| Project/Area Number |
10470458
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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 |
Periodontal dentistry
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| Research Institution | Niigata University |
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Principal Investigator |
YAMAZAKI Kazuhisa Faculty of Dentistry, Niigata University, Associate Professor, 歯学部, 助教授 (00182478)
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| Co-Investigator(Kenkyū-buntansha) |
AOYAGI Toshihiko Niigata University Dental Hospital, Assistant, 歯学部・附属病院, 助手 (80283018)
中島 貴子 新潟大学, 歯学部, 助手 (40303143)
原 耕二 新潟大学, 歯学部, 教授 (20018419)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥13,300,000 (Direct Cost: ¥13,300,000)
Fiscal Year 2000: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 1999: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 1998: ¥5,100,000 (Direct Cost: ¥5,100,000)
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| Keywords | Periodontitis / HSP60 / TCR / Molecular Mimicry / Th1 / SSCP / Sequencing / Heat Shock Protein / Porphyromonas gingivalis / T cell clonotype / Periodontitis / RT-PCR / Periodentitis |
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| Research Abstract |
Our previous studies using RT-PCR-SSCP analysis demonstrated the high clonality of T cells infiltrating into periodontitis lesion similar to that in inflammatory lesion of autoimmune diseases such as rheumatoid arthritis. Considering that the complex microbial flora in the periodontal pocket, it was speculated that T cells are recognizing antigens of bacteria which are homologous to host components. Because heat shock protein 6Os are remarkably immunogenic, despite their high degree of evolutionary conservation, both T cell and antibody responses to hsp60 have been reported in a variety of inflammatory conditions. In order to clarify the role of hsp60s on the T cell response in periodontitis, we examined the proliferative response of peripheral blood mononuclear cells (PBMC) as well as cytokine profile and clonality of T cells upon stimulation with recombinant human hsp6O and Porphyromonas gingivalis (P.gingivalis) GroEL from periodontitis patients and control subjects. Furthermore, nu
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cleotide sequences within the CDR3 region of the T cell receptor β-chain was compared between hsp60-reactive PBMC and periodontitis lesion-infiltrating T cells. In periodontitis patients significantly higher proliferative response of PBMC to human hsp60 but not to P.gingivalis GroEL than in control subjects. Analysis of the nucleotide sequences within the CDR3 region clearly demonstrated that hsp60-reactive T cell clones and periodontitis lesion-infiltrating T cells expressed the same receptors suggesting that hsp60-reactive T cells accumulated in periodontitis lesion. The analysis of cytokine profile demonstrated that hsp60-reactive PBMC produced significant level of IFN-γ in periodontitis patients, whereas P.gingivalis GroEL did not induce any skewing towards type1 or type2. In control subjects no significant expression of IFN-γ or IL-4 was induced upon stimulation with either hsp60 or P.gingivalis GroEL.These results suggest that in periodontitis patients infection with periodontopathic bacteria may induce the activation of self hsp60-reactive T cells with type1 cytokine profile resulting the stimulation of macrophage to produce proinflammatory cytokines leading to the tissue destruction. Less
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