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首页> 外文期刊>Nature immunology >The helminth product ES-62 protects against septic shock via Toll-like receptor 4-dependent autophagosomal degradation of the adaptor MyD88.
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The helminth product ES-62 protects against septic shock via Toll-like receptor 4-dependent autophagosomal degradation of the adaptor MyD88.

机译：蠕虫产品ES-62通过适配器MyD88的Toll样受体4依赖性自噬体降解来防止败血性休克。

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摘要

Sepsis is one of the most challenging health problems worldwide. Here we found that phagocytes from patients with sepsis had considerable upregulation of Toll-like receptor 4 (TLR4) and TLR2; however, shock-inducing inflammatory responses mediated by these TLRs were inhibited by ES-62, an immunomodulator secreted by the filarial nematode Acanthocheilonema viteae. ES-62 subverted TLR4 signaling to block TLR2- and TLR4-driven inflammatory responses via autophagosome-mediated downregulation of the TLR adaptor-transducer MyD88. In vivo, ES-62 protected mice against endotoxic and polymicrobial septic shock by TLR4-mediated induction of autophagy and was protective even when administered after the induction of sepsis. Given that the treatments for septic shock at present are inadequate, the autophagy-dependent mechanism of action by ES-62 might form the basis for urgently needed therapeutic intervention against this life-threatening condition.
机译：败血症是全球最具挑战性的健康问题之一。在这里，我们发现败血症患者的吞噬细胞具有明显的Toll样受体4（TLR4）和TLR2上调。然而，由这些TLRs介导的休克诱导的炎症反应被丝虫线虫棘皮动物蛋白（Acanthocheilonema viteae）分泌的免疫调节剂ES-62抑制。 ES-62通过自噬体介导的TLR衔接子-转换器MyD88的下调，破坏了TLR4信号传导，从而阻止TLR2和TLR4驱动的炎症反应。在体内，ES-62通过TLR4介导的自噬诱导小鼠免受内毒素和微生物败血症性休克的侵害，即使在败血症诱导后给药也具有保护作用。鉴于目前对败血性休克的治疗还不够，ES-62依赖自噬的作用机制可能构成了针对这种危及生命的疾病迫切需要的治疗干预的基础。

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