| Project/Area Number |
12672041
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Tokyo University of Science |
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Principal Investigator |
NOBUMICHI Hozumi Research Institute for Biological Sciences Tokyo University of Science, Pofessor, 生命科学研究所, 教授 (60051744)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIYUKI Hakeda Departmentfof Oral Anatomy, Faculty of Dentistry,Meikai University, Associate Professor, 歯学部・口腔解剖学講座, 助教授 (90164772)
KENICHI Tezuka Research Institute for Biological Science, Tokyo University of Science, Assistant Professor, 生命科学研究所, 講師 (50236973)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | NOD-SCID mouse / Actinohacilllis actinnmycetemcomitans / periodontitis / human immune response / CD4+ T cells / NOD / SCODマウス / Actinobacillus actionomycetemcomitans / Limiting Dilution Assay / IgG |
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| Research Abstract |
Juvenile periodontal diseases are heterogenous and are the result of specific microbial infection leading to host immune and/or inflammatory responses in the tooth-supporting tissues. Actinobacillus actinomycetemcomitans (Aa) is speculated to be responsible for the disease. We established a noble mouse model to elucidate the molecular mechanism involved in Aa infection-induced periodontitis. NOD-SCID mice were engrafted with peripheral blood lymphocytes from periodontitis patients. Then, these mice were inoculated with Aa (10^9 pfu) orally. Aa challenge (3 x wk) were repeated for 3-4 consecutive weeks. Mice were sacrificed and human lymphocytes isolated from periodontal tissues were analyzed by immunological methods. Periodontal tissues were examined by histological experiments as well. Infiltration of human. CD4^+T cells were observed in the tissues. Peripheral human T cells isolated from the mice were demonstrated to mount anti-Aa response. Depletion of human CD4 T cells resulted in a significant reduction of periodontal inflammation and bone destruction. These results suggest that the animal model should be quite versatile for the experiments of Aa infection-induced periodontitis.
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