| Project/Area Number |
16591889
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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 |
Pathobiological dentistry/Dental radiology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
AIDA Yoshitomi Kyushu University, Section of Periodontology, Division of Oral Rehabilitation, Faculty of Dental Science, Associate Professor, 歯学研究院, 助教授 (10127954)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2004: ¥2,300,000 (Direct Cost: ¥2,300,000)
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| Keywords | local anesthetics / neutrophil / priming / lipopolysaccharide / superoxide / cytochrome b558 / p38 MAPK / 単球 |
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| Research Abstract |
Fimbriae has been thought to be an important virulence factor of P.gingivalis in the pathogenesis of periodontitis. Fimbriae has been reported to mediate adherence of bacterial cells to epithelium and induce cytokines in human monocyte or epitherial cells. In this study, effects of fimbriae on the cellular activity of neutrophil was investigated. Fimbriae was purified from P. gingivalis and lipopolysaccharide contaminated in fimbriae was depleted by phase separation using Triton X-114. LPS-depleted fimbriae was tested for activation of neutrophil. Results were as follows : 1) Fimbriae did not prime neutrophils for enhanced release of superoxide in response to fMLP. 2) Activated neutrophils produced superoxide in response to adherence to fimbriae-coated polystyrene. 3) Fimbriae induced interleukin 8 production in neutrophils and this response was inhibited by antibody to Toll-like receptor 4. 4) Fimbriae did not appear to activate p38 MAP kinase in neutrophils. On the basis of these results, fimbriae did not appear to be an active virulence factor in neutrophil-mediated pathogenesis of periodontitis.
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