Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells

被引:43
作者
Jian, Congxiang [1 ,2 ]
Li, Chenjun [2 ]
Ren, Yu [2 ]
He, Yong [2 ]
Li, Yunming [2 ]
Feng, Xiaodan [1 ]
Zhang, Gang [1 ]
Tan, Yinghui [1 ]
机构
[1] Third Mil Med Univ, Affiliated Hosp 2, Dept Oral & Maxillofacial Surg, Chongqing 400038, Peoples R China
[2] PLA Gen Hosp Chengdu Mil Reg, Dept Stomatolog, Chengdu 610083, Sichuan, Peoples R China
基金
中国国家自然科学基金;
关键词
hypoxia; lipopolysaccharide; periodontal ligament cells; periodontitis; nuclear factor kappa B; NF-KAPPA-B; ACTINOBACILLUS-ACTINOMYCETEMCOMITANS; DISEASE; FIBROBLASTS; GINGIVALIS; ACTIVATION; RATS;
D O I
10.1007/s10753-014-9865-6
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:1413 / 1423
页数:11
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