• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Infection and immunity >Role of Interleukin-18 (IL-18) during Lethal Shock: Decreased Lipopolysaccharide Sensitivity but Normal Superantigen Reaction in IL-18-Deficient Mice
【24h】

Role of Interleukin-18 (IL-18) during Lethal Shock: Decreased Lipopolysaccharide Sensitivity but Normal Superantigen Reaction in IL-18-Deficient Mice

机译：白细胞介素18（IL-18）在致命性休克中的作用：IL-18缺陷小鼠脂多糖敏感性降低，但超抗原反应正常

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Lethal shock can be associated with excessive secretion of cytokines such as tumor necrosis factor (TNF) and gamma interferon (IFN-γ). IFN-γ mediates macrophage activation and appears to be controlled by interleukin (IL)-12 and IL-18. To investigate the role of IL-18 in vivo, we generated IL-18-deficient mice by gene targeting. IL-18?/? mice showed decreased sensitivity towards lipopolysaccharide (LPS)-induced shock. LPS-induced IFN-γ production was abrogated, yet induction of IL-12 and TNF was not affected. Both wild-type and IL-18-deficient mice succumbed to LPS-induced lethal shock after sensitization with d-galactosamine. However, in marked contrast to LPS, the bacterial superantigenStaphylococcus aureus enterotoxin B (SEB) induced comparable serum levels of IFN-γ in IL-18+/+ and IL-18?/? mice, accompanied by an upregulation of cell surface markers CD14, CD122 (IL-2Rβ), and CD132 (IL-2Rγ) on peritoneal macrophages. Moreover, SEB injection rendered IL-18-deficient mice sensitive for subsequent challenge with LPS. The degree of sensitization was comparable to that in wild-type controls with respect to lethality. However, LPS-induced TNF levels in serum were significantly reduced in SEB-sensitized IL-18-deficient mice. These results imply that IL-18 plays an important role in induction of IFN-γ and lethality in response to LPS.
机译：致命性休克可能与细胞因子的过度分泌有关，例如肿瘤坏死因子（TNF）和γ干扰素（IFN-γ）。 IFN-γ介导巨噬细胞激活，并似乎受白介素（IL）-12和IL-18的控制。为了研究IL-18在体内的作用，我们通过基因定位产生了IL-18缺陷小鼠。 IL-18？/？小鼠对脂多糖（LPS）诱发的休克表现出降低的敏感性。 LPS诱导的IFN-γ产生被取消，但IL-12和TNF的诱导不受影响。用d-半乳糖胺敏化后，野生型和IL-18缺陷型小鼠均死于LPS诱导的致命性休克。但是，与LPS形成鲜明对比的是，细菌超抗原金黄色葡萄球菌肠毒素B（SEB）在IL-18 + / +和IL-18β/β中诱导了相当水平的IFN-γ血清水平。小鼠，伴随着腹膜巨噬细胞上的细胞表面标记CD14，CD122（IL-2Rβ）和CD132（IL-2Rγ）上调。此外，SEB注射使IL-18缺陷型小鼠对随后的LPS攻击敏感。就致死性而言，致敏度与野生型对照相当。但是，在SEB敏感的IL-18缺陷小鼠中，LPS诱导的血清TNF水平显着降低。这些结果暗示IL-18在对LPS的应答中在IFN-γ的诱导和致死性中起重要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号