Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells
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Hypoxia Augments Lipopolysaccharide-Induced Cytokine Expression in Periodontal Ligament Cells Congxiang Jian,1,2 Chenjun Li,2 Yu Ren,2 Yong He,2 Yunming Li,2 Xiaodan Feng,1 Gang Zhang,1 and Yinghui Tan1,3
Abstract—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-α), interleukin (IL)-1β, and IL-6 expression by human periodontal ligament (hPDL) cells. We found that hypoxia augmented Pg LPS induced TNF-α, IL-1β, 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. KEY WORDS: hypoxia; lipopolysaccharide; periodontal ligament cells; periodontitis; nuclear factor κB.
INTRODUCTION Periodontitis is a chronic inflammatory disease characterized by the destruction of tooth supporting tissues [periodontal ligament (PDL), alveolar bone, and connective tissues] [1]. The disease is caused predominantly by Gram-negative anaerobes, such as porphyromonas gingivalis (Pg), and the immune responses against bacterial factors that result in the destruction of tooth-supporting tissues [2, 3]. Bacterial flora and its products/metabolites, especially lipopolysaccharide (LPS) is a significant inflammatory stimulus that triggers an innate immune response and causes a host-mediated immune response through C. Jian and C. Li contribute equally to this work as first authors. 1
Department of Oral and Maxillofacial Surgery, Second Affiliated Hospital, Third Military Medical University, Xinqiaozheng Street, Shapingba District, Chongqing, 400038, People’s Republic of China 2 Department of Stomatolog, PLA General Hospital of Chengdu Military Region, Chengdu, Sichuan Province 610083, People’s Republic of China 3 To whom correspondence should be addressed at Department of Oral and Maxillofacial Surgery, Second Affiliated Hospital, Third Military Medical University, Xinqiaozheng Street, Shapingba District, Chongqing, 400038, People’s Republic of China. E-mail: [email protected]
inflammatory cytokine secretion from immune cells that results in periodontal tissue destruction [4, 5]. Moreover, the injection of LPS into the gingival or periodontium tissues is an animal model similar to the other animal models for periodontitis [6]. The PDL cells, which lie between alveolar bone and cementum, are in close proximity to bacteria within the plaque and the pocket, and thus, these cells are readily accessible to bacterial endotoxins and other promoters of inflammation [7
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