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Determination of cytokines involved in initiation of acute inflammation.

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
负责人:
YOSHINAGA Masaru
金额:
$4.86万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (B)
财政年份:
1995
资助国家:
日本
项目状态:
已结题
起止时间:
1995 至 1996

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中文摘要
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英文摘要
To know the cytokines involved in the development of inflammation. We developed a subtraction gene library of rabbit and detected several candidate cytokines which are specifically expressed during the course of inflammation, i.e.TNFalpha), IL-8, IL-1beta and IL-1ra. Then, we made recombinants and antibodies of these gene products and investigated the significance of these cytokines in the pathogenesis of LPS-induced acute inflammation in rabbits.We conclude the followings :1. TNFalpha and IL-8 were produced during the initial stage (within 2 hrs). The production of these cytokines were mutually independent, namely inhibition of one of these did not suppressed the production of the other. The production was not reduced by depletion of neutrophils. Immunostaining revealed that resident cells were positive for these two cytokines, but not neutrophils.2. IL-1beta was produced during a later stage (peaked at 6 hrs). Production of IL-1beta was induced by both TNFalpha and IL-8 ; namely, inhibition of the two cytokines resulted in reduced production of IL-1beta. Recombinant TNFalpha or IL-8 induced the strong production of IL-1beta.3. IL-1 ra was produced by infiltrated neutrophils and macrophages and suppressed by inhibition of TNFalpha and IL-8. Recombinant IL-1ra suppressed the infiltration of neutrophils. Inhibition of IL-1ra produced enhanced neutrophil infiltration and tissue destruction.4. Inhibition of TNFalpha or IL-8 resulted in a partial inhibition of neutrophil infiltration at an early stage (2 hrs) of inflammation, but not those in a later stage (9 hrs).5. Inhibition of IL-1 resulted in reduced neutrophil infiltration at the later stage of inflammation. Then, we reached a conclusion that both TNFalpha and IL-8 act as initiation of inflammation and IL-1beta play a role in the amplification of acute inflammation.
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会议论文
Akihiro Matsukawa: "Analysis of the inflammatory cytokine network among TNFα,IL-1β,IL-1 receptor antagonist and IL-8 in LPS-induced rabbit arthritis." Laboratory Investigation. (印刷中). (1977)
Akihiro Matsukawa:“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”(正在出版)。
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通讯作者:
Dlsayd Y.A., et al.: "Expression of tissue factor and interleukin-1beta in a novel rabbit model of disseminated intravascular coagulation induced by carrageenan and lipopolysaccharide." Pathobiology. 63. 328-340 (1995)
Dlsayd Y.A. 等人:“角叉菜胶和脂多糖诱导的弥散性血管内凝血的新型兔模型中组织因子和白细胞介素 1β 的表达。”
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Sumitaka Imamura: "Involvement of tumor necrosis factor-α,interleukin-lβ,interleukin-8,and interleukin-l receptor antagonist in acute lung injury caused by local Shwartzman reaction." Pathology International,. 47. 16-24 (1997)
Sumitaka Imamura:“肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-8 和白细胞介素-1 受体拮抗剂参与局部 Shwartzman 反应引起的急性肺损伤。”47. 16-24 (1997)。
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通讯作者:
Yoshinaga M: "Role of TNFα,IL-1 and IL-1ra in the mediation of leukocyte infiltration and increased vascular permeability in rabbits with LPS-induced pleurisy." Clin.Immunol.Immunopathol.75. 68-74 (1995)
Yoshinaga M:“TNFα、IL-1 和 IL-1ra 在 LPS 诱导的胸膜炎兔子介导白细胞浸润和血管通透性增加中的作用。”Clin.Immunol.Immunopathol.75 (1995)。
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31
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