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首页> 外文期刊>Journal of Allergy >IL-17F Induces CCL20 in Bronchial Epithelial Cells
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IL-17F Induces CCL20 in Bronchial Epithelial Cells

机译：IL-17F在支气管上皮细胞中诱导CCL20

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摘要

IL-17F plays a crucial role in airway inflammatory diseases including asthma, but its function has not been fully elucidated. CCL20 is also involved in allergic airway inflammation, while its regulatory mechanisms remain to be defined. To further identify a novel role of IL-17F, the expression of CCL20 by IL-17F in bronchial epithelial cells and the signaling mechanisms involved were investigated. Bronchial epithelial cells were stimulated with IL-17F, and the levels of CCL20 gene and protein measured, with the effects of the addition of various kinase inhibitors and siRNAs also investigated. IL-17F significantly induced the expression of CCL20 gene and protein. Pretreatment with inhibitors for MEK1/2, Raf1 and MSK1, and overexpression of a Raf1 dominant-negative mutant significantly diminished IL-17F-induced CCL20 production. Moreover, transfection of the siRNAs targeting MSK1, p90RSK, and CREB blocked CCL20 expression. These findings suggest that IL-17F is able to induce CCL20 via Raf1-MEK1/2-ERK1/2-MSK1/p90RSK-CREB signaling pathway in bronchial epithelial cells. The IL-17F/CCL20 axis may be a novel pharmacological target for asthma.
机译：IL-17F在包括哮喘在内的气道炎性疾病中起着至关重要的作用，但其功能尚未完全阐明。 CCL20也参与过敏性气道炎症，但其调节机制尚待确定。为了进一步确定IL-17F的新作用，研究了IL-17F在支气管上皮细胞中CCL20的表达及其涉及的信号传导机制。用IL-17F刺激支气管上皮细胞，并测量CCL20基因和蛋白质的水平，还研究了添加各种激酶抑制剂和siRNA的影响。 IL-17F显着诱导CCL20基因和蛋白的表达。用MEK1 / 2，Raf1和MSK1抑制剂预处理以及Raf1显性负突变体的过表达显着减少了IL-17F诱导的CCL20的产生。此外，针对MSK1，p90RSK和CREB的siRNA的转染可阻断CCL20的表达。这些发现表明IL-17F能够通过Raf1-MEK1 / 2-ERK1 / 2-MSK1 / p90RSK-CREB信号转导途径在支气管上皮细胞中诱导CCL20。 IL-17F / CCL20轴可能是哮喘的新型药理靶标。

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