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

机译：哮喘中脂联素，瘦素和抵抗素：通过人群研究的基本机制

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摘要

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 among women and peripubertal girls. Further, higher serum total adiponectin may 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 associations may be stronger among women, postpubertal girls, and prepubertal boys. The role of adipokines in asthma is still evolving, and it is not currently known whether modulation of adipokines may be helpful in asthma prevention or treatment.
机译：脂肪组织产生的因子脂肪因子可能是促炎性的（例如瘦素和抵抗素）或消炎性的（例如脂联素）。这些脂肪因子对肺部的影响可能诱发或加剧哮喘。这篇综述总结了通过基于人群的临床研究得出的基本机制数据，这些研究针对的是脂肪因子在哮喘中的潜在作用。增加脂联素的循环浓度可减轻小鼠的过敏性气道炎症和气道高反应性。鼠类数据得到了人类数据的支持，这些数据表明，血清脂联素低与妇女和青春期女童患哮喘的风险更高有关。此外，较高的血清总脂联素可能与哮喘儿童和妇女的临床哮喘严重程度降低有关。相反，瘦素的外源给药导致小鼠变态反应性气道高反应性增强。从肥胖的哮喘患者获得的肺泡巨噬细胞就其增强炎症的潜力对瘦素具有独特的敏感性。与此基本的力学数据相一致，流行病学研究表明，血清瘦素水平较高与哮喘患病率和/或严重程度相关，并且这些相关性在女性，青春期后的女孩和青春期前的男孩中可能更强。脂肪因子在哮喘中的作用仍在发展，目前尚不清楚调节脂肪因子是否可能有助于哮喘的预防或治疗。

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