Proinflammatory potential of the airway epithelium in bronchial asthma

Abstract

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