Effect of interleukin-17 on the expression of chemokines in gingival epithelial cells
Effect of interleukin-17 on the expression of chemokines in gingival epithelial cells
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DOI：
10.1111/j.1600-0722.2011.00842.x
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发表时间：
2011-10-01
影响因子：
1.9
通讯作者：
Yamazaki, Kazuhisa
中科院分区：
文献类型：
--
作者：
Takahashi, Naoki;Okui, Takafumi;Yamazaki, Kazuhisa
白细胞介素（IL）-17在炎症细胞通讯中的作用已被充分描述，牙周炎的严重程度与IL-17水平呈正相关。虽然上皮细胞是IL-17的主要靶点，但关于IL-17对人牙龈上皮细胞（HGECs）产生趋化因子的影响知之甚少。我们使用定量实时PCR和ELISA评估IL-17对HGECs表达CXCL 8和CCL 2的影响。此外，核因子（NF）-κ B信号通路的IL-17介导的趋化因子的表达的作用进行了评估，使用特定的抑制剂。IL-17刺激上调HGECs中CXCL 8 mRNA的表达，但不上调CCL 2 mRNA的表达，而肿瘤坏死因子-α（TNF-α）则上调两种趋化因子的mRNA表达。IL-17刺激可上调CXCL 8蛋白的分泌，但不上调CCL 2蛋白的分泌。使用抗IL-17 R IG抑制IL-17对CXCL 8产生的作用，表明特异性受体-配体相互作用的作用。NF-κ B信号通路的抑制表明NF-κ B活化是HGEC中CXCL 8表达所需的。总之，IL-17通过诱导CXCL 8产生参与HGECs中先天免疫应答的调节。
The role of interleukin (IL)-17 in cellular communication in inflammation has been well described, and a positive correlation between the severity of periodontitis and the level of IL-17 was reported. Although epithelial cells are a major target of IL-17, little is known about the effect of IL-17 on the production of chemokines by human gingival epithelial cells (HGECs). We evaluated the effects of IL-17 on the expression of CXCL8 and CCL2 by HGECs using quantitative real-time PCR and ELISA. In addition, the role of the nuclear factor (NF)-kappa B signalling pathway in the IL-17-mediated expression of chemokines was assessed using a specific inhibitor. Stimulation with IL-17 up-regulated the expression of CXCL8 mRNA but not of CCL2 mRNA in HGECs, whereas tumour necrosis factor-alpha (TNF-alpha) elevated the expression of mRNA for both chemokines. Stimulation with IL-17 up-regulated the secretion of CXCL8 protein, but not the secretion of CCL2 protein. The effect of IL-17 on CXCL8 production was suppressed using an anti-IL-17R Ig, suggesting a role for a specific receptor-ligand interaction. Inhibition of the NF-kappa B signalling pathway demonstrated that NF-kappa B activation is required for the CXCL8 expression in HGECs. In conclusion, IL-17 is involved in the regulation of the innate immune response in HGECs by inducing CXCL8 production.