Phagocyte respiratory burst activates macrophage erythropoietin signalling to promote acute inflammation resolution

Bangwei Luo, Jinsong Wang, Zongwei Liu, Zigang Shen, Rongchen Shi, Yu-Qi Liu, Yu Liu, Man Jiang, Yuzhang Wu () and Zhiren Zhang ()
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Bangwei Luo: Institute of Immunology, Third Military Medical University of PLA
Jinsong Wang: Institute of Immunology, Third Military Medical University of PLA
Zongwei Liu: Institute of Immunology, Third Military Medical University of PLA
Zigang Shen: Institute of Immunology, Third Military Medical University of PLA
Rongchen Shi: Institute of Immunology, Third Military Medical University of PLA
Yu-Qi Liu: Institute of Immunology, Third Military Medical University of PLA
Yu Liu: Institute of Immunology, Third Military Medical University of PLA
Man Jiang: Institute of Immunology, Third Military Medical University of PLA
Yuzhang Wu: Institute of Immunology, Third Military Medical University of PLA
Zhiren Zhang: Institute of Immunology, Third Military Medical University of PLA

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Inflammation resolution is an active process, the failure of which causes uncontrolled inflammation which underlies many chronic diseases. Therefore, endogenous pathways that regulate inflammation resolution are fundamental and of wide interest. Here, we demonstrate that phagocyte respiratory burst-induced hypoxia activates macrophage erythropoietin signalling to promote acute inflammation resolution. This signalling is activated following acute but not chronic inflammation. Pharmacological or genetical inhibition of the respiratory burst suppresses hypoxia and macrophage erythropoietin signalling. Macrophage-specific erythropoietin receptor-deficient mice and chronic granulomatous disease (CGD) mice, which lack the capacity for respiratory burst, display impaired inflammation resolution, and exogenous erythropoietin enhances this resolution in WT and CGD mice. Mechanistically, erythropoietin increases macrophage engulfment of apoptotic neutrophils via PPARγ, promotes macrophage removal of debris and enhances macrophage migration to draining lymph nodes. Together, our results provide evidences of an endogenous pathway that regulates inflammation resolution, with important implications for treating inflammatory conditions.

Date: 2016
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DOI: 10.1038/ncomms12177

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