Neutrophils promote the development of reparative macrophages mediated by ROS to orchestrate liver repair

Wenting Yang, Yuandong Tao, Yan Wu, Xinyuan Zhao, Weijie Ye, Dianyuan Zhao, Ling Fu, Caiping Tian, Jing Yang, Fuchu He () and Li Tang ()
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Wenting Yang: Beijing Institute of Lifeomics
Yuandong Tao: Beijing Institute of Lifeomics
Yan Wu: Beijing Institute of Lifeomics
Xinyuan Zhao: Beijing Institute of Lifeomics
Weijie Ye: Beijing Institute of Lifeomics
Dianyuan Zhao: Beijing Institute of Lifeomics
Ling Fu: Beijing Institute of Lifeomics
Caiping Tian: Beijing Institute of Lifeomics
Jing Yang: Beijing Institute of Lifeomics
Fuchu He: Beijing Institute of Lifeomics
Li Tang: Beijing Institute of Lifeomics

Nature Communications, 2019, vol. 10, issue 1, 1-14

Abstract: Abstract 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 Ly6ChiCX3CR1lo monocytes/macrophages to pro-resolving Ly6CloCX3CR1hi 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.

Date: 2019
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DOI: 10.1038/s41467-019-09046-8

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