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-kappaB 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.