus infection. l-carbocisteine reduced the expression of intercellular adhesion molecule (ICAM)-1, an RS virus receptor, on the cells. However, l-carbocisteine had no effects on the expression of heparan sulfate, a glycosaminoglycan that binds to the RS virus attachment protein, or on the amount of intracellular activated-RhoA, isoform A of the Ras-homologous family, that binds to the RS virus fusion protein. These findings suggest that l-carbocisteine may inhibit RS virus infection by reducing the expression of ICAM-1. It may also modulate airway inflammation during RS virus infection.

Original languageEnglish
Pages (from-to)112-118
Number of pages7
JournalRespiratory Physiology and Neurobiology
Issue number1
Publication statusPublished - 2012 Jan 15


  • Bronchial asthma
  • COPD
  • Carbocisteine
  • ICAM-1
  • Respiratory syncytial virus

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology
  • Pulmonary and Respiratory Medicine


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