Peroxiredoxin-1 aggravates lipopolysaccharide-induced septic shock via promoting inflammation
Peroxiredoxin-1 aggravates lipopolysaccharide-induced septic shock via promoting inflammation
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Peroxiredoxin-1 通过促进炎症加重脂多糖诱导的败血性休克
DOI：
10.1016/j.bbrc.2020.04.149
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发表时间：
2020-07-05
影响因子：
3.1
通讯作者：
Yang, Huixiang
中科院分区：
文献类型：
--
作者：
He, Ying;Peng, Yu;Yang, Huixiang
脂多糖（LPS）引起的感染性休克的特点是严重的全身炎症反应和活化的巨噬细胞大量产生促炎细胞因子。由活化的巨噬细胞分泌的损伤相关分子模式（DAMP）是感染性休克的关键因素。然而，目前对于那些在 LPS 诱导的感染性休克下促进炎症反应的 DAMP 的了解仍然知之甚少。在此，我们报告过氧化还原蛋白 1 (Prdx1) 在 LPS 诱导的感染性休克中发挥有害作用。腹腔注射 LPS 会引起小鼠进行性感染性休克，其特点是具有显着的致死率以及细胞因子（IL-1β、IL-6 和 TNF-α）的大量产生。去除 Prdx1 可以有效保护小鼠免受 LPS 诱导的死亡，并减少 IL-1β、IL-6 和 TNF-α 的产生。此外，缺乏 Prdx1 的初级巨噬细胞产生更多 IL-1β、IL-6 和 TNF-α 的能力较差。总的来说，我们证明了 Prdx1 可能通过促进炎症而导致 LPS 诱导的败血性休克。 (C) 2020 Elsevier Inc. 保留所有权利。
Septic shock induced by lipopolysaccharide (LPS) is characterized by serious systemic inflammatory response and robust production of pro-inflammatory cytokines from activated macrophages. Damage-associated molecular patterns (DAMPs) secreted by activated macrophages are key contributors to septic shock. However, the current knowledge on those DAMPs that promote inflammatory response under LPS-induced septic shock remains poorly understood. Here, we report that Peroxiredoxin 1 (Prdx1) plays a detrimental role in LPS-induced septic shock. Intraperitoneal injection of LPS elicited a progressive course of septic shock in mice, which was characterized by significant lethality along with robust production of cytokines (IL-1 beta, IL-6 and TNF-alpha). Removal of Prdx1 strongly protected mice from LPS-induced death, and decreased IL-1 beta, IL-6 and TNF-alpha productions. Additionally, primary macrophages deficient in Prdx1 are less able to produce much more IL-1 beta, IL-6 and TNF-alpha. Collectively, we provide a demonstration for Prdx1 contributing to LPS-induced septic shock likely via promoting inflammation. (C) 2020 Elsevier Inc. All rights reserved.