Journal of Applied Physiology
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J Appl Physiol 90: 713-723, 2001;
8750-7587/01 $5.00
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Vol. 90, Issue 2, 713-723, February 2001

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

Steven R. Kleeberger, Yoshinori Ohtsuka, Liu-Yi Zhang, and Malinda Longphre

Department of Environmental Health Sciences, Division of Physiology, The Johns Hopkins University, Baltimore, Maryland 21205

Airways inflammation and epithelial injury induced by chronic ozone (O3) in genetically mast cell-deficient mice (KitW/KitW-v) were compared with those in mast cell-sufficient mice (+/+) and KitW/KitW-v mice repleted of mast cells (KitW/KitW-v-BMT). Mice were exposed to 0.26 ppm O3 8 h/day, 5 days/wk, for 1-90 days. Background was 0.06 ppm O3. Age-matched mice were exposed to filtered air for O3 controls. Reversibility of lesions was evaluated 35 days after exposure. Compared with KitW/KitW-v, O3 caused greater increases in lavageable macrophages, epithelial cells, and polymorphonuclear leukocytes in +/+ and KitW/KitW-v-BMT mice. O3 also caused lung hyperpermeability, but the genotypic groups were not different. Cells and permeability returned to air control levels after O3. O3 induced lung cell proliferation only in +/+ and KitW/KitW-v-BMT mice; proliferation remained elevated or increased in +/+ and KitW/KitW-v-BMT mice after O3. Greater O3-induced cell proliferation was found in nasal epithelium of +/+ and KitW/KitW-v-BMT mice compared with KitW/KitW-v mice. Results are consistent with the hypothesis that mast cells affect airway responses induced by chronic O3 exposure.

inflammation; proliferation; mast cell-deficient mouse; stem cell factor; air pollution


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