蛋白质科学中心:中性粒细胞促进巨噬细胞修复
创作:szx 审核:szx 2019年03月21日
  • 中性粒细胞促进Ly6C(hi)CX3CR1(lo)促炎症性巨噬细胞向Ly6C(lo)CX3CR1(hi)修复性巨噬细胞的转化,在肝脏修复中发挥重要作用;
  • 使用抗Ly6G抗体去除中性粒细胞、敲除粒细胞集落刺激因子(G-CSF)或敲除NADPH氧化酶2(Nox2)均可抑制巨噬细胞的上述转化;
  • 机制上,中性粒细胞产生的活性氧介导了巨噬细胞的转化;
  • 在去除中性粒细胞的小鼠中,过继转移野生型中性粒细胞可恢复巨噬细胞的转化,敲除Nox2的中性粒细胞无法恢复巨噬细胞的转化。
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来自国家蛋白质科学中心的贺福初院士团队在《Nature Communications》上发表的一项最新研究,揭示了中性粒细胞通过产生活性氧,促进巨噬细胞的M2极化,从而介导肝脏修复的机制。
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Neutrophils promote the development of reparative macrophages mediated by ROS to orchestrate liver repair

中性粒细胞通过活性氧介导修复性巨噬细胞的发育以协调肝脏修复

10.1038/s41467-019-09046-8

2019-03-06, Article

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Phagocytes, including neutrophils and macrophages, have been suggested to function in a cooperative way in the initial phase of inflammatory responses, but their interaction and integration in the resolution of inflammation and tissue repair remain unclear. Here we show that neutrophils have crucial functions in liver repair by promoting the phenotypic conversion of pro-inflammatory Ly6CCXCR1 monocytes/macrophages to pro-resolving Ly6CCXCR1 macrophages. Intriguingly, reactive oxygen species (ROS), expressed predominantly by neutrophils, are important mediators that trigger this phenotypic conversion to promote liver repair. Moreover, this conversion is prevented by the depletion of neutrophils via anti-Ly6G antibody, genetic deficiency of granulocyte colony-stimulating factor, or genetic deficiency of NADPH oxidase 2 (Nox2). By contrast, adoptive transfer of WT rather than Nox2 neutrophils rescues the impaired phenotypic conversion of macrophages in neutrophil-depleted mice. Our findings thus identify an intricate cooperation between neutrophils and macrophages that orchestrate resolution of inflammation and tissue repair.

First Authors:
Wenting Yang,Yuandong Tao

Correspondence Authors:
Fuchu He,Li Tang

All Authors:
Wenting Yang,Yuandong Tao,Yan Wu,Xinyuan Zhao,Weijie Ye,Dianyuan Zhao,Ling Fu,Caiping Tian,Jing Yang,Fuchu He,Li Tang

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