ABSTRACT
The airway wall in chronic inflammatory states is known to be the subject of
tissue remodeling (1-3). Changes in the architecture of the bronchus result in
airway wall thickening (4), with luminal narrowing, airflow obstruction, and
hyperreactivity to inhaled stimuli. Studies using bronchial biopsies have
shown this thickening to be due to changes in specific components of the
airway wall, including epithelium (5), subepithelial collagen (6,7), submucosal
collagen (8), submucosal vascularity (9), cellular infiltrate (10), and smooth
muscle (11).
