PROINFLAMMATORY POTENTIAL OF THE AIRWAY EPITHELIUM IN BRONCHIAL-ASTHMA

Histopathological studies of asthmatic airways removed postmortem or b y bronchial biopsy show marked inflammatory changes, notably epithelia l cell disruption and damage, and the presence of large numbers of eos inophils. The epithelial damage is seen in mild, asymptomatic asthmati cs as well as in patients who have died in status asthmaticus. Damage to the epithelium may also correlate with bronchial hyperreactivity. T he epithelium has been suggested to be a target for inflammatory cell mediators and cytokines. Recently, the airway epithelium has itself be en shown to produce and release several proinflammatory mediators and cytokines, and to express adhesion molecules for inflammatory cells. T he epithelium, thus, may actively participate in the inflammatory chan ges in asthma, where it may be a source as epithelium well as a target . Drug therapy aimed at preventing inflammatory changes in the epithel ium, such as cytokine and adhesion molecule expression, may be an impo rtant step forward in halting disease progression in asthma.