Analysis of T cell apoptosis induced by volatile fatty acids

挥发性脂肪酸诱导T细胞凋亡分析

基本信息

  • 批准号:
    09671872
  • 负责人:
  • 金额:
    $ 0.45万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
  • 财政年份:
    1997
  • 资助国家:
    日本
  • 起止时间:
    1997 至 1998
  • 项目状态:
    已结题

项目摘要

(1) Volatile fatty acids, especially butyric acid, metabolic by-products of periodontopathic bacteria, induced apoptosis in murine thymocytes, splenic T cells, human peripheral blood mononuclear cells (PBMC), and Jurkat cells. The apoptosis sensitivity of these cells to butyric acid was thymocytes > Jurkat cells> splenic T cells> PBMC.(2) Western blotting analysis which was used to study the expression of bcl-2, Bax, Fas and FasL, involved in the response to DNA damage and the induction of apoptosis, indicated that expression of bcl-2 was reduced and phosphorylated bcl-2 was also disappeared in butyric acid-treated cells. No changes in Bax, Fas and Fas-L was demonstrated. FACS analysis revealed that butyric acid suppressed the ratio of bcl-2^+ cells but not of Fas^+ cells.(3) RT-PCR and Western blotting analysis indicated that there was no increase in p53 expression in butyric acid-induced T cell apoptosis. The DNA fragmentation assay indicated that T cell blasts derived from mice containing a germ-line deficiency of the p53 tumor suppressor gene were susceptible to butyric acid-induced apoptosis to the same degree as wild-type T cells.(4) Annexin V binding experiments in flow cytometly revealed that butyric acid increased the number of early- and late-stage apoptotic cells.(5) Butyric acid-induced T cell apoptosis was accompanied by Caspase 3 and Caspase 6 protease activities but not by Caspase 1 and Caspase 8 protease activities.
(1)挥发性脂肪酸,特别是丁酸,牙周病细菌的代谢副产品,诱导小鼠胸腺细胞,脾T细胞,人外周血单核细胞(PBMC),和Jurkat细胞的凋亡。细胞对丁酸的凋亡敏感性为胸腺细胞> Jurkat细胞>脾T细胞> PBMC。(2)Western blotting分析与DNA损伤反应和诱导凋亡有关的bcl-2、Bax、Fas和FasL的表达,发现丁酸处理后bcl-2表达减少,磷酸化bcl-2消失。Bax、Fas和Fas-L无明显变化。流式细胞仪分析显示,丁酸抑制bcl-2^+细胞的比例,但不抑制Fas^+细胞的比例。(3)RT-PCR和Western blotting分析表明,p53蛋白在丁酸诱导的T细胞凋亡中的表达没有增加。DNA片段分析表明,T细胞母细胞来源于含有p53肿瘤抑制基因的生殖系缺陷的小鼠,对丁酸诱导的细胞凋亡的敏感程度与野生型T细胞相同。(4)流式细胞仪中的膜联蛋白V结合实验显示,丁酸增加了早期和晚期凋亡细胞的数量。(5)丁酸诱导的T细胞凋亡伴随Caspase 3和Caspase 6蛋白酶活性,但不伴随Caspase 1和Caspase 8蛋白酶活性。

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Tomoko Kurita-Ochiai: "Lipopolysaccharide stimulates butyric acid-induced apoptosis in human peripheral blood mononuclear cells." Infection and Immunity. Vol.67. 22-29 (1999)
Tomoko Kurita-Ochiai:“脂多糖刺激丁酸诱导的人外周血单核细胞凋亡。”
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    0
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  • 通讯作者:
Tomoko Kurita-Ochiai: "Volatile fatty acids, metabolic by-product of penodontopathic bacteria induces apoptosis in WEHI231 and RAJI B lymphoma cells and splenic B cells." Infection and Immunity. Vol.66. 2587-2594 (1998)
Tomoko Kurita-Ochiai:“挥发性脂肪酸是阴茎病细菌的代谢副产物,可诱导 WEHI231 和 RAJI B 淋巴瘤细胞以及脾 B 细胞凋亡。”
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  • 影响因子:
    0
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OCHIAI Tomoko其他文献

OCHIAI Tomoko的其他文献

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{{ truncateString('OCHIAI Tomoko', 18)}}的其他基金

Effects of periodontitis induced inflammasome activation on arteriosclerosis and its control
牙周炎诱导的炎症小体激活对动脉硬化的影响及其控制
  • 批准号:
    26463145
  • 财政年份:
    2014
  • 资助金额:
    $ 0.45万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Elucidation of autoummune condition in periodontitis-accelerated atherosclerosis and control by oral tolerance
阐明牙周炎加速动脉粥样硬化的自身免疫状况并通过口服耐受进行控制
  • 批准号:
    22390398
  • 财政年份:
    2010
  • 资助金额:
    $ 0.45万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Acceleration of atherosclerosis by periodontopathic bacteria and development of preventive vaccine
牙周病细菌加速动脉粥样硬化和预防性疫苗的开发
  • 批准号:
    19390537
  • 财政年份:
    2007
  • 资助金额:
    $ 0.45万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Characterization of cell growth and apoptosis in cell cycle analysis induced by butyric acid
丁酸诱导的细胞周期分析中细胞生长和凋亡的表征
  • 批准号:
    13671915
  • 财政年份:
    2001
  • 资助金额:
    $ 0.45万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
ENHANCEMENT OF GROWTH OF PERIODONTOPATHIC BACTERIA BY PRO-INFLAMMATORY CYTOKINES
促炎性细胞因子促进牙周病细菌的生长
  • 批准号:
    05671520
  • 财政年份:
    1993
  • 资助金额:
    $ 0.45万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (C)

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