IL-33 通过促进脓毒症中 IFN-γ 的产生来降低死亡率。
IL-33 attenuates mortality by promoting IFN-γ production in sepsis.
机构信息
Department of Anesthesiology, Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Zhejiang, China.
出版信息
Inflamm Res. 2018 Jun;67(6):531-538. doi: 10.1007/s00011-018-1144-9. Epub 2018 Apr 2.
OBJECTIVE AND DESIGN
Sepsis remains a major clinical problem with high morbidity and mortality. Interleukin (IL)-33 is a recently described member of the IL-1 family that is widely expressed and functions as a new inflammatory mediator. IL-33 has been reported to protect sepsis, but the underlying mechanisms are not well-elucidated.
MATERIALS AND METHODS
We measured the interferon gamma (IFN-γ) production in septic mice after IL-33 treatment.
RESULTS
IL-33 treatment enhanced the IFN-γ level in blood and promoted mice's survival, so the protective effects of IL-33 depend on IFN-γ. The IL-33 treatment also promoted both γδ T cells and NK cells in septic mice.
CONCLUSION
Our data showed that IL-33 attenuates mortality by promoting IFN-γ production in sepsis.
目的和设计
脓毒症仍然是一个主要的临床问题，具有高发病率和死亡率。白细胞介素（IL）-33 是最近描述的 IL-1 家族的一员，广泛表达并作为一种新的炎症介质发挥作用。IL-33 已被报道可保护脓毒症，但潜在机制尚不清楚。
材料和方法
我们测量了 IL-33 治疗后脓毒症小鼠的干扰素γ（IFN-γ）产生。
结果
IL-33 治疗增强了血液中的 IFN-γ 水平并促进了小鼠的存活，因此 IL-33 的保护作用依赖于 IFN-γ。IL-33 治疗还促进了脓毒症小鼠中的γδ T 细胞和 NK 细胞。
结论
我们的数据表明，IL-33 通过促进脓毒症中 IFN-γ 的产生来减轻死亡率。
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