Mechanism of delayed phase of increased vascular permeabitity in acute inflammation

急性炎症血管通透性增加延迟期的机制

基本信息

  • 批准号:
    09470065
  • 负责人:
  • 金额:
    $ 7.74万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (B).
  • 财政年份:
    1997
  • 资助国家:
    日本
  • 起止时间:
    1997 至 2000
  • 项目状态:
    已结题

项目摘要

To investigate the mechanism of increased vascular permeability (IVP) in acute inflammation, we developed the recombinant cytokines, including interleukin (IL)-1β, tumor necerosis factor-α (TNFα), IL-1receptor antagonist (IL-1a), IL-8, growth stimulating oncogene (GRO), monocyte chemoattractant protein-1 (MCP-1) and their antibodies, together with immunoassay systems. Using rabbits with LPS-induced pleurisy as well as the above mentioned materials and methods, we determined interleukin (IL)-8 as a direct mediator for delayed phase of IVP in acute inflammation on the basis of the following series of evidence ; (1) We reconfirmed that the IVP showed biphasic pattern in the LPS-induced pleurisy similarly to the other types of acute inflammation, and the immediate phase is mediated by histamine. (2) Either blocking of TNFα or IL-8 with corresponding antibodies, resulted in disappearance of the delayed permeability, while the duration and the degree of intensity of immediate permeability was not affected. IL-1ra did not suppress the delayed IVP.(3) The delayed permeability was not observed in neutro-phil-depleted rabbits, but the production of TNFα was maintained. (4) Intrapleural injections of either rabbit recombinant TNFα or IL-8 induced a delayed type of IVP that was not inhibited with antihistamine. (5) Injection of TNFα induced the production of IL-8. (6) IL-8 but not TNFα induced the delayed type IVP in the neutrophil-depleted rabbits. (7) GRO induced a delayed type of IVP via inducing the production of TNFα. Thus, TNFα-induced IL-8 is responsible for the mediation of delayed IVP in LPS-induced pleurisy of rabbits. This mechanism may generally be applicable to many types of acute inflammations, because similar IVP was also observed in inflammations at different site of the body, i.e. articular cavity and vitreal space as well as the inflammation with a different stimuli, i.e. urea crystal in rabbits.
为了研究急性炎症中血管通透性增加(IVP)的机制,我们开发了重组细胞因子,包括白细胞介素(IL)-1β、肿瘤坏死因子-α (TNFα)、IL-1受体拮抗剂(IL-1a)、IL-8、促生长癌基因(GRO)、单核细胞趋化蛋白-1 (MCP-1)及其抗体,以及免疫分析系统。采用lps诱导的胸膜炎家兔及上述材料和方法,基于以下一系列证据,我们确定了白细胞介素(IL)-8是急性炎症中IVP延迟期的直接介质;(1)我们再次证实lps诱导的胸膜炎IVP与其他类型的急性炎症相似,呈双相模式,且直接期是由组胺介导的。(2)用相应抗体阻断TNFα或IL-8均可导致延迟性通透性消失,而即时通透性持续时间和强度程度不受影响。IL-1ra对延迟IVP无抑制作用。(3)中性粒细胞耗竭的家兔没有观察到延迟通透性,但TNFα的产生维持。(4)兔胸膜内注射重组TNFα或IL-8诱导延迟型IVP,抗组胺药不抑制。(5)注射TNFα诱导IL-8的产生。(6) IL-8诱导中性粒细胞缺失家兔迟发性IVP, TNFα不诱导。(7) GRO通过诱导TNFα的产生诱导延迟型IVP。由此可见,tnf α-诱导的IL-8参与了lps致兔胸膜炎延迟性IVP的介导作用。这一机制可能普遍适用于许多类型的急性炎症,因为在身体不同部位的炎症,如关节腔和玻璃腔,以及兔体内不同刺激的炎症,如尿素晶体,也可以观察到类似的IVP。

