Project/Area Number |
09671864
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Morphological basic dentistry
|
Research Institution | Meikai University |
Principal Investigator |
HANAZAWA Shigemasa Meikai University School of Dentistry, Prof., 歯学部, 教授 (60060258)
|
Co-Investigator(Kenkyū-buntansha) |
MURAKAMI Yukio Meikai University School of Dentistry, Res.Asso., 歯学部, 助手 (00286014)
TAKESHITA Akira Meikai University School of Dentistry, Res.Asso., 歯学部, 助手 (70236454)
|
Project Period (FY) |
1997 – 1998
|
Project Status |
Completed (Fiscal Year 1998)
|
Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 1998: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1997: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | P.gingivalis / Gingival fibroblasts / Lipopolysaccharide / CD14 / Signal transduction / Inflammatory cytokine / リポ多多糖体 / LPS / 歯周疾患 / 骨芽細胞 / 骨吸収刺激作用 / Interleukin-1 |
Research Abstract |
Lipopolysaccharide(LPS) of Porphyrom onas gin givalis(P.gin givalis), a pathogenic bacterium of periodontal disease, has been considered an important pathogenic component of the organism in the initiation and development of periodontal diseases, because bacterial LPS is known to be a potent stimulator of inflammatory cytokine production and bone resorption. One target of LPS is the human gingival fibroblast, a cell that play an important role in the remodeling of periodontal soft tissues. These fibroblasts may also function as a regulator of the cytokine network of periodontal tissues, because they produce several kinds of cytokine when stimulated by inflammatory cytokines and bacterial cell components. P.gin givalis LPS stimulates interleukin(IL)-1, IL-8, and IL-6 production by human gingival fibroblasts. More recently, a very interesting study has demonstrated that CD14 gene expression in the mouse is not restricted to myeloid cells only, but also occurs in epithelial cells of various organs. This demonstration suggested to us that LPS maybe involved actively in inflammatory reactions of various tissues via CD14. Therefore, it is very important to examine whether human gingival fibroblasts express CD14 on their cell surface. If they do, it would be of interest to elucidate the CD14-mediated signal transducing mechanism of P.gingivalis LPS in these gingival fibroblasts. In the present study, we demonstrated that human gingival fibroblasts express CDI4 and also demonstrated CD14 mediation of the signal pathway of P.gin givalis LPS in the cells.
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