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哮喘中的脂联素、瘦素和抵抗素:基于人群研究的基本机制

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

作者信息

Sood Akshay, Shore Stephanie A

机构信息

School of Medicine, Department of Medicine, University of New Mexico, MSC 10 5550, Albuquerque, NM 87131, USA.

出版信息

J Allergy (Cairo). 2013;2013:785835. doi: 10.1155/2013/785835. Epub 2013 Oct 30.

DOI:10.1155/2013/785835
PMID:24288549
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3832971/
Abstract

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.

摘要

脂肪因子是由脂肪组织产生的因子,可能具有促炎作用(如瘦素和抵抗素)或抗炎作用(如脂联素)。这些脂肪因子对肺部的影响有可能引发或加重哮喘。本综述通过基于人群的研究和临床研究总结了关于脂肪因子在哮喘中潜在作用的基础机制数据。提高循环中脂联素的浓度可减轻小鼠的过敏性气道炎症和气道高反应性。人体数据支持了小鼠实验数据,这些数据表明低血清脂联素与女性和青春期前女孩患哮喘的风险增加有关。此外,血清总脂联素水平较高可能与哮喘儿童和女性较低的临床哮喘严重程度有关。相比之下,外源性给予瘦素会导致小鼠过敏性气道高反应性增强。从肥胖哮喘患者中获得的肺泡巨噬细胞在增强炎症方面对瘦素具有独特的敏感性。与这些基础机制数据一致,流行病学研究表明,血清瘦素水平较高与哮喘患病率和/或严重程度增加有关,而且这些关联在女性、青春期后女孩和青春期前男孩中可能更强。脂肪因子在哮喘中的作用仍在不断演变,目前尚不清楚调节脂肪因子是否有助于哮喘的预防或治疗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/5724aa985c56/JA2013-785835.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/64bc6e539be5/JA2013-785835.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/5724aa985c56/JA2013-785835.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/64bc6e539be5/JA2013-785835.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/807d7731fd34/JA2013-785835.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/cf75f0f09a9d/JA2013-785835.003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/529c/3832971/5724aa985c56/JA2013-785835.005.jpg

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