项目成果

期刊论文数量(122)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
Makoto Kimura 他: "Blocking of TNF-α and IL-1 inhibits leukocyte infiltration at early, but not at late stage of Staphylococcus aureus-induced arthritis and concomitant cartilage destruction in rabbits."Clinical Immunology and Immunopathology. 82. 18-25 (1
Makoto Kimura 等人:“阻断 TNF-α 和 IL-1 可以抑制金黄色葡萄球菌诱导的兔子关节炎和伴随软骨破坏的早期白细胞浸润,但不能抑制晚期白细胞浸润。”临床免疫学和免疫病理学。 25(1)
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Takumi Fukumoto 他: "IL-8 is an essential mediator of the increased delayed-phase vascular permeability in LPS-induced rabbit pleurisy."Journal of Leukocyte Biology. 63. 584-590 (1998)
Takumi Fukumoto 等人:“IL-8 是 LPS 诱导的兔胸膜炎延迟相血管通透性增加的重要介质。”白细胞生物学杂志 63. 584-590 (1998)
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    0
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Jun-Song Mo 他: "CXC chemokine GRO is essential for neutrophil infiltration in LPS-induced uveitis in rabbits."Experimental Eye Research. 70. 221-226 (2000)
Jun-Song Mo 等人:“CXC 趋化因子 GRO 对于 LPS 诱导的兔子葡萄膜炎中性粒细胞浸润至关重要。”实验眼科研究。70. 221-226 (2000)
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    0
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A.Matsukawa, T.Yoshimura, K.Miyamoto, S.Ohkawara, and M.Yoshinaga: "Analysis of the inflammatory cytokine network among TNFα, IL-1β, IL-1 receptor antagonist and IL-8 in LPS-induced rabbit arthritis."Lab.Invest.. 76. 629-638 (1997)
A.Matsukawa、T.Yoshimura、K.Miyamoto、S.Ohkawara 和 M.Yoshinaga:“LPS 诱导的兔关节炎中 TNFα、IL-1β、IL-1 受体拮抗剂和 IL-8 之间的炎症细胞因子网络分析.“实验室投资.. 76. 629-638 (1997)
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A.Matsukawa, T.Yoshimura, K.Fujiwara, T.Maeda, S.Ohkawara and M.Yoshinaga: "Involvement of growth related protein (GRO) in lipopolysaccharide-induced rabbit arthritis : Cooperation between GRO and interleukin (IL)-8, and interre-lated recrulation among tu
A.Matsukawa、T.Yoshimura、K.Fujiwara、T.Maeda、S.Ohkawara 和 M.Yoshinaga:“生长相关蛋白 (GRO) 参与脂多糖诱导的兔关节炎:GRO 与白细胞介素 (IL)-8 之间的合作
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YOSHINAGA Masaru其他文献

YOSHINAGA Masaru的其他文献

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{{ truncateString('YOSHINAGA Masaru', 18)}}的其他基金

Determination of cytokines involved in initiation of acute inflammation.
测定参与急性炎症引发的细胞因子。
  • 批准号:
    07457060
  • 财政年份:
    1995
  • 资助金额:
    $ 7.74万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Regulation of inflammatory response by an inhibitory cytokine in a mode of inhiditory cybemetics
抑制性细胞因子在抑制性控制学模式下调节炎症反应
  • 批准号:
    05454182
  • 财政年份:
    1993
  • 资助金额:
    $ 7.74万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Structure and Functions of an IL-1 inhibitor found at inflammatory site in rabbit.
兔炎症部位发现的 IL-1 抑制剂的结构和功能。
  • 批准号:
    03454172
  • 财政年份:
    1991
  • 资助金额:
    $ 7.74万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
A New Aspect of Neutrophil Function Dependent on Their Protein Synthesis.
中性粒细胞功能依赖于其蛋白质合成的新方面。
  • 批准号:
    01480166
  • 财政年份:
    1989
  • 资助金额:
    $ 7.74万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)
Polymorphonuclear leukocytes as an inflammatory hormone-producing argan.
多形核白细胞作为产生炎症激素的摩洛哥坚果。
  • 批准号:
    62480143
  • 财政年份:
    1987
  • 资助金额:
    $ 7.74万
  • 项目类别:
    Grant-in-Aid for General Scientific Research (B)

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血管通透性增加参与硼替佐米诱导的肺毒性
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Development of approaches to control vascular permeability using mouse models with increased vascular permeability
使用血管通透性增加的小鼠模型开发控制血管通透性的方法
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  • 财政年份:
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Mechanisms of increased vascular permeability associated with sympathetic excitability and the development of treatment strategy of ARDS.
血管通透性增加与交感神经兴奋相关的机制及ARDS治疗策略的制定。
  • 批准号:
    16390448
  • 财政年份:
    2004
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    $ 7.74万
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Study on the Mechanism of Increased Vascular Permeability in Pulmonary Edema
肺水肿血管通透性增加的机制研究
  • 批准号:
    06454443
  • 财政年份:
    1994
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    $ 7.74万
  • 项目类别:
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PREVENTION OF INCREASED VASCULAR PERMEABILITY
预防血管通透性增加
  • 批准号:
    2219096
  • 财政年份:
    1988
  • 资助金额:
    $ 7.74万
  • 项目类别:
PREVENTION OF INCREASED VASCULAR PERMEABILITY
预防血管通透性增加
  • 批准号:
    3355344
  • 财政年份:
    1988
  • 资助金额:
    $ 7.74万
  • 项目类别:
PREVENTION OF INCREASED VASCULAR PERMEABILITY
预防血管通透性增加
  • 批准号:
    3355342
  • 财政年份:
    1988
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    $ 7.74万
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PREVENTION OF INCREASED VASCULAR PERMEABILITY
预防血管通透性增加
  • 批准号:
    3355346
  • 财政年份:
    1988
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    $ 7.74万
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PREVENTION OF INCREASED VASCULAR PERMEABILITY
预防血管通透性增加
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    3355345
  • 财政年份:
    1988
  • 资助金额:
    $ 7.74万
  • 项目类别:
PREVENTION OF INCREASED VASCULAR PERMEABILITY
预防血管通透性增加
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    3355347
  • 财政年份:
    1988
  • 资助金额:
    $ 7.74万
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