HIGHLIGHTED TOPIC Pulmonary Physiology and Pathophysiology in Obesity Obesity and lung inflammation

prevalence of obesity has increased dramatically worldwide, predisposing individ-uals 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 re-sponses in the lung have been shown to influence the production of the adipocy-tokines, leptin and adiponectin, cytokines, acute phase proteins, and other media-tors 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 environ-mental 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