Airway responses to chronic ozone exposure are partially mediated through mast cells

Airways inflammation and epithelial injury induced by chronic ozone (O-3) i n genetically mast cell-deficient mice (Kit(W)/Kit(W-v)) were compared with those in mast cell-sufficient mice (+/+) and Kit(W)/Kit(W-v) mice repleted of mast cells (Kit(W)/Kit(W-v)-BMT). Mice were exposed to 0.26 ppm O-3 8 h /day, 5 days/wk, for 1-90 days. Background was 0.06 ppm O-3. Age-matched mi ce were exposed to filtered air for O-3 controls. Reversibility of lesions was evaluated 35 days after exposure. Compared with Kit(W)/Kit(W-v), O-3 ca used greater increases in lavageable macrophages, epithelial cells, and pol ymorphonuclear leukocytes in +/+ and Kit(W)/Kit(W-v)-BMT mice. O-3 also cau sed lung hyper permeability, but the genotypic groups were not different. C ells and permeability returned to air control levels after O-3. O-3 induced lung cell proliferation only in +/+ and Kit(W)/Kit(W-v)-BMT mice; prolifer ation remained elevated or increased in +/+ and Kit(W)/Kit(W-v)-BMT mice af ter O-3. Greater O-3-induced cell proliferation was found in nasal epitheli um of +/+ and Kit(W)/Kit(W-v)-BMT mice compared with Kit(W)/Kit(W-v) mice. Results are consistent with the hypothesis that mast cells affect airway re sponses induced by chronic O-3 exposure.