Department of Periodontology and Operative Dentistry, University Medical Center, University of Mainz, 55131 Mainz, Germany.
Section of Experimental Dento-Maxillo-Facial Medicine, Center of Dento-Maxillo-Facial Medicine, University of Bonn, 53111 Bonn, Germany.
Int J Mol Sci. 2021 Jan 27;22(3):1235. doi: 10.3390/ijms22031235.
There is little known about the effect of the periodontopathogen on macrophages as key cells of the innate immune defense in the periodontium. Therefore, the aim of the present study was to investigate the effect of and additionally of the pro-inflammatory cytokine tumor necrosis factor-alpha (TNFα) on visfatin and other pro-inflammatory and proteolytic molecules associated with periodontitis in human macrophages. The presence of macrophage markers CD14, CD86, CD68, and CD163 was examined in gingival biopsies from healthy individuals and periodontitis patients. Human macrophages were incubated with and TNFα for up to 2 d. The effects of both stimulants on macrophages were determined by real-time PCR, ELISA, immunocytochemistry, and immunofluorescence. was able to significantly stimulate the synthesis of visfatin by human macrophages using TLR2 and MAPK pathways. In addition to visfatin, was also able to increase the synthesis of cyclooxygenase 2, TNFα, and matrix metalloproteinase 1. Like , TNFα was also able to stimulate the production of these proinflammatory and proteolytic molecules. Our results highlight the pathogenetic role of in periodontal diseases and also underline the involvement of visfatin in the aetiopathogenesis of periodontitis.
关于牙周病原体对作为牙周固有免疫防御关键细胞的巨噬细胞的影响知之甚少。因此,本研究的目的是研究 以及促炎细胞因子肿瘤坏死因子-α(TNFα)对人巨噬细胞中与牙周炎相关的内脂素和其他促炎及蛋白水解分子的影响。在健康个体和牙周炎患者的牙龈活检中检查了巨噬细胞标志物 CD14、CD86、CD68 和 CD163 的存在。用 和 TNFα 孵育人巨噬细胞长达 2 天。通过实时 PCR、ELISA、免疫细胞化学和免疫荧光测定这两种刺激物对巨噬细胞的影响。TLR2 和 MAPK 途径能够显著刺激人巨噬细胞合成内脂素。除了内脂素,还能够增加环氧合酶 2、TNFα 和基质金属蛋白酶 1 的合成。与 一样,TNFα 也能够刺激这些促炎和蛋白水解分子的产生。我们的结果强调了 在牙周病中的致病作用,并强调了内脂素在牙周炎发病机制中的参与。