Department of Periodontics, College of Dentistry, The University of Iowa, Iowa City, IA 52242, USA.
J Clin Periodontol. 2011 Mar;38(3):219-28. doi: 10.1111/j.1600-051X.2010.01684.x. Epub 2010 Dec 29.
The aim of this study was to compare the expression of 22 chemokines and cytokines in gingival crevicular fluid (GCF) from smokers and non-smokers with periodontitis and periodontally healthy control subjects.
Forty subjects with generalized severe chronic periodontitis (20 smokers and 20 non-smokers) and 12 periodontally healthy control subjects participated in this study. Four diseased and two healthy sites were selected from each of the periodontitis subjects. GCF samples were collected and cytokines analysed utilizing a multiplexed immunoassay (Luminex(®) ). Statistical analyses employed non-parametric tests including the Mann-Whitney and Wilcoxon matched-pairs signed-rank tests.
Compared with healthy control subjects, GCF in subjects with chronic periodontitis contained significantly higher amounts of interleukin (IL)-1α, IL-1β, IL-6, IL-12(p40) (pro-inflammatory cytokines); IL-8, macrophage chemotactic protein (MCP)-1, macrophage inflammatory protein (MIP)-1α, regulated on activation normal T-cell expressed and secreted (RANTES) (chemokines); IL-2, IFN-γ, IL-3, IL-4 (Th1/Th2 cytokines); IL-15 [regulator of T-cells and natural killer (NK) cells]. Smokers displayed decreased amounts of pro-inflammatory cytokines [IL-1α, IL-6, IL-12(p40)], chemokines (IL-8, MCP-1, MIP-1, RANTES), and regulators of T-cells and NK cells (IL-7, IL-15).
Periodontitis subjects had significantly elevated cytokine and chemokine profiles. Smokers exhibited a decrease in several pro-inflammatory cytokines and chemokines and certain regulators of T-cells and NK-cells. This reflects the immunosuppressant effects of smoking which may contribute to an enhanced susceptibility to periodontitis.
本研究旨在比较吸烟和非吸烟牙周炎及牙周健康对照受试者龈沟液(GCF)中 22 种趋化因子和细胞因子的表达。
本研究纳入了 40 名患有广泛性严重慢性牙周炎的受试者(20 名吸烟者和 20 名非吸烟者)和 12 名牙周健康对照受试者。从每位牙周炎受试者中选择 4 个患病部位和 2 个健康部位。采集 GCF 样本并利用多重免疫分析(Luminex®)分析细胞因子。统计学分析采用非参数检验,包括 Mann-Whitney 和 Wilcoxon 配对符号秩检验。
与牙周健康对照受试者相比,慢性牙周炎受试者的 GCF 中含有明显更高水平的白细胞介素(IL)-1α、IL-1β、IL-6、IL-12(p40)(促炎细胞因子);IL-8、单核细胞趋化蛋白(MCP)-1、巨噬细胞炎性蛋白(MIP)-1α、调节激活正常 T 细胞表达和分泌(RANTES)(趋化因子);IL-2、IFN-γ、IL-3、IL-4(Th1/Th2 细胞因子);IL-15[调节 T 细胞和自然杀伤(NK)细胞]。吸烟者显示促炎细胞因子[IL-1α、IL-6、IL-12(p40)]、趋化因子(IL-8、MCP-1、MIP-1、RANTES)和 T 细胞及 NK 细胞调节剂(IL-7、IL-15)的含量减少。
牙周炎受试者的细胞因子和趋化因子谱显著升高。吸烟者表现出几种促炎细胞因子和趋化因子以及某些 T 细胞和 NK 细胞调节剂的减少。这反映了吸烟的免疫抑制作用,可能导致对牙周炎的易感性增强。