Cited by 339Traumatic Brain Injury and Neurovascular DisturbancesNeuroinflammation and Neurodegeneration MechanismsTraumatic Brain Injury Research

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Microglial/Macrophage Polarization Dynamics following Traumatic Brain Injury

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Kumar, Alok, Alvarez-Croda, Dulce-Mariely, Stoica, Bogdan A., Faden, Alan I., Loane, David J.·2016·Journal of Neurotrauma

DOI 10.1089/neu.2015.4268PMC PMC5065034

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Abstract

Activated microglia and macrophages exert dual beneficial and detrimental roles after central nervous system injury, which are thought to be due to their polarization along a continuum from a classical pro-inflammatory M1-like state to an alternative anti-inflammatory M2-like state. The goal of the present study was to analyze the temporal dynamics of microglia/macrophage polarization within the lesion micro-environment following traumatic brain injury (TBI) using a moderate-level controlled cortical impact (CCI) model in mice. We performed a detailed phenotypic analysis of M1- and M2-like polarized microglia/macrophages, as well as nicotinamide adenine dinucleotide phosphate oxidase (NOX2) expression, through 7 days post-injury using real-time polymerase chain reaction (qPCR), flow cytometry and image analyses. We demonstrated that microglia/macrophages express both M1- and M2-like phenotypic markers early after TBI, but the transient up-regulation of the M2-like phenotype was replaced by a predominant M1- or mixed transitional (Mtran) phenotype that expressed high levels of NOX2 at 7 days post-injury. The shift towards the M1-like and Mtran phenotype was associated with increased cortical and hippocampal neurodegeneration. In a follow up study, we administered a selective NOX2 inhibitor, gp91ds-tat, to CCI mice starting at 24 h post-injury to investigate the relationship between NOX2 and M1-like/Mtran phenotypes. Delayed gp91ds-tat treatment altered M1-/M2-like balance in favor of the anti-inflammatory M2-like phenotype, and significantly reduced oxidative damage in neurons at 7 days post-injury. Therefore, our data suggest that despite M1-like and M2-like polarized microglia/macrophages being activated after TBI, the early M2-like response becomes dysfunctional over time, resulting in development of pathological M1-like and Mtran phenotypes driven by increased NOX2 activity.

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Background
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Authors: Kumar, A., Alvarez-Croda, D.-M., Stoica, B. A., Faden, A. I., & Loane, D. J.
Affiliations: University of Maryland, Baltimore (US)
Department of Anesthesiology and Shock, Trauma and Anesthesiology Research (STAR) Center, University of Maryland School of Medicine, Baltimore, Maryland.
Corresponding author: Loane, David J.
ORCID: Kumar, Alok
Stoica, Bogdan A.
Faden, Alan I.
Loane, David J.
Venue: Journal of Neurotrauma
Publisher: SAGE Publications
Published: 2016-10
Volume: 33
Issue: 19
Pages: 1732-1750
ISSN: 0897-7151 (ISSN-L)
1557-9042
DOI: 10.1089/neu.2015.4268
PMC: PMC5065034
OpenAlex: W2209119157
Cited by: 339
References: 52
Citations by year: 2026: 14 · 2025: 26 · 2024: 27 · 2023: 30 · 2022: 41 · 2021: 55 · 2020: 39 · 2019: 31 · 2018: 27 · 2017: 24 · 2016: 23
FWCI: 17.56
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.liebertpub.com/nv/resources-tools/text-and-data-mining-policy/121/ (tdm)
Locations: Journal of Neurotrauma (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (AG028747)
National Institute on Aging (AG028747, P30AG028747)
National Institute of Neurological Disorders and Stroke (R01NS037313, R01NS082308)
Topics: Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury and Neurovascular Disturbances
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Clinical Neurology › Traumatic Brain Injury Research
Keywords: microglial polarization, macrophage polarization, traumatic brain injury, M1/M2 phenotype, NOX2, controlled cortical impact, neuroinflammation, neurodegeneration, oxidative damage, hippocampus, cortical injury, temporal dynamics

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Microglial/Macrophage Polarization Dynamics following Traumatic Brain Injury

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