| Project/Area Number |
09670301
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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 |
Bacteriology (including Mycology)
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| Research Institution | Kanagawa Dental College |
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Principal Investigator |
KUMADA Hidefumi Kanagawa Dental College, School of Dentistry, Oral Microbiology, assistant professor, 歯学部, 講師 (60120995)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Kiyoko Kanagawa Dental College, School of Dentistry, Oral Microbiology, research associ, 歯学部, 助手 (70148021)
棚元 憲一 国立医薬品食品衛生研究所(旧国立衛生試験所), 衛生微生物部, 室長
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Porphyromonas gingivalis / endotoxin / synthetic lipid A / Limulus amoebocyte / maitogenic activity / TNFalpha activity / IL-6 activity / C3H / HeJ mouse / マイトジェン / リムルス / IL-6 / TNFα / HeJマウス |
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| Research Abstract |
Porphyromonas gingivalis has been implicated as one of the major periodontal pathogens. The lipopolysaccharide (LPS) expresses typical activities directly associated with the periodontal diseases of bone resorption, induction of various inflammatory cytokines, and induction of periodontal tissue alterations and destruction including attachment loss, collagen degradation and alveolar bone loss. The LPS also has a far more moderate endotoxic activity than the LPS from enterobacteria, and is able to activate splenocyte mitogenicity, cytokine release from peritoneal macrophages in LPS-nonresponsive C3H/HeJ mouse to the same extent as in LPS-responsive mouse. However, the study of the structural-activity relationship concerning these facts f is not yet done, especially, the interest is had very much about the fact in which Pg LPS activates the LPS-nonresponsive mouse cells.
The lipid A part of Porphyromonas gingivalis lipopolysaccharide (LPS) was chemically synthesized to elucidate the essen
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tial activity of lipid A itself, the active center of LPS.Since the LPS or native lipid A preparation of P.gingivalis has been found to induce splenocyte mitogenicity, cytokine release from peritoneal macrophages in LPS-nonresponsive C3H/HeJ mouse to the same extent as in LPS-responsive mouse.
In this study, no the synthetic lipid A of P.gingivalis certainly exhibited biological activity in the assay tested ; mitogenicity in spleen cells and the release of TNF-alpha and IL-6 from peritoneal macrophages of C3H/HeJ mouse, however the native lipid. A strongly exhibited those activities. The synthetic lipid A of P.gingivalis also exhibited biological activity a little less than those observed for Escherichia coli synthetic lipid A (506) used as a positive control, when measured those in LPS-responsive C3H/HeN mice. It was concluded that the LPS itself of P.gingivalis could not be to activate the cells of LPS-nonresponsive mouse, despite the native lipid A was able to activate. The responsibility of LPS-nonresponsive mouse cells to LPS or native lipid A of P.gingivalis reported by several groups may thought that the active material in these preparations is contaminants ; outer membrane proteins et al.. Less
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