Project/Area Number |
18592274
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Periodontal dentistry
|
Research Institution | Hyogo College of Medicine |
Principal Investigator |
OHYAMA Hideki Hyogo College of Medicine, Faculty of Medicine, Assistant Professor (90280685)
|
Co-Investigator(Kenkyū-buntansha) |
TERADA Nobuyuki Hyogo College of Medicine, Faculty of Medicine, Professor (50150339)
NAKASHO Keiji Hyogo College of Medicine, Faculty of Medicine, Assistant Professor (00217712)
YAMADA Naoko Hyogo College of Medicine, Faculty of Medicine, Assistant Professor (10319858)
NISHIMURA Fusanori Hiroshima University, Graduate School of Biomedical Sciences, Professor (80208222)
HASHITANI Susumu Hyogo College of Medicine, Faculty of Medicine, Instructor (00330449)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥4,010,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥510,000)
Fiscal Year 2007: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | IL-22 / periodontitis / β-defensin / T cells / keratinocytes / β-ディフェンシン2,3 |
Research Abstract |
Interleukin (IL)-22, which is one of cytokines produced from activated helper T cells, plays an important role in the host defence against the bacterial infection by inducing the expression of β-defensin from keratinocytes. In contrast, since IL-22 is mostly produced from Th17 cells, which are implicated in the cell-mediated tissue damage, it is also likely that IL-22 is one of possible cytokines involved in the progression of the disease. In order to assess the involvement of IL-22 in periodontal diseases, we evaluated the expression level of IL-22 and IL-22 receptors in the periodontal lesions and the production level of IL-22 of peripheral blood T cells specific to periodontal antigens. Firstly, gene expression of IL22 and IL22RA were evaluated in the lesional sites and their control sites in each gingival biopsy sample. As a result, we could detect IL22RA expression in almost all gingival biopsy samples; however, the expression of IL22 could be detected in only a few samples. When compared between lesional sites and control sites, the gene expression levels of IL22RA in lesional sites were significantly higher than control sites. Next, we evaluated the IL-22 production of Th cell clones specific to Ag53 of P. gingivalis, which were derived from PBMCs. As a result, we could detect the IL-22 production in many T cell clones established in this study. Most of Th cell clones also had potential to produce IL-13 and IFN-γ, however, we could not find the correlations between IL-22 productivities and the production of these cytokines. From these findings, it might be implicated in the pathogenesis of the periodontal diseases that there are few numbers of Th cell producing IL-22 in periodontal lesions as compared with the numbers of IL-22 producing cells in the peripheral blood Th cells responding specific to the periodontal bacterial antigens.
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