1998 Fiscal Year Final Research Report Summary
Development of Immunological Procedure for Prevention of Periodontal Disease Using
| Project/Area Number |
08457572
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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 |
矯正・小児・社会系歯学
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
KOGA Toshihiko Faculty of Dentistry, KYUSHU UNIVERSITY,Professor, 歯学部, 教授 (10037541)
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| Co-Investigator(Kenkyū-buntansha) |
SHIBATA Yukie Faculty of Dentistry, KYUSHU UNIVERSITY,Research Associate, 歯学部, 助手 (30274476)
YAMAGUCHI Noboru Faculty of Dentistry, KYUSHU UNIVERSITY,Research Associate, 歯学部, 助手 (00230368)
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| Project Period (FY) |
1996 – 1998
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| Keywords | Periodontal Disease / Periodontitis / Periodontopathic Bacteria / Monoclonal Antibody / Carbohydrate Antigen / Lipopolysaccharide |
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| Research Abstract |
In this study, monoclonal antibodies and polyclonal antibodies against cell-surface antigens of periodontopathic Actinobacillus actinomycetemcomitans (Aa) and Porphvromonas gingivalis. Using these antibodies, we have obtained the results described below.
1) A large gene cluster associated with the biosynthesis of the serotype-specific polysaccharide antigen (SPA) of Aa Y4 (serotype b) was cloned and characterized. Escherichia coli containing a plasmid carrying this cluster, produced a polysaccharide which reacted with a monoclonal antibody directed against the SPA of Aa Y4.2) Gene clusters involved in the synthesis of the serotype a antigen and the serotype c antigen of Aa were cloned. 3) SPA extracted from whole cells of Aa Y4 by autoclaving and purified by chromatography on DEAE-Sephadex A-25 and Sephacryl S-300 induced the release of monocyte chemotactic factor and inflammatory cytokines by human monocytes. The release of the factor was inhibited by monoclonal antibodies against SPA, but not by monoclonal antibodies of lipopolysaccharide from strain Y4.4) The ability of Aa Y4 and its SPA-defective variants to elicit the chemiluminescence response of human polymorphonuclear leukocytes in the presence of complement. The chemiluminescence response of leukocytes to strain Y4 was weak, but that to the SPA-defective variants was high. Monoclonal antibodies against SPA enhanced significantly the response of leukocytes to strain Y4.
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