欢迎访问《现代生物医学进展》编辑部！

目的：有研究发现白介素-17（IL-17）作为炎症反应的重要标志物在炎症反应中具有重要作用，并且其表达水平的高低与牙周疾病的严重程度有着正相关性，但是目前为止白介素-17 对于牙龈上皮细胞的趋化因子生成的影响尚没有研究，所以本课题主要探索在牙龈上皮细胞（human gingival epithelial cells，HGECs）中白介素-17 如何通过趋化因子调控炎症反应，并进一步探究其作用机制。方法：酶联免疫吸附剂测定法（enzyme linked immunosorbent assay，ELISA）观察细胞中相关趋化因子分泌，同时蛋白印迹法（western blot）观察细胞中核转录因子κB的变化。结果：无IL-17 刺激组与IL-17 刺激组比较，IL-17 刺激组的趋化因子白介素8（CXCL8）分泌量显著性增加而另一趋化因子单核细胞趋化蛋白-1（CCL2）却没有显著变化，并且通过磷酸化I资B 的表达量显著性增加提示NF-κB 被激活(P<0.05)；同时IL-17 刺激组与IL-17+NF-κB抑制剂组比较，IL-17 +NF-κB抑制剂组的CXCL8 分泌量显著降低，而通过磷酸化I资B的表达量显著减少提示NF-κB 的活性被抑制(P<0.05)。结论：NF-κB 对IL-17 刺激下的牙龈上皮细胞趋化因子的表达调控具有关键性作用，同时可能也为将来治疗IL-17 诱导的牙周炎症性疾病提供了新的靶点。

英文摘要:

Objective: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). The effects and the mechanism of IL-17 have been evaluated on the expression of CXCL8 and CCL2 by HGECs.Methods:After IL-17 stimulated the human gingival epithelial cells, We evaluated the effects of IL-17 on the expression of CXCL8 and CCL2 by HGECs using ELISA. In addition, the role of the nuclear factor (NF)-κB signalling pathway in the IL-17-mediated expression of chemokines was assessed using a specific inhibitor by WESTERN BOLT.Results:Comparing no stimulation of IL-17 group with under stimulation of IL-17 group, the secretion of CXCL8 protein had significantly increased. And the protein expression of p-IκB significantly increased indicate the activation of NF-κB (P<0.05). Meanwhile, comparing stimulation of IL-17 group with stimulation of IL-17 plus the inhibitor of NF-κB group, the secretion of CXCL8 protein had significantly dcressed. And the protein expression of p-IκB significantly decressed indicate the inhibition of NF-κB (P<0.05).Conclusion:IL-17 is involved in the regulation of the innate immune response in HGECs by inducing CXCL8 production and the NF-jB signalling pathway is involved, while it provides a new target for treatment of periodontitis induced by IL-17.

View Full Text View/Add Comment Download reader