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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IκB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IκB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。
OBJECTIVE: It has been found that interleukin-17 (IL-17) plays an important role in the inflammatory response as an important marker of inflammation and its expression level is positively correlated with the severity of periodontal disease. However, interleukin-17 -17 has not been studied for the chemotactic production of gingival epithelial cells. Therefore, this study mainly explored how interleukin-17 regulates inflammatory response by chemokines in human gingival epithelial cells (HGECs) and further explored Its mechanism of action. Methods: The enzyme-linked immunosorbent assay (ELISA) was used to observe the secretion of chemokines in the cells. At the same time, the changes of nuclear factor kappa B in cells were observed by western blot. Results: Compared with IL-17-stimulated group, the secretion of chemokine interleukin-8 (CXCL8) in IL-17-stimulated group was significantly increased compared with IL-17-stimulated group, while the chemotactic monocyte chemoattractant protein-1 CCL2) did not change significantly, and the significant increase of IκB phosphorylation indicated that NF-κB was activated (P <0.05); IL-17 stimulated group compared with IL-17 + NF-κB inhibitor group, IL -17 + NF-κB inhibitor group, the expression of CXCL8 was significantly decreased, while the phosphorylation of IκB significantly decreased, suggesting that NF-κB activity was inhibited (P <0.05). CONCLUSION: NF-κB plays a key role in the regulation of chemokine expression on gingival epithelial cells stimulated by IL-17 and may also provide a new target for future treatment of IL-17-induced periodontal inflammatory diseases.