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Harry et al. Neuroimmunol Neuroinflammation 2020;7:150-65          Neuroimmunology
               DOI: 10.20517/2347-8659.2020.07                              and Neuroinflammation




               Review                                                                        Open Access


               An association between mitochondria and microglia

               effector function: what do we think we know?


               Gaylia Jean Harry , Gabrielle Childers , Sahana Giridharan , Irisyunuel Lopez Hernandes
                                                1,2
                               1
                                                                  1,3
                                                                                             1
               1 National Toxicology Program Laboratory, National Institute of Environmental Health Sciences, Durham, NC 27709, USA.
               2 (Current affiliation) Gabrielle Childers, University of Albama at Birmingham, Birmingham, AL 35294, USA.
               3 Sahana Giridharan, Duke University, Durham, NC 27708, USA.
               Correspondence to: Gaylia Jean Harry, National Institute of Environmental Health Sciences, P.O. Box 12233, MD E1-07,  Durham,
               NC 27709, USA. E-mail: harry@nih.gov


               How to cite this article: Harry GJ, Childers G, Giridharan S, Lopez Hernandes I. An association between mitochondria and
               microglia effector function: what do we think we know? Neuroimmunol Neuroinflammation 2020;7:150-65.
               http://dx.doi.org/10.20517/2347-8659.2020.07

               Received: 14 Jan 2020    First Decision: 24 Feb 2020    Revised: 7 Apr 2020    Accepted: 7 Apr 2020    Available online: 16 Jun 2020

               Science Editor: Jeffrey Bajramovic    Copy Editor: Jing-Wen Zhang    Production Editor: Tian Zhang


               Abstract
               While resident innate immune cells of the central nervous system, the microglia, represent a cell population unique
               in origin, microenvironment, and longevity, they assume many properties displayed by peripheral macrophages.
               One prominent shared property is the ability to undergo a metabolic switch towards glycolysis and away from
               oxidative phosphorylation (OXPHOS) upon activation by the pro-inflammatory stimuli lipopolysaccharide.
               This shift serves to meet specific cellular demands and allows for cell survival, similar to the Warburg effect
               demonstrated in cancer cells. In contrast, normal surveillance phenotype or stimulation to a non-proinflammatory
               phenotype relies primarily on OXPHOS and fatty acid oxidation. Thus, mitochondria appear to function as a
               pivotal signaling platform linking energy metabolism and macrophage polarization upon activation. These unique
               shifts in cell bioenergetics in response to different stimuli are essential for proper effector responses at sites of
               infection, inflammation, or injury. Here, we present a summary of recent developments as to how these dynamics
               characterized in peripheral macrophages are displayed in microglia. The new insights provided by an increased
               understanding of metabolic reprogramming in macrophages may allow for translation to the central nervous
               system and a better understanding of microglia heterogeneity, regulation, and function.


               Keywords: Mitochondria bioenergetics, inflammasome, microglia, pro-inflammatory, anti-inflammatory,
               polarization



                           © The Author(s) 2020. Open Access This article is licensed under a Creative Commons Attribution 4.0
                           International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use,
                sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long
                as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
                and indicate if changes were made.


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