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Am J Physiol Lung Cell Mol Physiol (December 22, 2005). doi:10.1152/ajplung.00386.2005
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Submitted on September 9, 2005
Accepted on December 14, 2005

Increased pulmonary responses to acute ozone exposure in obese db/db mice

Frank L Lu1, Richard A Johnston2, Lesley Flynt2, Todd A Theman2, Raya D Terry2, Igor N Schwartzman2, Anna Lee2, and Stephanie A Shore2*

1 Environmental Health, Harvard School of Public Health, Boston, MA, USA; Department of Pediatrics, National Taiwan University Hospital and Medical College, Taipei, Taiwan
2 Environmental Health, Harvard School of Public Health, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: sshore{at}hsph.harvard.edu.

Epidemiological studies indicate that the incidence of asthma is increased in obese and overweight humans. Responses to ozone (O3), an asthma trigger, are increased in obese (ob/ob) mice lacking the satiety hormone leptin. The long form of the leptin receptor (Ob-Rb) is required for satiety and mice lacking this receptor (db/db mice) are also substantially obese. Here, wildtype and db/db mice were exposed to air or O3 (2 ppm) for 3 hours. Airway responsiveness, measured by the forced oscillation technique, was greater in db/db than wildtype mice after air exposure. O3-induced increases in pulmonary resistance and airway responsiveness were also greater in db/db mice. Bronchoalveolar lavage fluid eotaxin, IL-6, KC, and MIP-2 increased 4 h after O3 exposure and subsided by 24 h, whereas protein and neutrophils continued to increase through 24 h. For each outcome, the effect of O3 was significantly greater in db/db than wildtype mice. Previously published results obtained in ob/ob mice were similar except for O3-induced neutrophils and MIP-2, which were not different from wildtype mice. O3 also induced pulmonary IL-1{beta} and TNF{alpha} mRNA expression in db/db but not ob/ob mice. Leptin was increased in serum of db/db mice, and pulmonary mRNA expression of the short form of the leptin receptor (Ob-Ra) was similar in db/db and wildtype mice. These data confirm that obese mice have innate airway hyperresponsiveness and increased pulmonary responses to O3. Differences between ob/ob mice, which lack leptin, and db/db mice, which lack Ob-Rb but not Ob-Ra, suggest that leptin, acting through Ob-Ra, can modify some pulmonary responses to O3.




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