Abstract
Asthma is a disease of the airways characterized by variable airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Asthma is also accompanied by changes to the structure and composition of the airway walls, collectively termed airway remodeling.1 Cardinal features of airway remodeling include increased numbers of mucus-secreting epithelial cells, thickening of the subepithelial collagen layer, and increases in vascularity and smooth-muscle mass around the airways. There is a strong consensus that airway remodeling contributes to the decline in lung function and the development of fixed airway obstruction present in patients with chronic, persistent asthma.2 Evidence indicates that aspects of airway remodeling . . .
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