| Project/Area Number |
15390551
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Morphological basic dentistry
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| Research Institution | Tohoku University |
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Principal Investigator |
SUGAWARA Shunji Tohoku University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (10241639)
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| Co-Investigator(Kenkyū-buntansha) |
TAKADA Haruhiko Tohoku University, Graduate School of Dentistry, Professor, 大学院・歯学研究科, 教授 (30135743)
NEMOTO Eiji Tohoku University, Graduate School of Dentistry, Assistant Professor, 大学院・歯学研究科, 助手 (40292221)
ENDO Yasuo Tohoku University, Graduate School of Dentistry, Associate Professor, 大学院・歯学研究科, 助教授 (50005039)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥14,000,000 (Direct Cost: ¥14,000,000)
Fiscal Year 2004: ¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 2003: ¥7,300,000 (Direct Cost: ¥7,300,000)
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| Keywords | periodontopathic bacteria / neutrophils / proteases / protease-activated receptors / innate immunity / oral mucosa / cytokines / 血小板 |
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| Research Abstract |
Research results of this project are as follows,
1.Neutrophil serine proteases (elastase, cathepsin G, and proteinase 3 (PR3)) activate human non-epithelial cells (i.e.human gingival fibroblasts (HGF)) through G-protein-coupled protease-activated receptor-2 (PAR-2) and induce cytokine production from the cells. PR3 but not elastase and cathepsin G activates oral epithelial cells, due to secretory leukocyte inhibitor (an inhibitor of elastase and cathepsin G but not PR3) from the epithelial cells.
2.Inflamed oral epithelium expresses PR3. Proinflammatory cytokines induce PR3 as membrane-bound and secretory forms with enzymatic activity. Antibodies to PR3 activate the cells through PAR-2 and induce chemokine production from the cells.
3.As T cells accumulate in the inflamed lamina propria of gingival tissue from patients with adult periodontitis, immune responses of gingival cells to T cell cytokines, interleukin-2 (IL-2) and IL-15 was investigated. Endogenous IL-15 expressed in HGF sustains recruitment of IL-2/15 receptor β and common γ through nuclear factor-κB activation in normal and inflamed HGF.
4.A trypsin-like proteases, gingipains, from periodontopathic bacteria cleave intercellular adhesion molecule-1 (CD54) expressed on oral epithelial cells, and consequently disrupt neutrophil-oral epithelial cell interaction.
5.SalivaCD14, an important molecule in innate immunity, promotes the invasion of oral epithelial cells by periodontopathic bacteria and consequently augments the production of chemokine, playing an important role in innate immunity in the oral cavity.
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