Asthma is a common inflammatory disorder of the airways, affecting about 300 million people worldwide.
Asthmatic individuals are frequently allergic and show an exaggerated response to environmental agents that are either innocuous or cause only transient inflammatory reactions in the airways of normal subjects. The primary pathogenetic alterations that predispose to this hyperresponsiveness are still largely unknown. Possible candidates are intrinsic defects of the airway epithelium, which would favor the frequently observed sensitization to a number of airborne antigens and the development of inflammatory reactions by allowing the penetration of antigens and irritants through the dysfuntional epithelial barrier.
The disorder usually exhibits a chronically relapsing course. Recurrent episodes of wheezing and shortness of breath manifest in concomitance with a worsening of the inflammatory infiltrate in the airways, and an abnormal broncho-constrictive response to a variety of inhaled agents persists in the remission phases. Patients with long-standing disease can experience irreversible airflow obstruction and a progressive decline in lung function as a consequence of the persisting structural alterations and remodeling of the normal bronchial architecture.
The current approach to asthma treatment is unsatisfactory because it is directed to suppressing the clinical manifestations of inflammation and airway remodeling rather than preventing or reversing primary pathogenetic alterations.
