Ozone is a major component of photochemical smog and one of the most important air pollutants worldwide. Short-term ozone exposure causes epithelial necrosis in the lung, primarily of type I and ciliated cells in centriacinar regions. Recent experimental investigations have shown that the neutrophilic influx, which progresses to sites of epithelial injury, aids in the removal of necrotic epithelial cells and expedites epithelial repair. IL-8 production is upregulated by ozone exposed airway epithelium, but its' function relative to the neutrophil influx is not well defined. The mechanisms by which neutrophils traffic to an area of ozone injury and aid in the removal of ozone injured airway epithelial cells are unknown. After in vitro ozone exposure of immortalized and primary human and Rhesus monkey bronchial epithelial cells, the following specific aims will be investigated: 1) characterize the phenotype of the airway epithelial cell(s) that produce IL-8 after exposure to ambient levels of ozone 2) determine whether neutrophils migrate directly to ozone injured airway epithelial cells 3) determine if IL-8 production by airway epithelium exposed to ambient levels of ozone correlates with the co-localization of neutrophils.
