Induction of cytokines by oral bacterial stimulation and its arthropathic properties

口腔细菌刺激诱导细胞因子及其关节病特性

基本信息

  • 批准号:
    02670824
  • 负责人:
  • 金额:
    $ 1.34万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)
  • 财政年份:
    1990
  • 资助国家:
    日本
  • 起止时间:
    1990 至 1991
  • 项目状态:
    已结题

项目摘要

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.
本实验检测了革兰氏阳性球菌肽聚糖(PG)片段体外对小鼠脾单个核细胞(SMNC)的增殖和产生细胞因子的作用,以及在体内诱导炎症反应的活性。C3H/HEN小鼠SMNC在体外向PG的增殖在第3天达到最大,高于Balb/c小鼠的SMNC。结果表明,C3H/HEN小鼠SMNC对PG的反应细胞主要为Ia~+细胞。注射后3h,C3H/HEN小鼠肺组织中GM-CSFmRNA的表达明显高于Balb/c小鼠。注射PG后,BALB/c小鼠易患急性关节炎,而C3H/HEN和C57BL/6小鼠未发生急性关节炎。化脓性链球菌的细胞质膜蛋白(MAP)与人外周血淋巴细胞孵育5-7天后,不产生IL-2,但不能诱导PG等人外周血淋巴细胞的多克隆活化。活化的T细胞包括CD^&lt;4+&gt;CD^&lt;8-&gt;辅助性T细胞。我们已经获得了一些关于单个核细胞对细菌细胞成分,特别是细胞因子产生和激活细胞的责任的信息。这些因素形成了一个复杂的网络,而对关节炎所涉及的机制到细菌亚组分的完全了解,还必须等待详细的研究。

项目成果

期刊论文数量(23)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
関 修司: "Identification of activated T cell receptor γδ lymphocytes in the liver of tumorーbearing hosts." Journal of Clinical Immunology. 86. 409-415 (1990)
Shuji Seki:“荷瘤宿主肝脏中激活的 T 细胞受体 γδ 淋巴细胞的鉴定。”《临床免疫学杂志》86. 409-415 (1990)。
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    0
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Katsuo Kumagai: "PERIODONTAL DISEASE:PATHOGENS and HOST IMMUNE RESPONSES" S.Hamada,S.C.Holt and J.R.McGhee, (1991)
Katsuo Kumagai:“牙周疾病:病原体和宿主免疫反应”S.Hamada、S.C.Holt 和 J.R.McGhee,(1991)
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    0
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T. Abo: "induction of human TCR_<gamma>delta^+ and TCR_<gamma>delta^-CD2^+CD3^- double negative lymphocytes by bacterial stimulation." International Immunology. 2. 775-785 (1990)
T. Abo:“通过细菌刺激诱导人类 TCR_<gamma>delta^ 和 TCR_<gamma>delta^-CD2^ CD3^- 双阴性淋巴细胞。”
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    0
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川村 勝: "Further characterization of the autologous mixedーlymphocyte reaction:Induction of double negative γδ lymphocytes." Cellular Immunology. 133. 468-483 (1991)
Masaru Kawamura:“自体混合淋巴细胞反应的进一步表征:双阴性 γδ 淋巴细胞的诱导。” 133. 468-483 (1991)
  • DOI:
  • 发表时间:
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  • 影响因子:
    0
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  • 通讯作者:
川村 勝: "Further characterization of the autologous mixedーlymphocyte reaction;Induction of double negative γ δ lymphocytes." Cellular Immunology. 133. 468-483 (1991)
Masaru Kawamura:“自体混合淋巴细胞反应的进一步表征;双阴性 γ δ 淋巴细胞的诱导。” 133. 468-483 (1991)
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RIKIISHI Hidemi其他文献

RIKIISHI Hidemi的其他文献

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{{ truncateString('RIKIISHI Hidemi', 18)}}的其他基金

Mechanisms of Taxotere-induced apoptosis in or a squamous cell carcinoma.
泰索帝诱导鳞状细胞癌凋亡的机制。
  • 批准号:
    16390577
  • 财政年份:
    2004
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Selective apoptosis during treatment with superantigen and lipopolysaccharide
超抗原和脂多糖治疗期间的选择性细胞凋亡
  • 批准号:
    14571726
  • 财政年份:
    2002
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Inhibition of superantigen-induced apoptosis by LPS
LPS 抑制超抗原诱导的细胞凋亡
  • 批准号:
    12671759
  • 财政年份:
    2000
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
The etiological significance of superantigen in periodontal disease and its possible role
超抗原在牙周病中的病因学意义及其可能的作用
  • 批准号:
    10671695
  • 财政年份:
    1998
  • 资助金额:
    $ 1.34万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
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