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Induction of cytokines by oral bacterial stimulation and its arthropathic properties

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
批准号:
02670824
负责人:
RIKIISHI Hidemi
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
项目状态:
已结题
起止时间:
1990 至 1991

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中文摘要
翻译
本文研究了革兰氏阳性球菌肽聚糖(PG)片段在体外对小鼠脾单个核细胞(SMNC)的增殖和产生细胞因子的活性,以及在体内诱导炎症反应的活性。C3 H/HeN小鼠SMNC在体外对PG的增殖在第3天达到高峰,且高于Balb/c小鼠SMNC。结果表明,C3 H/HeN小鼠SMNC对PG的反应细胞主要为Ia^+ Mac^<2+>细胞。C3 H/HeN小鼠肺组织中GM-CSF的mRNA转录水平明显高于Balb/c小鼠。Balb/c小鼠在注射PG后易发生急性关节炎,而C3 H/HeN和C57 BL/6小鼠则不能发生急性关节炎。化脓性链球菌的胞质膜蛋白(MAP),而不是PG和其他,当与人外周血淋巴细胞孵育时,诱导T细胞的多克隆活化后,孵育5-7天,没有IL-2的生产。活化的T细胞包括CD^&lt;4+&gt; CD^<8->辅助T细胞。我们已经获得了一些关于单核细胞对细菌细胞成分,特别是细胞因子产生和活化细胞的反应的信息。这些因素形成了一个复杂的网络,而对关节炎与细菌亚类相关机制的完整理解,必须等待详细的研究。
英文摘要
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.
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会议论文
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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通讯作者:
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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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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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)
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