Department of Periodontology, School of Dentistry, Aichi Gakuin University, 2-11 Suemoridori, Chikusa-ku, Nagoya, Aichi 464-8651, Japan.
Arch Oral Biol. 2013 Oct;58(10):1541-8. doi: 10.1016/j.archoralbio.2013.06.020. Epub 2013 Jul 25.
Oral epithelial cells act not only as mechanical barriers but also as immunological barriers by producing various mediators such as cytokines. Since, in periodontal disease, limited information is available regarding the role of oral epithelial cell-derived cytokines on T cell activation, we investigated the responses of human T cells (Jurkat cell) to cytokines in KB cells (an oral epithelial cell line) that had been stimulated with Aggregatibacter actinomycetemcomitans lipopolysaccharide (LPS).
To evaluate T cell activation in response to the culture supernatant of KB cells, we examined cell proliferation and interferon gamma (IFN-γ) production, which is closely related to periodontal disease, in Jurkat cells. Culture supernatant of LPS-stimulated KB cells enhanced cell proliferation and IFN-γ production in Jurkat cells. To determine the active component within the culture supernatant, the production of epithelial cell-derived cytokines, interleukin-12 (IL-12), IL-15 and IL-18, in LPS-stimulated KB cells was analysed.
IL-15, but not IL-18, was significantly increased in the culture supernatant of LPS-stimulated KB cells. Moreover, additional anti-IL-15 neutralizing antibody abolished culture supernatant-induced IFN-γ expression in Jurkat cells.
These results suggest that periodontal pathogens induce the production of IL-15 from epithelial cells, and leading the activation of T cells in periodontal lesions.
口腔上皮细胞不仅作为机械屏障，还通过产生各种介质（如细胞因子）发挥免疫屏障作用。由于在牙周病中，关于口腔上皮细胞来源的细胞因子对 T 细胞活化的作用的信息有限，我们研究了人 T 细胞（Jurkat 细胞）对被牙龈卟啉单胞菌脂多糖（LPS）刺激的 KB 细胞（一种口腔上皮细胞系）来源的细胞因子的反应。
为了评估 KB 细胞培养上清液对 T 细胞活化的影响，我们检测了 Jurkat 细胞的增殖和干扰素γ（IFN-γ）产生，IFN-γ与牙周病密切相关。LPS 刺激的 KB 细胞的培养上清液增强了 Jurkat 细胞的增殖和 IFN-γ产生。为了确定培养上清液中的活性成分，分析了 LPS 刺激的 KB 细胞中上皮细胞来源的细胞因子白细胞介素 12（IL-12）、IL-15 和 IL-18 的产生。
LPS 刺激的 KB 细胞培养上清液中 IL-15 显著增加，而 IL-18 则没有。此外，额外的抗 IL-15 中和抗体消除了培养上清液诱导 Jurkat 细胞中 IFN-γ表达。
这些结果表明，牙周病病原体诱导上皮细胞产生 IL-15，并导致牙周病损中 T 细胞的活化。
