Hypoxia Impairs Mesenchymal Stromal Cell-Induced Macrophage M1 to M2 Transition

The transition of macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype is crucial for the progression of normal wound healing. Persistent M1 macrophages within the injury site may lead to an uncontrolled macrophage-mediated inflammatory response and ultimately a failure of...

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Bibliographic Details
Published inTechnology (Singapore) Vol. 5; no. 2; p. 81
Main Authors Faulknor, Renea A, Olekson, Melissa A, Ekwueme, Emmanuel C, Krzyszczyk, Paulina, Freeman, Joseph W, Berthiaume, François
Format Journal Article
LanguageEnglish
Published Singapore 01.06.2017
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Summary:The transition of macrophages from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype is crucial for the progression of normal wound healing. Persistent M1 macrophages within the injury site may lead to an uncontrolled macrophage-mediated inflammatory response and ultimately a failure of the wound healing cascade, leading to chronic wounds. Mesenchymal stromal cells (MSCs) have been widely reported to promote M1 to M2 macrophage transition; however, it is unclear whether MSCs can drive this transition in the hypoxic environment typically observed in chronic wounds. Here we report on the effect of hypoxia (1% O ) on MSCs' ability to transition macrophages from the M1 to the M2 phenotype. While hypoxia had no effect on MSC secretion, it inhibited MSC-induced M1 to M2 macrophage transition, and suppressed macrophage expression and production of the anti-inflammatory mediator interleukin-10 (IL-10). These results suggest that hypoxic environments may impede the therapeutic effects of MSCs.
ISSN:2339-5478
DOI:10.1142/S2339547817500042