Erythromycin attenuates MUC5AC synthesis and secretion in cultured human tracheal cells infected with RV14

Respirology. 2008 Mar;13(2):215-20. doi: 10.1111/j.1440-1843.2007.01227.x.

Abstract

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.

MeSH terms

  • Aged
  • Cell Culture Techniques
  • Common Cold / metabolism*
  • Epithelial Cells / drug effects*
  • Epithelial Cells / metabolism
  • Erythromycin / pharmacology*
  • Extracellular Signal-Regulated MAP Kinases / physiology
  • Female
  • Humans
  • Male
  • Middle Aged
  • Mucin 5AC
  • Mucins / genetics
  • Mucins / metabolism*
  • Protein Synthesis Inhibitors / pharmacology*
  • RNA, Messenger / metabolism
  • Trachea / drug effects*
  • Trachea / metabolism
  • Trachea / pathology

Substances

  • MUC5AC protein, human
  • Mucin 5AC
  • Mucins
  • Protein Synthesis Inhibitors
  • RNA, Messenger
  • Erythromycin
  • Extracellular Signal-Regulated MAP Kinases