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1 Physiology Program, Harvard School of Public Health, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.
Epidemiological data indicate an increased incidence of asthma in overweight adults and children. Ozone (O3) is a common trigger for asthma. Accordingly, the purpose of this study was to compare O3-induced airway hyperresponsiveness (AHR) and airway inflammation in lean, wildtype (C57BL/6J) mice and mice obese as a consequence of a defect in the gene encoding the satiety hormone leptin (ob/ob mice). Ob/ob mice eat excessively, and weighed more than twice as much as age and gender matched wildtype mice. Airway responsiveness to intravenous methacholine was measured by forced oscillation. In air exposed controls, baseline pulmonary resistance (RL) was greater and the dose of methacholine required to double RL was lower in ob/ob than wildtype mice. Exposure to O3 (2 ppm for 3 h) caused AHR and airway inflammation in both groups of mice, but responses to O3 were enhanced in ob/ob compared to wildtype mice. Administration of exogenous leptin did not reverse the enhanced inflammatory response observed in ob/ob mice but augmented airway inflammation in wildtype mice. The inhaled dose of O3 per gram of lung tissue was greater in ob/ob than wildtype mice. Our results indicate that O3-induced airway responses are enhanced in ob/ob mice, and suggest that inhaled O3 dose may be one factor contributing to this difference, but other aspects of the obese phenotype may also contribute. Our results also indicate that the hormone leptin, which is increased in the obese, has the capacity to increase airway inflammation.
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