Structural changes in the airway walls that are probably driven by mediator
s released as a consequence of chronic allergic inflammation are prominent
features of asthma. However, it is not clear how each of the many changes t
hat occur in the airway wall contribute to altered airway function in asthm
a. Collagen deposition in the subepithelial matrix, around and inside the s
mooth muscle, would be expected to oppose the effect of smooth-muscle contr
action. Conversely, geometric factors would result in exaggerated airway na
rrowing for a given degree of smooth-muscle shortening; decreased airway wa
ll stiffness and increased airway narrowing for a given amount of force gen
erated by the smooth muscle. Degradation of the matrix may alter the coupli
ng between muscle and lung recoil, allowing exaggerated smooth-muscle short
ening. Increase in muscle mass associated with preservation of its contract
ile capacity could be the most important contributor to exaggerated airway
narrowing.