| Project/Area Number |
06672059
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
矯正・小児・社会系歯学
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| Research Institution | The University of Tokushima |
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Principal Investigator |
HIROTA Katsuhiko The University of Tokushima, Dentistry, Research Associate, 歯学部, 助手 (60199130)
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| Co-Investigator(Kenkyū-buntansha) |
NEMOTO Ken The University of Tokushima, Dentistry, Research Associate, 歯学部, 助手 (10218274)
ONO Tsuneko The University of Tokushima, Dentistry, Assistant Professor, 歯学部, 講師 (40035514)
MIYAKE Yoichiro The University of Tokushima, Dentistry, Professor, 歯学部, 教授 (80136093)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1995: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1994: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | heart disease / oral streptococci / Kawasaki syndrome / sialy Lewis^X / translocation / sialyl Lewis^X |
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| Research Abstract |
The expression of sialyl-Lewis^X (sLe^X ; Neu5Ac alpha2-3 Gal beta1-4 (Fuc alpha1-3) GlcNAc-R) on oral bacteria producing infective endocarditis was determined by a whole-cell enzyme linked immuno-sorbent assay and an immuno-electron microscopy using the well-characterized anti-sLe^X monoclonal antibody SNH-3 (MAb SNH-3 ; IgM class). mAb SNH-3 reacted strongly with whole cells of oral bacteria-Streptococcus sanguis, Streptococcus mutans, Streptococcus mitis, Streptococcus salivarius, Streptococcus intermedius, Streptococcus constellatus, Streptococcus anginosus, Streptococcus pyogenes, Actinobacillus actinomycetemcomitans, Eikenella corrodens and Porphyromonas gingivalis. The negatively stained immuno-electron micrograph of Streptococcus pyogenes showed many reactive gold particles on the cell surface. Our findings demonstrated the existence of immunologic mimicry between the sLe^X oligosaccharide and cell surface antigens of many species associated with infective endocarditis. We propose the hypothesis that if these bacteria escape their normal habitats, the surface components that mimic the sLe^X oligosaccharide might bind to host antigens of the selectin family which could promote binding to endothelial cells and, consequently, initiation of the events leading to infective endocarditis.
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