Journal
JOURNAL OF APPLIED PHYSIOLOGY
Volume 108, Issue 3, Pages 722-728Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/japplphysiol.00781.2009
Keywords
macrophage; pneumonia; chronic obstructive pulmonary disease
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Funding
- National Heart, Lung, and Blood Institute [HL077417]
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL077417] Funding Source: NIH RePORTER
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Mancuso P. Obesity and lung inflammation. J Appl Physiol 108: 722-728, 2010. First published October 29, 2009; doi: 10.1152/japplphysiol.00781.2009.-The prevalence of obesity has increased dramatically worldwide, predisposing individuals to an increased risk of morbidity and mortality due to cardiovascular disease and type 2 diabetes. Less recognized is the fact that obesity may play a significant role in the pathogenesis of pulmonary diseases through mechanisms that may involve proinflammatory mediators produced in adipose tissue that contribute to a low-grade state of systemic inflammation. In animal models, inflammatory responses in the lung have been shown to influence the production of the adipocytokines, leptin and adiponectin, cytokines, acute phase proteins, and other mediators produced by adipose tissue that may participate in immune responses of the lung. An increased adipose tissue mass may also influence susceptibility to pulmonary infections, enhance pulmonary inflammation associated with environmental exposures, and exacerbate airway obstruction in preexisting lung disease. An increased understanding of the mechanisms by which obesity influences pulmonary inflammation may facilitate the development of novel therapeutic interventions for the treatment of lung disease.
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