Enteric helminth-induced type I interferon signaling protects against pulmonary virus infection through interaction with the microbiota.
Enteric helminth-induced type I interferon signaling protects against pulmonary virus infection through interaction with the microbiota.
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肠蠕虫诱导的I型干扰素信号传导通过与微生物群相互作用来预防肺病毒感染。
DOI：
10.1016/j.jaci.2017.01.016
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发表时间：
2017-10
期刊：
影响因子：
--
通讯作者：
Schwarze J
中科院分区：
文献类型：
--
作者：
McFarlane AJ;McSorley HJ;Davidson DJ;Fitch PM;Errington C;Mackenzie KJ;Gollwitzer ES;Johnston CJC;MacDonald AS;Edwards MR;Harris NL;Marsland BJ;Maizels RM;Schwarze J
据报道，蠕虫寄生虫在过敏和自身免疫条件下发挥有益的免疫调节作用，而在结核病和一些病毒感染中起有害作用。它们在呼吸道病毒合并感染中的作用尚不清楚。在这里，我们在一个小鼠模型中研究了多回螺旋体肠道蠕虫感染对呼吸道合胞病毒(RSV)感染的影响。感染多脑回的小鼠在RSV感染后表现出明显的疾病和肺部炎症，与病毒载量的减少有关。由于IL-4R、α-/-和RAG1-/-小鼠对呼吸道合胞病毒的保护作用维持，2型和获得性免疫反应不是必需的。重要的是，多脑回病毒感染上调了干扰素-β和干扰素刺激基因在十二指肠和肺中的表达，并且在IFNAR1/-和无菌小鼠中失去了保护作用，揭示了I型干扰素信号和微生物区系在多回病毒诱导的保护中的重要作用。总之，我们证明了严格的肠道蠕虫感染可以通过诱导依赖微生物区系的I型干扰素反应在肺部具有保护性的抗病毒作用。
Helminth parasites have been reported to exert beneficial immune modulatory roles in allergic and autoimmune conditions and detrimental effects in tuberculosis and some viral infections. Their role in co-infection with respiratory viruses is not clear. Here, we investigated the effects of strictly enteric helminth infection with Heligmosomoides polygyrus on respiratory syncytial virus (RSV) infection in a mouse model. H. polygyrus infected mice showed significantly less disease and pulmonary inflammation after RSV infection, associated with reduced viral load. Type 2 and adaptive immune responses were not essential since protection against RSV was maintained in IL-4Rα-/- and RAG1-/- mice. Importantly, H. polygyrus infection upregulated expression of IFN-β and IFN stimulated genes (ISG) in both the duodenum and the lung, and its protective effects were lost in IFNAR1-/- and germ-free mice, revealing essential roles for type I IFN signaling and microbiota in H. polygyrus induced protection against RSV. In conclusion, we demonstrate that a strictly enteric helminth infection can have protective antiviral effects in the lung through induction of a microbiota-dependent type I IFN response.
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