PT  - JOURNAL ARTICLE
AU  - H. Yasuda
AU  - M. Yamaya
AU  - T. Sasaki
AU  - D. Inoue
AU  - K. Nakayama
AU  - M. Yamada
AU  - M. Asada
AU  - M. Yoshida
AU  - T. Suzuki
AU  - H. Nishimura
AU  - H. Sasaki
TI  - Carbocisteine inhibits rhinovirus infection in human tracheal epithelial cells
AID  - 10.1183/09031936.06.00058505
DP  - 2006 Jul 01
TA  - European Respiratory Journal
PG  - 51--58
VI  - 28
IP  - 1
4099  - http://erj.ersjournals.com/content/28/1/51.short
4100  - http://erj.ersjournals.com/content/28/1/51.full
SO  - Eur Respir J2006 Jul 01; 28
AB  - The aim of the study was to examine the effects of a mucolytic drug, carbocisteine, on rhinovirus (RV) infection in the airways. Human tracheal epithelial cells were infected with a major-group RV, RV14. RV14 infection increased virus titres and the cytokine content of supernatants. Carbocisteine reduced supernatant virus titres, the amount of RV14 RNA in cells, cell susceptibility to RV infection and supernatant cytokine concentrations, including interleukin (IL)-6 and IL-8, after RV14 infection. Carbocisteine reduced the expression of mRNA encoding intercellular adhesion molecule (ICAM)-1, the receptor for the major group of RVs. It also reduced the supernatant concentration of a soluble form of ICAM-1, the number and fluorescence intensity of acidic endosomes in the cells before RV infection, and nuclear factor-κB activation by RV14. Carbocisteine also reduced the supernatant virus titres of the minor group RV, RV2, although carbocisteine did not reduce the expression of mRNA encoding a low density lipoprotein receptor, the receptor for RV2. These results suggest that carbocisteine inhibits rhinovirus 2 infection by blocking rhinovirus RNA entry into the endosomes, and inhibits rhinovirus 14 infection by the same mechanism as well as by reducing intercellular adhesion molecule-1 levels. Carbocisteine may modulate airway inflammation by reducing the production of cytokines in rhinovirus infection.