A model of chronic inflammation and pulmonary emphysema after multiple ozone exposures in mice.

TitleA model of chronic inflammation and pulmonary emphysema after multiple ozone exposures in mice.
Publication TypeJournal Article
Year of Publication2011
AuthorsTriantaphyllopoulos K, Hussain F, Pinart M, Zhang M, Li F, Adcock I, Kirkham P, Zhu J, Chung K F
JournalAm J Physiol Lung Cell Mol Physiol
Volume300
Issue5
PaginationL691-700
Date Published2011 May
ISSN1522-1504
KeywordsAnimals, Bronchoalveolar Lavage Fluid, Caspase 3, Gene Expression Profiling, Heme Oxygenase-1, Lung, Male, Matrix Metalloproteinase 12, Mice, Mice, Inbred BALB C, Oxidative Stress, Ozone, Pneumonia, Pulmonary Alveoli, Pulmonary Disease, Chronic Obstructive, Pulmonary Emphysema, Smoking
Abstract

Oxidative stress plays a role in the pathophysiology of emphysema through the activation of tissue proteases and apoptosis. We examined the effects of ozone exposure by exposing BALB/c mice to either a single 3-h exposure or multiple exposures over 3 or 6 wk, with two 3-h exposures per week. Compared with air-exposed mice, the increase in neutrophils in bronchoalveolar lavage fluid and lung inflammation index was greatest in mice exposed for 3 and 6 wk. Lung volumes were increased in 3- and 6-wk-exposed mice but not in single-exposed. Alveolar space and mean linear intercept were increased in 6- but not 3-wk-exposed mice. Caspase-3 and apoptosis protease activating factor-1 immunoreactivity was increased in the airway and alveolar epithelium and macrophages of 3- and 6-wk-exposed mice. Interleukin-13, keratinocyte chemoattractant, caspase-3, and IFN-γ mRNA were increased in the 6-wk-exposed group, but heme oxygenase-1 (HO-1) mRNA decreased. matrix metalloproteinase-12 (MMP-12) and caspase-3 protein expression increased in lungs of 6-wk-exposed mice. Collagen area increased and epithelial area decreased in airway wall at 3- and 6-wk exposure. Exposure of mice to ozone for 6 wk induced a chronic inflammatory process, with alveolar enlargement and damage linked to epithelial apoptosis and increased protease expression.

DOI10.1152/ajplung.00252.2010
Alternate JournalAm. J. Physiol. Lung Cell Mol. Physiol.
PubMed ID21355040