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首页> 外文期刊>Nature immunology >Type i interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium
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Type i interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium

机译：I型干扰素在肠炎沙门氏菌血清鼠伤寒感染过程中诱导巨噬细胞坏死性坏死

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摘要

Salmonella enterica serovar Typhimurium (S. Typhimurium) is a virulent pathogen that induces rapid host death. Here we observed that host survival after infection with S. Typhimurium was enhanced in the absence of type I interferon signaling, with improved survival of mice deficient in the receptor for type I interferons (Ifnar1 -/- mice) that was attributed to macrophages. Although there was no impairment in cytokine expression or inflammasome activation in Ifnar1 -/- macrophages, they were highly resistant to S. Typhimurium-induced cell death. Specific inhibition of the kinase RIP1 or knockdown of the gene encoding the kinase RIP3 prevented the death of wild-type macrophages, which indicated that necroptosis was a mechanism of cell death. Finally, RIP3-deficient macrophages, which cannot undergo necroptosis, had similarly less death and enhanced control of S. Typhimurium in vivo. Thus, we propose that S. Typhimurium induces the production of type I interferon, which drives necroptosis of macrophages and allows them to evade the immune response.
机译：肠炎沙门氏菌鼠伤寒沙门氏菌（S. Typhimurium）是一种致病性致病菌，可引起快速的宿主死亡。在这里，我们观察到在没有I型干扰素信号传导的情况下，鼠伤寒沙门氏菌感染后宿主的存活率得到了提高，而归因于巨噬细胞的I型干扰素受体（Ifnar1-/-小鼠）缺乏的小鼠的存活率得到了提高。尽管在Ifnar1-/-巨噬细胞中细胞因子表达或炎性体激活没有受到损害，但它们对鼠伤寒沙门氏菌诱导的细胞死亡具有高度抵抗力。对激酶RIP1的特异性抑制或编码激酶RIP3的基因的敲低阻止了野生型巨噬细胞的死亡，这表明坏死性坏死是细胞死亡的一种机制。最后，不能进行尸检的RIP3缺陷型巨噬细胞具有相似的更少的死亡并增强了对鼠伤寒沙门氏菌的体内控制。因此，我们建议鼠伤寒沙门氏菌诱导I型干扰素的产生，它驱动巨噬细胞坏死性坏死并使其逃避免疫反应。

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