Review Article Adiponectin, Leptin, and Resistin in Asthma: Basic Mechanisms through Population Studies

License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Adipokines, factors produced by adipose tissue, may be proinflammatory (such as leptin and resistin) or anti-inflammatory (such as adiponectin). Effects of these adipokines on the lungs have the potential to evoke or exacerbate asthma.This review summarizes basic mechanistic data through population-based and clinical studies addressing the potential role of adipokines in asthma. Augmenting circulating concentrations of adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. Murine data is supported by human data that suggest that low serum adiponectin is associated with greater risk for asthma amongwomen and peripubertal girls. Further, higher serum total adiponectinmay be associated with lower clinical asthma severity among children and women with asthma. In contrast, exogenous administration of leptin results in augmented allergic airway hyperresponsiveness in mice. Alveolar macrophages obtained from obese asthmatics are uniquely sensitive to leptin in terms of their potential to augment inflammation. Consistent with this basic mechanistic data, epidemiologic studies demonstrate that higher serum leptin is associated with greater asthma prevalence and/or severity and that these associationsmay be stronger among women, postpubertal girls, and prepubertal boys. The role of adipokines in asthma is still evolving, and it is not currently know