4.5 Review

Obesity, airway hyperresponsiveness, and inflammation

Journal

JOURNAL OF APPLIED PHYSIOLOGY
Volume 108, Issue 3, Pages 735-743

Publisher

AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00749.2009

Keywords

mice; leptin; adiponectin; tumor necrosis factor-alpha; adipokines

Funding

  1. National Institute of Environmental Health Sciences [ES-013307, ES-000002]
  2. National Heart, Lung, and Blood Institute [HL-084044]
  3. NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL084044] Funding Source: NIH RePORTER
  4. NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [R01ES013307, P30ES000002] Funding Source: NIH RePORTER

Ask authors/readers for more resources

Shore SA. Obesity, airway hyperresponsiveness, and inflammation. J Appl Physiol 108: 735-743, 2010. First published October 29, 2009; doi: 10.1152/japplphysiol.00749.2009.-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.

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