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著者: Masanori Asada, Motoki Yoshida, Yukimasa Hatachi, Takahiko Sasaki, Hiroyasu Yasuda, Xue Deng, Hidekazu Nishimura, Hiroshi Kubo, Ryoichi Nagatomi, Mutsuo Yamaya
雑誌名: Respir Physiol Neurobiol. 2012 Jan 15;180(1):112-8. doi: 10.1016/j.resp.2011.10.017. Epub 2011 Nov 7.
Abstract/Text
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.
Copyright © 2011 Elsevier B.V. All rights reserved.
PMID 22080978 Respir Physiol Neurobiol. 2012 Jan 15;180(1):112-8. doi: 10.1016/j.resp.2011.10.017. Epub 2011 Nov 7.
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