Nicotine favors osteoclastogenesis in human periodontal ligament cells co-cultured with CD4+ T cells by upregulating IL-1β

  • Authors:
    • Li-Zheng Wu
    • Duo-Mo Duan
    • Ying-Feng Liu
    • Xin Ge
    • Zhi-Fei Zhou
    • Xiao-Jing Wang
  • View Affiliations

  • Published online on: January 30, 2013     https://doi.org/10.3892/ijmm.2013.1259
  • Pages: 938-942
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Abstract

Periodontitis, which is the main cause of tooth loss, is one of the most common chronic oral diseases in adults. Tooth loss is mainly a result of alveolar bone resorption, which reflects an increased osteoclast formation and activation. Osteoclast formation in periodontal tissue is a multistep process driven by osteoclastogenesis supporting cells such as human periodontal ligament (PDL) cells and CD4+ T cells. Inflammatory cytokines, such as interleukin-1β (IL-1β), can induce osteoclastogenesis by affecting the expression of receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in human PDL cells. Nicotine, the major component in tobacco smoking and a specific agonist of the α7 nicotinic acetylcholine receptor (α7 nAChR), has been proven to regulate the expression of inflammatory cytokines in smoking-associated periodontitis. In this study, we investigated the mechanism(s) through which nicotine affects osteoclastogenesis in human PDL cells co-cultured/non-co-cultured with CD4+ T cells. Human PDL cells were stimulated with nicotine (10-5 M) and/or α-bungarotoxin (α-BTX, specific antagonist of α7 nAChR, 10-8 M) before being co-cultured with CD4+ T cells. Compared with mono-culture systems, stimulation with nicotine caused an increased secretion of IL-1β in serum of human PDL cell-CD4+ T cell co-culture, and the expression of RANKL in human PDL cells was further upregulated co-cultured with CD4+ T cells, while no differences were observed in the expression of OPG between the co-culture and mono-culture systems. Our data suggested that nicotine upregulated IL-1β secretion, further upregulated RANKL expression in smoking-associated periodontitis, which may aid in the better understanding of the relationship between nicotine and alveolar bone resorption.
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April 2013
Volume 31 Issue 4

Print ISSN: 1107-3756
Online ISSN:1791-244X

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Spandidos Publications style
Wu L, Duan D, Liu Y, Ge X, Zhou Z and Wang X: Nicotine favors osteoclastogenesis in human periodontal ligament cells co-cultured with CD4+ T cells by upregulating IL-1β. Int J Mol Med 31: 938-942, 2013
APA
Wu, L., Duan, D., Liu, Y., Ge, X., Zhou, Z., & Wang, X. (2013). Nicotine favors osteoclastogenesis in human periodontal ligament cells co-cultured with CD4+ T cells by upregulating IL-1β. International Journal of Molecular Medicine, 31, 938-942. https://doi.org/10.3892/ijmm.2013.1259
MLA
Wu, L., Duan, D., Liu, Y., Ge, X., Zhou, Z., Wang, X."Nicotine favors osteoclastogenesis in human periodontal ligament cells co-cultured with CD4+ T cells by upregulating IL-1β". International Journal of Molecular Medicine 31.4 (2013): 938-942.
Chicago
Wu, L., Duan, D., Liu, Y., Ge, X., Zhou, Z., Wang, X."Nicotine favors osteoclastogenesis in human periodontal ligament cells co-cultured with CD4+ T cells by upregulating IL-1β". International Journal of Molecular Medicine 31, no. 4 (2013): 938-942. https://doi.org/10.3892/ijmm.2013.1259