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Obesity and eosinophilic inflammation: Does leptin play a role?

机译:肥胖和嗜酸性粒细胞炎症:瘦素是否起作用?

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摘要

It has been pointed out that obesity is a risk factor for, and is involved in the exacerbation of asthma. Mounting evidence about adipose tissue-derived proteins (adipokines) gave rise to the current understanding of obesity as a systemic inflammatory disorder. In this review, we summarized the involvement of leptin, focusing on eosinophil functions. Several studies have indicated that leptin can restrain eosinophil apoptosis, enhance migration, increase adhesion molecules and induce cytokine production. Since leptin also acts on a variety of immune cells related to allergic response, increased leptin in obese individuals potentially explains the mechanism by which obesity leads to an exacerbation of asthma. Further studies targeting adipokines will delineate the association between obesity and eosinophil-associated diseases.
机译:已经指出,肥胖是哮喘的危险因素,并且与哮喘的发作有关。关于脂肪组织衍生蛋白(adipokines)的越来越多的证据引起了人们对肥胖作为一种系统性炎性疾病的当前理解。在这篇综述中,我们总结了瘦素的参与,着重于嗜酸性粒细胞功能。几项研究表明,瘦素可以抑制嗜酸性粒细胞凋亡,增强迁移,增加粘附分子并诱导细胞因子的产生。由于瘦素还作用于与过敏反应相关的多种免疫细胞,因此肥胖个体中瘦素的增加可能解释了肥胖导致哮喘恶化的机制。针对脂肪因子的进一步研究将描述肥胖与嗜酸性粒细胞相关疾病之间的关联。

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