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10.1038/ncomms12177

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suck abstract from ncbi


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pmid27397585
      Nat+Commun 2016 ; 7 (ä): 12177
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  • Phagocyte respiratory burst activates macrophage erythropoietin signalling to promote acute inflammation resolution #MMPMID27397585
  • Luo B ; Wang J ; Liu Z ; Shen Z ; Shi R ; Liu YQ ; Liu Y ; Jiang M ; Wu Y ; Zhang Z
  • Nat Commun 2016[Jul]; 7 (ä): 12177 PMID27397585 show ga
  • 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 PPAR?, 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.
  • |*Phagocytosis [MESH]
  • |*Respiratory Burst [MESH]
  • |Animals [MESH]
  • |Cell Movement [MESH]
  • |Erythropoietin/*metabolism [MESH]
  • |Hypoxia/metabolism [MESH]
  • |Inflammation/immunology/*metabolism [MESH]
  • |Lymph Nodes/immunology [MESH]
  • |Macrophages/*metabolism [MESH]
  • |Male [MESH]
  • |Mice, Inbred C57BL [MESH]
  • |Mice, Knockout [MESH]
  • |PPAR gamma/metabolism [MESH]
  • |Receptors, Erythropoietin/metabolism [MESH]


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