慢性牙周炎患者血清IL-33、TNF-α、IL-6的检测及意义

doi:10.3969/j.issn.1006-7795.2016.03.001

首都医科大学学报 ›› 2016, Vol. 37 ›› Issue (3): 255-259.doi: 10.3969/j.issn.1006-7795.2016.03.001

慢性牙周炎患者血清IL-33、TNF-α、IL-6的检测及意义

林梅, 张冬雪, 刘志强, 王左敏

首都医科大学附属北京朝阳医院口腔科, 北京 100020

收稿日期:2016-03-29 出版日期:2016-06-21 发布日期:2016-06-13
通讯作者: 王左敏 E-mail:wzuomin@sina.com
基金资助:
国家自然科学基金面上项目(81271158),北京市科学技术委员会首都市民健康项目培育项目(Z131100006813027)。

Levels of IL-33, TNF-α, and IL-6 in peripheral blood of the patients with chronic periodontitis

Lin Mei, Zhang Dongxue, Liu Zhiqiang, Wang Zuomin

Department of Stomatology, Beijing Chaoyang Hospital, Capital Medical University, Beijing 100020, China

Received:2016-03-29 Online:2016-06-21 Published:2016-06-13
Supported by:
This study was supported by National Natural Science Foundation Of China(81271158), Fund of the Capital Public Health Project from Beijing Municipal Commission of Science and Technology(Z131100006813027).

摘要/Abstract

摘要： 目的检测并分析慢性牙周炎患者血清中白细胞介素(interleukin, IL)-33、肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)、IL-6的浓度。方法选取慢性牙周炎患者和健康人群共218人,采用酶联免疫吸附法(enzyme linked immunosorbent assay, ELISA)检测牙周炎患者的血清中IL-33、TNF-α、IL-6的浓度。结果与健康人群相比,中度及重度牙周炎患者血清中的IL-33显著降低(P <0.01),而重度牙周炎患者血清中的TNF-α显著升高(P <0.01),中度及重度牙周炎患者血清中的IL-6浓度显著升高(P=0.042,P <0.001)。结论血清中TNF-α、IL-6浓度与牙周组织炎性反应呈正相关关系,可以作为提示牙周炎活跃期的一个信号分子,而IL-33浓度与牙周组织炎性反应呈负相关关系,在慢性牙周炎病理过程中可能具有保护协调性的作用。

关键词: 白细胞介素-33, 肿瘤坏死因子-α, 白细胞介素-6, 慢性牙周炎

Abstract: Objective To investigate the levels of interleukin (IL)-33, tumor necrosis factor-α(TNF-α), IL-6 expression in peripheral blood of the patients with chronic periodontitis(CP). Methods Thirty-one healthy controls,187 cases with CP who were divided into 4 groups: healthy controls, mild periodontitis, moderate periodontitis, severe periodontitis were enrolled.IL-33,TNF-α,IL-6 were examined by enzyme linked immunosorbent assay (ELISA).Periodontal indexes were measured.Results In the CP group of moderate and severe periodontitis, IL-33 were significantly lower than that of healthy controls (P <0.01).TNF-α in severe periodontitis was higher than those in the control group (P <0.01) (between moderate periodontitis and healthy controls,P >0.05), and IL-6 in the group of moderate and severe periodontitis were significantly higher than healthy control(P=0.042, P <0.01). Conclusion The levels of TNF-α and IL-6 in serum positively correlated with periodontal tissue inflammation, and therefore they may be used as signal molecules suggestive of active stage periodontitis; IL-33 level negatively correlated with inflammation of periodontal tissue, which may have protective coordinating effects in the pathological processes of chronic periodontitis.

Key words: interleukin-33, tumor necrosis factor-α, interleukin-6, chronic periodontitis

中图分类号:

R781.4

林梅, 张冬雪, 刘志强, 王左敏. 慢性牙周炎患者血清IL-33、TNF-α、IL-6的检测及意义[J]. 首都医科大学学报, 2016, 37(3): 255-259.

Lin Mei, Zhang Dongxue, Liu Zhiqiang, Wang Zuomin. Levels of IL-33, TNF-α, and IL-6 in peripheral blood of the patients with chronic periodontitis[J]. Journal of Capital Medical University, 2016, 37(3): 255-259.

