Host liver-derived extracellular vesicles deliver miR-142a-3p induces neutrophil extracellular traps via targeting WASL to block the development of Schistosoma japonicum.
Host liver-derived extracellular vesicles deliver miR-142a-3p induces neutrophil extracellular traps via targeting WASL to block the development of Schistosoma japonicum.
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宿主肝源性细胞外囊泡传递 miR-142a-3p 通过靶向 WASL 诱导中性粒细胞细胞外陷阱阻止日本血吸虫的发育
DOI：
10.1016/j.ymthe.2022.03.016
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发表时间：
2022-05-04
影响因子：
12.4
通讯作者：
Sun, Xi
中科院分区：
文献类型：
--
作者：
Wang, Lifu;Zhu, Zifeng;Liao, Yao;Zhang, Lichao;Yu, Zilong;Yang, Ruibing;Wu, Ji;Wu, Zhongdao;Sun, Xi
血吸虫病是一种重要的被忽视的热带疾病。宿主免疫系统和血吸虫之间的相互作用是复杂的。中性粒细胞主要通过释放中性粒细胞胞外陷阱（NETs）来清除大型病原体。然而，NETs在清除血吸虫中的功能作用尚不清楚。本文中，我们报道了来自日本血吸虫感染小鼠肝脏（il - ev）的细胞外囊泡（ev）通过递送miR-142a-3p靶向WASL并阻断日本血吸虫的发育来诱导NET释放。WASL基因敲除加速了net的形成，从而阻断了日本血吸虫的进一步发育。miR-142a-3p和NETs上调CCL2的表达，CCL2招募巨噬细胞，阻断日本血吸虫的发育。然而，日本血吸虫通过上调宿主白细胞介素-10 （IL-10）的表达来抑制野生型小鼠的NET形成。相反，在WASL敲除小鼠中，IL-10表达下调，日本血吸虫介导的NET形成抑制显著降低。因此，il - ev介导的NET形成是一种抗血吸虫反应，可以被日本血吸虫抵消。这些发现表明，il - ev介导的NET形成在血吸虫感染中起着关键作用，WASL是血吸虫病和其他传染病的潜在治疗靶点。Wu， Sun等人报道，来自日本血吸虫感染小鼠（il - ev）肝脏的细胞外囊泡通过递送miR-142a-3p靶向WASL并阻断日本血吸虫的发展来诱导NET释放。这些发现表明，il - ev介导的NET形成在血吸虫感染中起关键作用。
Schistosomiasis is an important neglected tropical disease. Interactions between the host immune system and schistosomes are complex. Neutrophils contribute to clearance of large pathogens primarily by releasing neutrophil extracellular traps (NETs). However, the functional role of NETs in clearing schistosomes remains unclear. Herein, we report that extracellular vesicles (EVs) derived from the liver of Schistosoma japonicum-infected mice (IL-EVs) induce NET release by delivering miR-142a-3p to target WASL and block the development of S. japonicum. WASL knockout accelerated the formation of NETs that blocked further development of S. japonicum. miR-142a-3p and NETs upregulated the expression of CCL2, which recruits macrophages that block S. japonicum development. However, S. japonicum inhibited NET formation in wild-type mice by upregulating host interleukin-10 (IL-10) expression. In contrast, in WASL knockout mice, IL-10 expression was downregulated, and S. japonicum-mediated inhibition of NET formation was significantly reduced. IL-EV-mediated induction of NET formation is thus an anti-schistosome response that can be counteracted by S. japonicum. These findings suggest that IL-EV-mediated induction of NET formation plays a key role in schistosome infection and that WASL is a potential therapeutic target in schistosomiasis and other infectious diseases. Wu, Sun, and colleagues report that extracellular vesicles derived from the liver of Schistosoma japonicum-infected mice (IL-EVs) induce NET release by delivering miR-142a-3p to target WASL and block the development of S. japonicum. These findings suggest that IL-EV-mediated induction of NET formation plays a key role in schistosomes infection.
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