[The role of radical oxygen species in airway inflammation]

Abstract

Reactive oxygen species (ROS) are among numerous mediators of airway inflammation. They are playing a key role in asthma, chronic obturative pulmonary disease (COPD), adult respiratory distress syndrome (ARDS) and lung fibrosis (LF) pathogenesis. In view of very short half-life, their effects are local, related to the site of their formation. Generated either by epithelial or infiltrating cells, ROS cause epithelial damage, increase vascular leakage, induce smooth muscle proliferation and enhance pro-inflammatory gene expression. They also increase arachidonic acid mediator release through cytosolic phospholipase A2 phosphorylation. Drugs inhibiting ROS generation have become the first line of treatment of airway inflammatory disorders.