参考文献

[1] Pihlstrom B L, Michalowicz B S, Johnson N W. Periodontal diseases[J]. Lancet, 2005, 366(9499):1809-1820.
[2] AIJehani Y A. Risk factors of periodontal disease: review of the literature[J]. Int J Dent, 2014: 182513.
[3] Yucel O O, Berker E, Gariboqlu S, et al. Interleukin-11, interleukin-1beta, interleukin-12 and the pathogenesis of inflammatory periodontal diseases[J]. J Clin Periodontol, 2008, 35(5): 365-370.
[4] Lingel A, Weiss T M, Niebuhr M, et al. The structure of interleukin-33 and its interaction with the ST2 and IL-1RAcP receptors-insight into the arrangement of heterotrimeric interleukin-1 signaling complexes[J]. Structure, 2009, 17(10): 1398-1410.
[5] Schmitz J, Owyang A, Oldham E, et al. IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines[J]. Immunity, 2005, 23(5): 479-490.
[6] Moradi J,Abbasipour F,Zaringhalam J, et al. Anethole,a medicinal plant compound,decreases the production of pro-inflammatory TNF-alpha and IL-lbeta in a rat model of LPS-Induced periodontitis[J]. Iran J Pharm Res, 2014, 13(4): 1319-1325.
[7] Jiang Z L,Cui Y Q,Gao R,et al. Study of TNF-alpha, IL-lbeta and LPS levels in the gingival crevicular fluid of a rat model of diabetes mellitus and periodontitis[J]. Dis Markers, 2013, 34(5): 295-304.
[8] Reis C, DA Costa A V, Guimarães J T, et al. Clinical improvement following therapy for periodontitis: association with a decrease in IL-1 and IL-6[J]. Exp Ther Med, 2014, 8(1): 323-327.
[9] Carriere V, Roussel L, Ortega N, et al. IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factor in vivo[J]. Proc Natl Acad Sci USA, 2007, 104(1): 282-287.
[10] da Luz F A, Oliveira A P, Borges D, et al. The physiopathological role of IL-33: new highlights in bone biology and a proposed role in periodontal disease[J]. Mediators Inflamm, 2014, 2014: 342410.
[11] Nakao A, Fukushima H, Kajiya H, et al. RANKL-stimulated TNFalpha production in osteoclast precursor cells promotes osteoclastogenesis by modulating RANK signaling pathways[J]. Biochem Biophys Res Commun, 2007, 357(4):945-950.
[12] Souto G R, Queiroz-Junior C M, de Abreu M H, et al. Pro-inflammatory, Thl, Th2, Thl7 cytokines and dendritic cells: across-sectional study in chronic periodontitis[J]. PLoS One, 2014, 9(3): e91636.
[13] Brunetti G,Colucci S,Pignataro P,et al. T cells support osteoclastogenesis in an in vitro model derived from human periodontitis patients[J]. J Periodontol, 2005, 76(10): 1675-1680.
[14] Oates T W,Graves D T,Cochran D L. Clinical, radiographic and biochemical assessment of IL-1/TNF-alpha antagonist inhibition of bone loss in experimental periodontitis[J]. J Clin Periodontol, 2002, 29(2): 137-143.
[15] Preshaw P M,Taylor J J. How has research into cytokine interactions and their role in driving immune responses impacted our understanding of periodontitis?[J]. J Clin Periodontol, 2011, 38(Suppl 11): 60-84.
[16] Zheng P, Chen H, Shi S, et al. Periodontal parameters and platelet-activating factor levels in serum and gingival crevicular fluid in a Chinese population[J]. J Clin Periodontol, 2006, 33(11): 797-802.
[17] 常春荣,韩东,孙尚敏,等. 牙周基础治疗对慢性牙周炎患者龈沟液白细胞介素6、肿瘤坏死因子α及血清高敏C反应蛋白的影响[J]. 中国医科大学学报,2013,42(2):135-137.
[18] 丁芳,吕亚林,王杰,等. 认知行为干预对维持慢性牙周炎治疗效果的作用[J]. 首都医科大学学报,2015,36(5):768-772.

慢性牙周炎患者血清IL-33、TNF-α、IL-6的检测及意义

Levels of IL-33, TNF-α, and IL-6 in peripheral blood of the patients with chronic periodontitis

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