Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells
Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells
复制标题
DOI：
10.1007/s10753-014-9865-6
复制
发表时间：
2014-10-01
期刊：
影响因子：
5.1
通讯作者：
Tan, Yinghui
中科院分区：
文献类型：
--
作者：
Jian, Congxiang;Li, Chenjun;Tan, Yinghui
牙周炎是一种以破坏牙齿支撑组织为特征的慢性炎症性疾病。高原环境的主要变化是缺氧，动物实验表明缺氧可诱发严重的牙周炎。然而，关于缺氧和脂多糖（LPS）诱导的牙周韧带（PDL）细胞因子表达的信息很少。在这篇文章中，我们描述了缺氧或牙龈P.脂多糖（Pg LPS）诱导人牙周韧带（hPDL）细胞表达肿瘤坏死因子α (tnf - α)、白细胞介素(IL)-1 β和IL-6。我们发现缺氧增强的Pg LPS诱导hPDL细胞中tnf - α、IL-1 β和IL-6的表达。我们还证实了核因子κ B通路参与了缺氧增强Pg LPS诱导的hPDL细胞因子表达。因此，我们的研究结果表明，缺氧环境可能增强由Pg LPS诱导的hPDL细胞的免疫功能。
Periodontitis is a chronic inflammatory disease characterized by the destruction of tooth supporting tissues. Hypoxia, the mainly changes of the plateau environment, can induce severe periodontitis by animal experiments. There is, however, very little information on hypoxia and lipopolysaccharide (LPS) induced cytokine expression in periodontal ligament (PDL) cells. In this article, we characterized hypoxia or P. gingivalis lipopolysaccharide (Pg LPS) induced tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1 beta, and IL-6 expression by human periodontal ligament (hPDL) cells. We found that hypoxia augmented Pg LPS induced TNF-alpha, IL-1 beta, and IL-6 expression in hPDL cells. We also demonstrated that nuclear factor kappa B pathway was involved in hypoxia augmenting Pg LPS induced cytokine expression in hPDL cells. Thus, our results suggest that the hypoxic environment may enhance the immune function of hPDL cells that is induced by Pg LPS.