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J Appl Physiol 102: 516-528, 2007. First published October 19, 2006; doi:10.1152/japplphysiol.00847.2006
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INVITED REVIEWS

Obesity and asthma: lessons from animal models

Stephanie A. Shore

Program in Molecular and Integrative Physiological Sciences, Harvard School of Public Health, Boston, Massachusetts

Epidemiological data indicate that obesity is a risk factor for asthma. These data are supported by observations in several murine models of obesity. Ob/ob, db/db, and Cpefat mice each exhibit innate airway hyperresponsiveness, a characteristic feature of asthma. These mice also respond more vigorously to common asthma triggers, including ozone. Here we discuss the implications of these data with respect to several mechanisms proposed to explain the relationship between obesity and asthma: 1) common etiologies; 2) comorbidities; 3) mechanical factors; and 4) adipokines. We focus on the role of adipokines, especially TNF-{alpha}, IL-6, leptin, and adiponectin. Understanding the mechanistic basis for the relationship between obesity and asthma may lead to novel therapeutic strategies for treatment of the obese asthmatic subject.

mice; leptin; adiponectin; tumor necrosis factor-{alpha}; interleukin-6; adipokines


Address for reprint requests and other correspondence: S. Shore, Program in Molecular and Integrative Physiological Sciences, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115 (e-mail: sshore{at}hsph.harvard.edu)




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