It has also been proposed that the remodeling process might be beneficial in airway diseases. Lambert and colleagues suggested that airway wall thickening protects against bronchoconstriction. Peribronchiolar fibrosis correlated with milder COPD stage, suggesting that fibrosis can be protective, preventing narrowing. Collagen deposition in subepithelial matrix may inhibit narrowing by making the airway wall stiffer, representing an additional load on ASM. Hyaluronan and versican deposition in and around the smooth muscle also counteracts airway narrowing and smooth-muscle shortening. Experiments conducted on rat models of allergen-induced asthma have suggested that airway responsiveness may increase following airway inflammation but may decrease with the development of airway remodeling.
Duration of asthma has been associated with reduced lung function, increased hyperresponsiveness and asthma symptoms, and greater use of medication. Airway remodeling may contribute to these features. The extent of epithelial injury has been statistically correlated to AHR. Functional consequences of epithelial alterations mostly refer to increased sputum production and airway narrowing. in detail
Some variable correlations have been found between the severity of asthma, AHR or attack score, and subepithelial collagen types I and III deposition in the airways. Proteoglycan deposition in the ECM and bronchial fibroblast production of proteoglycans also correlate with airway responsiveness in asthmatic subjects. Niimi and col-leagues showed than increased airway thickness measured by helical CT correlated inversely with AHR, suggesting that it is not only airway dimension that may affect airway function but probably other factors. Smooth-muscle cell hyperplasia and hypertrophy have been linked to asthma severity. Functional consequences of this increase in airway smooth-muscle mass have been proposed, such as airflow obstruction through airway wall thickening and increased airway responsiveness in both asthma and COPD.