Project/Area Number |
09671857
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Morphological basic dentistry
|
Research Institution | The University of Tokushima |
Principal Investigator |
MIYAKE Yoichiro Tokushima University School of Dentistry, Department of Microbiology, Professor, 歯学部, 教授 (80136093)
|
Co-Investigator(Kenkyū-buntansha) |
NEMOTO Ken Tokushima University School of Dentistry, Department of Microbiology, Instructor, 歯学部, 助手 (10218274)
HIROTA Katsuhiko Tokushima University School of Dentistry, Department of Microbiology, Instructor, 歯学部, 助手 (60199130)
ONO Tsuneko Tokushima University School of Dentistry, Department of Microbiology, Associate, 歯学部, 助教授 (40035514)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥2,500,000 (Direct Cost: ¥2,500,000)
|
Keywords | streptococci / CD15s / fosfomycin / autoimmunity / liver |
Research Abstract |
Streptococcus pyogenes and oral streptococci express CD15s-like antigen which may have a role in pathogenecity of the bacteria. Characterization of the antigen demonstrated the antigen being non-proteinous substance with its molecular size of 400-500 kDa, and contains N-acetylglucosamine, glucose, fructose, galactose, and sialic acid. We investigated the effect of antibiotics on the expression of the antigen by S.pyogenes. Among antibiotics tested, benzylpenicillin, a transpeptidase inhibitor, and fosfomycin reduced the expression of CD15s. It is worth noted that enantiomer fosfomycin, without any antibacterial activity, also reduced the antigen expression. Microorganisms which mimic human antigen, such as Helicobacter pylori and Schistosoma mansonii, induce autoimmune reaction of humans. We injected heat-killed S.intermedius repeatedly to mice from gingiva. As a result, antibody to CD15s was induced and the antibody reacted with mouse neutrophils. In the liver, inflammation occurred and hepatocytes in and around the inflammatory lesion expressed CD15s cytoplasmically. Cell adhesion molecules, E-selectin and ICAM-1 which have a role in infiltration of lymphocytes, were expressed by endothelial cells of central vein and sinusoid. Inflammatory lesion was dominated by lymphocytes while a small number of macrophages were also observed. Most of the infiltrating T cells were CD8+T cells. CD3+T cells and B220+B cells infiltrated in the liver had high binding ability to CD15s-probe. Apoptosis of the hepatocytes in and around inflammatory lesion was demonstrated by TUNEL method. Our results suggest that immunization with CD15s positive S.intermedius from gingiva induced the systemic immune response and trigger autoimmune response in the liver.
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