- 作者：Takayuki Suga ; Akio Mitani ; Makio Mogi ; Takeshi Kikuchi ; Takeki Fujimura ; Hiroaki Takeda ; Toshimitsu Hishikawa ; Genta Yamamoto ; Jun-ichiro Hayashi ; Yuichi Ishihara ; Toshihide Noguchi
- 关键词：Aggregatibacter actinomycetemcomitans (Actinobacillus actinomycetemcomitans) ; Interleukin-15 ; Periodontal diseases ; Epithelial cells ; Interferon-gamma
- 刊名：Archives of Oral Biology
- 出版年：2013
- 出版时间：October, 2013
- 年：2013
- 卷：58
- 期：10
- 页码：1541-1548
- 全文大小：706 K
Objective
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).Design
To evaluate T cell activation in response to the culture supernatant of KB cells, we examined cell proliferation and interferon gamma (IFN-¦Ã) production, which is closely related to periodontal disease, in Jurkat cells. Culture supernatant of LPS-stimulated KB cells enhanced cell proliferation and IFN-¦Ã 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.
Results
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-¦Ã expression in Jurkat cells.
Conclusion
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.