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Hookworms Evade Host Immunity by Secreting a Deoxyribonuclease to Degrade Neutrophil Extracellular Traps.
Cell Host & Microbe ( IF 20.6 ) Pub Date : 2020-02-12 , DOI: 10.1016/j.chom.2020.01.011 Tiffany Bouchery 1 , Mati Moyat 1 , Javier Sotillo 2 , Solomon Silverstein 3 , Beatrice Volpe 4 , Gillian Coakley 3 , Theodora-Dorita Tsourouktsoglou 5 , Luke Becker 6 , Kathleen Shah 4 , Manuel Kulagin 4 , Romain Guiet 7 , Mali Camberis 8 , Alfonso Schmidt 9 , Arne Seitz 7 , Paul Giacomin 6 , Graham Le Gros 8 , Venizelos Papayannopoulos 5 , Alex Loukas 6 , Nicola L Harris 3
Cell Host & Microbe ( IF 20.6 ) Pub Date : 2020-02-12 , DOI: 10.1016/j.chom.2020.01.011 Tiffany Bouchery 1 , Mati Moyat 1 , Javier Sotillo 2 , Solomon Silverstein 3 , Beatrice Volpe 4 , Gillian Coakley 3 , Theodora-Dorita Tsourouktsoglou 5 , Luke Becker 6 , Kathleen Shah 4 , Manuel Kulagin 4 , Romain Guiet 7 , Mali Camberis 8 , Alfonso Schmidt 9 , Arne Seitz 7 , Paul Giacomin 6 , Graham Le Gros 8 , Venizelos Papayannopoulos 5 , Alex Loukas 6 , Nicola L Harris 3
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Hookworms cause a major neglected tropical disease, occurring after larvae penetrate the host skin. Neutrophils are phagocytes that kill large pathogens by releasing neutrophil extracellular traps (NETs), but whether they target hookworms during skin infection is unknown. Using a murine hookworm, Nippostrongylus brasiliensis, we observed neutrophils being rapidly recruited and deploying NETs around skin-penetrating larvae. Neutrophils depletion or NET inhibition altered larvae behavior and enhanced the number of adult worms following murine infection. Nevertheless, larvae were able to mitigate the effect of NETs by secreting a deoxyribonuclease (Nb-DNase II) to degrade the DNA backbone. Critically, neutrophils were able to kill larvae in vitro, which was enhanced by neutralizing Nb-DNase II. Homologs of Nb-DNase II are present in other nematodes, including the human hookworm, Necator americanus, which also evaded NETs in vitro. These findings highlight the importance of neutrophils in hookworm infection and a potential conserved mechanism of immune evasion.
中文翻译：
钩虫通过分泌脱氧核糖核酸酶降解中性粒细胞胞外陷阱而逃避宿主免疫。
钩虫引起严重的被忽视的热带病，发生在幼虫穿透宿主皮肤后。中性粒细胞是吞噬细胞，可通过释放中性粒细胞胞外陷阱（NETs）杀死大量病原体，但尚不清楚它们是否在皮肤感染期间靶向钩虫。使用鼠钩虫Nippostrongylus brasiliensis，我们观察到嗜中性粒细胞迅速募集并在穿透皮肤的幼虫周围部署了NET。中性粒细胞耗竭或NET抑制改变了幼虫的行为，并增加了鼠感染后成虫的数量。然而，幼虫能够通过分泌脱氧核糖核酸酶（Nb-DNase II）来降解DNA骨架来减轻NET的影响。至关重要的是，中性粒细胞能够在体外杀死幼虫，而中和Nb-DNase II可以增强这种能力。Nb-DNase II的同系物存在于其他线虫中，包括人类钩虫，美国的Necator，也逃避了NET的攻击。这些发现突出了嗜中性粒细胞在钩虫感染中的重要性以及免疫逃避的潜在保守机制。
更新日期：2020-02-20
中文翻译：
钩虫通过分泌脱氧核糖核酸酶降解中性粒细胞胞外陷阱而逃避宿主免疫。
钩虫引起严重的被忽视的热带病，发生在幼虫穿透宿主皮肤后。中性粒细胞是吞噬细胞，可通过释放中性粒细胞胞外陷阱（NETs）杀死大量病原体，但尚不清楚它们是否在皮肤感染期间靶向钩虫。使用鼠钩虫Nippostrongylus brasiliensis，我们观察到嗜中性粒细胞迅速募集并在穿透皮肤的幼虫周围部署了NET。中性粒细胞耗竭或NET抑制改变了幼虫的行为，并增加了鼠感染后成虫的数量。然而，幼虫能够通过分泌脱氧核糖核酸酶（Nb-DNase II）来降解DNA骨架来减轻NET的影响。至关重要的是，中性粒细胞能够在体外杀死幼虫，而中和Nb-DNase II可以增强这种能力。Nb-DNase II的同系物存在于其他线虫中，包括人类钩虫，美国的Necator，也逃避了NET的攻击。这些发现突出了嗜中性粒细胞在钩虫感染中的重要性以及免疫逃避的潜在保守机制。
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