| Project/Area Number |
13671958
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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 |
Functional basic dentistry
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| Research Institution | Matsumoto Dental University (2002)
Osaka Dental University (2001) |
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Principal Investigator |
WANG Pao-li Matsumoto Dental University, Professor, 歯学部, 教授 (20213613)
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| Co-Investigator(Kenkyū-buntansha) |
NAITO Makoto Matsumoto Dental University, Instructor, 歯学部, 助手 (80329474)
AZUMA Yasutaka Osaka Dental University, Instructor, 歯学部, 助手 (50298816)
OHURA Kiyoshi Matsumoto Dental University, Professor, 歯学部, 教授 (20131378)
MIYAZAWA Yoshiko Matsumoto Dental University, Instructor, 歯学部, 助手 (10200164)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 2002: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Periodontal Disease / LPS / CD14 / TLR4 / Gingival Fibroblasts |
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| Research Abstract |
Porphyromonas gingivalis (P. gingivalis) is implicated in the initation and progression of periodontitis. Human gingival fibroblasts (HGFs) are the major constituent of gingival connective tissue. P. gingivalis or its components such as lipopolysaccharide (LPS) upregulate the production of various inflammatory cytokines including interleukin (IL)-1 and IL-6 HGFs. Recently, we demonstrated that the binding of P. gingivalis LPS to Toll-like receptor 4 (TLR4) on HGFs activates vatious second messenger systems. In the present study, we ezamined the level of TLR4 expression on HGFs by enzyme-linked *mosorbent assay (ELISA). Upon stimulation by P. gingivalis LPS for 24 h, HGFs that expressed a high level of TLR4 secreted significantly higher levels of IL-1 and IL-6 than HGFs that expressed a low level of TLR4. On the other hand, after stimulation with P. gingivalis LPS for 24 h, the level of TLR4 on the surface of HGFs decreased. These results suggest that the level of TLR4 expression on HGFs reflects the extent of inflammation in the gingival tissue, and that P. gingivalis LPS downregulates TLR4 expression on HGFs reflects the extent of inflammation in the gingival tissue, and that P. gingivalis LPS downregulates TLR4 expression on HGFs. These findings may be used to control inflammatory and immune responses in periodontal disease
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