Obesity, airway hyperresponsiveness, and inflammation.
Epidemiological data indicate that obesity is a risk factor for asthma, but the mechanistic basis for this relationship is not established. Here we review data from human subjects and animal models investigating the relationship between obesity and airway hyperresponsiveness, a characteristic feature of asthma. We discuss obesity as a state of chronic systemic inflammation resulting from interactions between adipocytes and adipose tissue macrophages that are recruited to obese adipose tissue. Finally, we focus on the possibility that aspects of this inflammation, particularly obesity-related changes in TNF-alpha, leptin, and adiponectin, may contribute to airway hyperresponsiveness in obesity. Determining how obesity promotes asthma may uncover novel therapeutic strategies that are effective in the obese asthmatic subject.
Shore
Stephanie A
SA
Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115, USA. sshore@hsph.harvard.edu
D052242:Adiponectin / Q000378:metabolism; D000273:Adipose Tissue / Q000276:immunology; D000328:Adult; D000818:Animals; D001249:Asthma / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D016535:Bronchial Hyperreactivity / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D002648:Child; D005260:Female; D006801:Humans; D007249:Inflammation / Q000209:etiology* / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000378:metabolism; D020738:Leptin / Q000378:metabolism; D008297:Male; D009765:Obesity / Q000150:complications* / Q000276:immunology / Q000503:physiopathology; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D052242:Adiponectin; D018836:Inflammation Mediators; D020738:Leptin; D014409:Tumor Necrosis Factor-alpha