| Project/Area Number |
02670824
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | Tohoku University |
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Principal Investigator |
RIKIISHI Hidemi Tohoku Univ. Dentistry Assistant Prof., 歯学部, 助手 (70091767)
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| Co-Investigator(Kenkyū-buntansha) |
KUMAGAI Katsuo Tohoku Univ. Dentistry, 歯学部, 教授 (00005018)
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| Project Period (FY) |
1990 – 1991
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| Project Status |
Completed (Fiscal Year 1991)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1991: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1990: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Peptidoglycan / Cytoplasmic membrane protein / GM-CSF / Arthropathic reaction / ペプチドグリカン刺激 / サイトカイン / マウス系統差 / 急性関節炎 |
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| Research Abstract |
The activities of peptidoglycan(PG)fragments derived from gram-positive cocci were examined to proliferate spleen mononuclear cells(SMNC)from murine various strains and to produce cytokines in vitro, and also examined to induce the inflammatory reaction in vivo. The proliferation of SMNC from C3H/HeN mice to PG in vitro were maximum on day 3, and greater than that of SMNC from Balb/c mice. It was indicated that the responsive cells of SMNC from C3H/HeN mouse to PG were mainly Ia^+ Mac^<2+> cells. mRNA transcripts of GM-CSF were detected in the lungs of C3H/HeN mouse much stronger than that of Balb/c mouse after 3 hr of injection. Balb/c mice were susceptible to acute arthritis after PG injection, whereas C3H/HeN and C57BL/6 mice failed to produce acute arthritis. The cytoplasmic membrane protein(MAP)of Streptococcus pyogenes, but not PG and others, when incubated with human peripheral blood lymphocytes, induced polyclonal activation of T cells after 5-7 days of incubation without IL-2 production. The activated T cells included CD^<4+> CD^<8-> helper T cells. We have obtained some informations on the responsibility of mononuclear cells to bacterial cell components, especially cytokine production and activated cells. These factors form a complex net work, and a complete understanding of the mechanisms involved in the arthritis to bacterial subfraction, must await detailed studies.
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