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首页> 外文期刊>American Journal of Physiology >Leptin enhances ICAM-1 expression, induces migration and cytokine synthesis, and prolongs survival of human airway epithelial cells
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Leptin enhances ICAM-1 expression, induces migration and cytokine synthesis, and prolongs survival of human airway epithelial cells

机译：瘦素增强了ICAM-1表达，诱导迁移和细胞因子合成，延长人气道上皮细胞的存活

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There is rising interest in how obesity affects respiratory diseases, since epidemiological findings indicate a strong relationship between the two conditions. Leptin is a potent adipokine produced mainly by adipocytes. It regulates energy storage and expenditure and also induces inflammation. Previous studies have shown that leptin is able to activate inflammatory cells such as lymphocytes and granulocytes, but little is known about its effect on lung structural cells. The present study investigated the effects of leptin on human airway epithelial cells by using human primary airway epithelial cells and a human airway epithelial cell line, BEAS-2B. Flow cytometry showed enhanced ICAM-1 expression by both of those cells in response to leptin, and that effect was abrogated by dexamethasone or NF-kappaB inhibitor. Flow cytometry and quantitative PCR showed that airway epithelial cells expressed leptin receptor (Ob-R), whose expression level was downregulated by leptin itself. Multiplex cytokine analysis demonstrated enhanced production of CCL11, G-CSF, VEGF, and 1L-6 by BEAS-2B cells stimulated with leptin. Furthermore, transfec-tion of Ob-R small interference RNA decreased the effect of leptin on CCL11 production as assessed by quantitative PCR. Finally, leptin induced migration of primary airway epithelial cells toward leptin, suppressed BEAS-2B apoptosis induced with TNF-alpha and IFN-gamma, and enhanced proliferation of primary airway epithelial cells. In summary, leptin was able to directly activate human airway epithelial cells by binding to Ob-R and by NF-kappaB activation, resulting in upregulation of ICAM-1 expression, induction of CCL11, VEGF, G-CSF, and IL-6 synthesis, induction of migration, inhibition of apoptosis, and enhancement of proliferation.
机译：肥胖如何影响呼吸系统疾病的兴趣兴起，因为流行病学发现表明了两种条件之间的牢固关系。瘦素是一种主要由脂肪细胞产生的强脂蛋白。它调节能量储存和支出，并诱导炎症。以前的研究表明，瘦素能够激活炎性细胞，如淋巴细胞和粒细胞，但大概是对其对肺部结构细胞的影响很少。本研究通过使用人的原发性气道上皮细胞和人气气道上皮细胞，BEA-2B研究了Leptin对人气道上皮细胞的影响。流式细胞术通过响应瘦素的两种细胞显示出增强的ICAM-1表达，并且该效果由地塞米松或NF-κB抑制剂消除。流式细胞术和定量PCR显示，气道上皮细胞表达瘦素受体（OB-R），其表达水平通过瘦素本身下调。多重细胞因子分析证明通过用瘦蛋白刺激的BEA-2B细胞增强了CCL11，G-CSF，VEGF和1L-6的产生。此外，OB-R小干扰RNA的转移降低了通过定量PCR评估的瘦素对CCL11生产的影响。最后，瘦素诱导原发性气道上皮细胞对瘦素的迁移，抑制了TNF-α和IFN-γ的诱导的BEA-2B凋亡，以及增强原代气道上皮细胞的增殖。总之，瘦素能够通过结合OB-R和NF-κB活化直接激活人气道上皮细胞，导致ICAM-1表达，CCL11，VEGF，G-CSF和IL-6合成的诱导，诱导迁移，抑制细胞凋亡，增强增强。

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