Inflammatory Disease (3) Role of Airway Mucins in Inflammatory Lung Diseases

Abstract

Homeostasis of the airways is maintained through a mucociliary clearance, which is a biological defense system that traps inhaled fine particles with mucus and eliminates them from the lower respiratory tract by ciliary movement. However, in airway inflammation, mucin gene expression in mucus-producing cells is stimulated by various inflammatory mediators, cytokines, growth factors, and reactive oxygen species that are produced by recruited inflammatory cells, such as neutrophils and eosinophils, thereby increasing the production and secretion of airway mucus. On the other hand, the ciliary transport function is remarkably impaired by inflammatory epithelial cell damage and changes in the biophysical properties of mucus, resulting in an airway hypersecretory condition. In particular, mucin 5AC, which is produced by goblet cells, plays a central role in the formation of mucus plugs, which contributes to the poor prognosis of airway hypersecretory diseases. Recently, a molecular biological analysis of airway mucins revealed the function, distribution, and gene regulatory mechanism of mucin in various pathological conditions of airway inflammation. This paper reviews the mechanism of action underlying airway hypersecretion and its therapeutic approaches in airway inflammatory diseases.