Mitochondrial arginase-2 is essential for IL-10 metabolic reprogramming of inflammatory macrophages


Jennifer K Dowling, Remsha Afzal, Linden J Gearing Mariana P Cervantes-Silva , Stephanie Annett Gavin M Davis , Chiara De Santi , Nadine Assmann, Katja Dettmer, Daniel J Gough , Glenn R Bantug , Fidinny I Hamid , Frances K Nally , Conor P Duffy , Aoife L Gorman , Alex M Liddicoat, Ed C Lavelle , Christoph Hess , Peter J Oefner , David K Finlay , Gavin P Davey , Tracy Robson, Annie M Curtis , Paul J Hertzog , Bryan R G Williams , Claire E McCoy

Macrophages are important immune cells that can exert either pro-inflammatory or anti-inflammatory functions, for innate as well as adaptive immune responses1. Metabolically, it has been shown that in vitro ‘M1-like’ inflammatory macrophages utilize aerobic glycolysis for the generation of ATP. This is accompanied with a downregulation of mitochondrial oxidative phosphorylation (OxPhos) and an accumulation of certain metabolites in the tricarboxylic acid (TCA) cycle, such as citrate and succinate. Conversely, diverse anti-inflammatory stimuli including IL-10, IL-4, and IL-13 are ‘M2-like’ anti-inflammatory phenotype inducers. M2-like cells are shown to favour the use of OxPhos, which has been linked to specific alterations in macrophage mitochondrial dynamics.

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