Premium
Erythromycin attenuates MUC5AC synthesis and secretion in cultured human tracheal cells infected with RV14
Author(s) -
INOUE Daisuke,
KUBO Hiroshi,
SASAKI Takahiko,
YASUDA Hiroyasu,
NUMASAKI Muneo,
SASAKI Hidetada,
YAMAYA Mutsuo
Publication year - 2008
Publication title -
respirology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 85
eISSN - 1440-1843
pISSN - 1323-7799
DOI - 10.1111/j.1440-1843.2007.01227.x
Subject(s) - mucin , overproduction , medicine , erythromycin , rhinovirus , mapk/erk pathway , secretion , protein kinase a , immunology , kinase , microbiology and biotechnology , respiratory system , biology , pathology , antibiotics , enzyme , biochemistry
Background and objective: The common cold is a major cause of asthma exacerbation and chronic obstructive lung disease. Rhinovirus is reported to be responsible for more than 50% of cases of the common cold. In a previous study, we reported that rhinovirus infection of cultured airway cells induced MUC5AC mucin overproduction and hypersecretion by activating the p44/42 mitogen‐activated protein kinase (p44/42 MAPK) pathway. The aim of this study was to examine the effect of erythromycin on RV14‐induced airway mucin overproduction and hypersecretion. Methods: RV14‐infected human tracheal epithelial cells were treated with erythromycin. Results: Erythromycin blocked RV14‐induced MUC5AC protein overproduction and hypersecretion, and also blocked RV14‐induced p44/42 MAPK activation in the cells. Conclusions: Erythromycin may attenuate RV14‐induced MUC5AC overproduction and hypersecretion by blocking the p44/42 MAPK pathway or its upstream regulators.