Obesity, airway hyperresponsiveness, and inflammation
1Department of Environmental Health, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115, USA. sshore@hsph.harvard.edu
Journal of Applied Physiology (Bethesda, Md. : 1985)
|October 31, 2009
Summary
Obesity increases asthma risk, potentially through chronic inflammation involving immune cells and signaling molecules like TNF-alpha, leptin, and adiponectin. Understanding this link may reveal new treatments for obese individuals with asthma.
Area of Science:
- Immunology
- Pulmonary Medicine
- Metabolic Disorders
Background:
- Epidemiological studies link obesity to increased asthma risk.
- The precise mechanisms connecting obesity and asthma remain unclear.
- Airway hyperresponsiveness is a key feature of asthma.
Purpose of the Study:
- To review the relationship between obesity and airway hyperresponsiveness.
- To explore the role of chronic inflammation in obesity-related asthma.
- To identify potential therapeutic targets for obese asthmatics.
Main Methods:
- Review of human and animal model data.
- Analysis of obesity-induced systemic inflammation.
- Investigation of inflammatory mediators such as TNF-alpha, leptin, and adiponectin.
Main Results:
- Obesity is characterized by chronic systemic inflammation.
- Adipose tissue macrophages contribute to this inflammation.
- Obesity-related inflammatory changes may drive airway hyperresponsiveness.
Conclusions:
- Obesity-associated inflammation, particularly involving TNF-alpha, leptin, and adiponectin, is a plausible contributor to airway hyperresponsiveness.
- Further research into these mechanisms could lead to novel asthma therapies for obese patients.
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