Airway remodeling in the pathogenesis of asthma

Abstract

Asthma is characterized by a chronic inflammatory process of the airways followed by healing, the end result of which is an altered structure referred to as airway remodeling. Although the mechanisms responsible for such structural alterations appear to be heterogeneous, it is likely that abnormal airway cell dedifferentiation, migration, and redifferentiation, together with changes in connective tissue deposition, contribute to the altered restitution of airway structure and function. This altered restitution is often seen as fibrosis and increased smooth muscle, mucus gland mass, and vessel area. As a consequence of these structural changes, the airway wall in asthma is usually characterized by increased thickness and markedly and permanently reduced airway caliber. These features may result in increased airflow resistance, particularly when there is bronchial contraction and bronchial hyperresponsiveness. The effect on airflow is compounded by increased mucus secretion and inflammatory exudate, which not only block the airway passages but also cause increased surface tension favoring airway closure.