Breathing pattern response and epithelial labeling in ozone-induced airwayinjury in neutrophil-depleted rats

To test the hypothesis that neutrophils enhance the repair of ozone (O-3)-i njured airway epithelium, we investigated breathing pattern responses and a irway epithelial injury and repair in rats depleted of neutrophils using ra bbit antirat neutrophil serum (ANS) and control rats treated with normal ra bbit serum (NRS). Thirty-seven Wistar rats were exposed to O-3 (1 ppm) or f iltered air (FA) for 8 h followed by 8 h in FA. O-3-exposed NRS- and ANS-tr eated rats showed similar progressive decreases in tidal volume and increas e in breathing frequency, with maximal changes occurring at 8 h of exposure , whereas FA-exposed rats showed no significant changes. O-3-exposed ANS-tr eated rats showed more epithelial necrosis in the nasal cavity, bronchi, an d distal airways than did O-3-exposed NRS-treated rats. Incorporation of 5- bromo-2-deoxyuridine (BrdU), a measure of cellular proliferation, was asses sed using an optical disector to count BrdU-labeled terminal bronchiolar ep ithelial cells. O-3-exposed ANS-treated rats had significantly less BrdU-la beled epithelial cells than did O-3-exposed NRS-treated rats. We conclude t hat neutrophils contribute to the repair process by enhancing the prolifera tion of O-3-injured airway epithelial cells.