Interleukin-18 protects mice from Enterovirus 71 infection
Interleukin-18 protects mice from Enterovirus 71 infection
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Interleukin-18 保护小鼠免受肠道病毒 71 感染
DOI：
10.1016/j.cyto.2017.04.002
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发表时间：
2017-08-01
期刊：
影响因子：
3.8
通讯作者：
Meng, Guangxun
中科院分区：
文献类型：
--
作者：
Li, Zheng;Wang, Hongbin;Meng, Guangxun
先前的研究表明，NLRP3炎症小体对保护小鼠宿主免受肠病毒71 （EV71）感染至关重要。然而，潜在的机制仍然未知。在这里，我们发现多效性细胞因子白介素-18 (IL-18)，一种NLRP3炎性体依赖的效应蛋白，对EV71的攻击表现出保护能力。小鼠体内缺乏IL-18会加重EV71感染，表现为病毒复制增加，干扰素（ifn - β、ifn - γ）、促炎细胞因子（tnf - α、IL-6）和趋化因子CCL2的产生增加，以及实验动物的存活率降低。相反，给药重组IL-18可显著抑制IL-18缺陷小鼠的EV71感染。因此，我们的研究结果揭示了IL-18对EV71攻击的保护作用，并表明IL-18在EV71相关的手足口病（HFMD）中的新的治疗应用。
Previous study has demonstrated that the NLRP3 inflammasome is essential for protecting murine host against Enterovirus 71 (EV71) infection. However, the underlying mechanism remained unknown. Here we discovered that the pleiotropic cytokine interleukin-18 (IL-18), an NLRP3 inflammasome-dependent effector protein, exhibits a protective capability against EV71 challenge. Deficiency of IL-18 in mice exacerbated EV71 infection, which was reflected by increased viral replication, elevated production of interferons (IFN-beta, IFN-gamma), proinflammatory cytokines (TNF-alpha, IL-6) and chemokine CCL2, as well as decreased survival of experimental animals. Conversely, administration of recombinant IL-18 considerably restrained EV71 infection in IL-18 deficient mice. Thus, our results revealed a protective role for IL-18 against EV71 challenge, and indicated a novel therapeutic application for IL-18 in EV71 associated hand, foot, and mouth disease (HFMD).