Fundamental Neurochemistry Review: Microglial immunometabolism in traumatic brain injury

Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microgli...

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Published inJournal of neurochemistry Vol. 167; no. 2; pp. 129 - 153
Main Authors Strogulski, Nathan R., Portela, Luis V., Polster, Brian M., Loane, David J.
Format Journal Article
LanguageEnglish
Published England Blackwell Publishing Ltd 01.10.2023
Subjects
Animals
Anti-Inflammatory Agents
Brain
Brain damage
Brain Injuries, Traumatic - metabolism
Environmental effects
Glycolysis
Head injuries
Immune response
Immune system
Immunosurveillance
Impact damage
Inflammation
Lipid peroxidation
Lipids
Macrophages
Metabolic disorders
Metabolic pathways
Metabolism
Metabolites
Mice
Mice, Inbred C57BL
Microglia
Microglia - metabolism
Mitochondria
Neurochemistry
Neurodegeneration
Neuroinflammatory Diseases
Neurological diseases
Oxidation
Oxidative metabolism
Pain perception
Pentose
Pentose phosphate pathway
Phagocytosis
Phenotypes
Phenotyping
Reactive oxygen species
Stimuli
Traumatic brain injury
traumatic brain injury
neuroimmunology
metabolism
microglia
mitochondria
Online AccessGet full text
ISSN0022-3042
1471-4159
1471-4159
DOI10.1111/jnc.15959

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Abstract Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain‐infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro‐ and anti‐inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro‐inflammatory activation is associated with decreased mitochondrial respiration, whereas anti‐inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post‐traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non‐resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post‐traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI. image
AbstractList Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain‐infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro‐ and anti‐inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro‐inflammatory activation is associated with decreased mitochondrial respiration, whereas anti‐inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post‐traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non‐resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post‐traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI.
Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain-infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro- and anti-inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro-inflammatory activation is associated with decreased mitochondrial respiration, whereas anti-inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post-traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non-resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post-traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI.Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain-infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro- and anti-inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro-inflammatory activation is associated with decreased mitochondrial respiration, whereas anti-inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post-traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non-resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post-traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI.
Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain‐infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro‐ and anti‐inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia's ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro‐inflammatory activation is associated with decreased mitochondrial respiration, whereas anti‐inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post‐traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include (a) the nature of microglial mitochondrial dysfunction after TBI, (b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and (c) how immunometabolism alters microglial phenotypes, culminating in chronic non‐resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post‐traumatic neuroinflammation, and set out future directions toward advancing immunometabolic phenotyping in TBI. image
Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic neurodegeneration. Key mechanisms believed to support secondary brain injury include mitochondrial dysfunction and chronic neuroinflammation. Microglia and brain-infiltrating macrophages are responsible for neuroinflammatory cytokine and reactive oxygen species (ROS) production after TBI. Their production is associated with loss of homeostatic microglial functions such as immunosurveillance, phagocytosis, and immune resolution. Beyond providing energy support, mitochondrial metabolic pathways reprogram the pro- and anti-inflammatory machinery in immune cells, providing a critical immunometabolic axis capable of regulating immunologic response to noxious stimuli. In the brain, the capacity to adapt to different environmental stimuli derives, in part, from microglia’s ability to recognize and respond to changes in extracellular and intracellular metabolite levels. This capacity is met by an equally plastic metabolism, capable of altering immune function. Microglial pro-inflammatory activation is associated with decreased mitochondrial respiration, whereas anti-inflammatory microglial polarization is supported by increased oxidative metabolism. These metabolic adaptations contribute to neuroimmune responses, placing mitochondria as a central regulator of post-traumatic neuroinflammation. Although it is established that profound neurometabolic changes occur following TBI, key questions related to metabolic shifts in microglia remain unresolved. These include, a) the nature of microglial mitochondrial dysfunction after TBI, b) the hierarchical positions of different metabolic pathways such as glycolysis, pentose phosphate pathway, glutaminolysis, and lipid oxidation during secondary injury and recovery, and c) how immunometabolism alters microglial phenotypes, culminating in chronic non-resolving neuroinflammation. In this basic neurochemistry review article, we describe the contributions of immunometabolism to TBI, detail primary evidence of mitochondrial dysfunction and metabolic impairments in microglia and macrophages, discuss how major metabolic pathways contribute to post-traumatic neuroinflammation, and set out future directions towards advancing immunometabolic phenotyping in TBI. In this fundamental neurochemistry review we examine the relationship between traumatic brain injury (TBI) and immune cell metabolism, primarily focusing on microglia. TBI leads to widespread damage and chronic neurodegeneration, with secondary brain injury involving mitochondrial dysfunction and ongoing neuroinflammation. Microglia contribute to inflammation via cytokine and reactive oxygen species production chronically post-TBI, and promote long-term neurodegeneration. Metabolic pathways in these cells regulate immune responses, with metabolic adaptations driving pro- or anti-inflammatory states. However, questions about microglial mitochondrial dysfunction, the roles of specific metabolic pathways, and how immunometabolism influences chronic neuroinflammation following TBI remain. The review explores these aspects to advance understanding of immunometabolic changes in TBI.
Author Polster, Brian M.
Strogulski, Nathan R.
Portela, Luis V.
Loane, David J.
AuthorAffiliation 1 School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland
3 Department of Anesthesiology and Shock, Trauma and Anesthesiology Research Center, University of Maryland School of Medicine, Baltimore, Maryland, USA
2 Neurotrauma and Biomarkers Laboratory, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
AuthorAffiliation_xml – name: 2 Neurotrauma and Biomarkers Laboratory, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil
– name: 1 School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland
– name: 3 Department of Anesthesiology and Shock, Trauma and Anesthesiology Research Center, University of Maryland School of Medicine, Baltimore, Maryland, USA
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  givenname: Nathan R.
  orcidid: 0000-0003-2166-2137
  surname: Strogulski
  fullname: Strogulski, Nathan R.
  organization: School of Biochemistry and Immunology Trinity Biomedical Sciences Institute Trinity College Dublin Dublin Ireland
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  givenname: Luis V.
  orcidid: 0000-0001-6113-8466
  surname: Portela
  fullname: Portela, Luis V.
  organization: Neurotrauma and Biomarkers Laboratory Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul Porto Alegre Brazil
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  surname: Loane
  fullname: Loane, David J.
  organization: School of Biochemistry and Immunology Trinity Biomedical Sciences Institute Trinity College Dublin Dublin Ireland, Department of Anesthesiology and Shock, Trauma and Anesthesiology Research Center University of Maryland School of Medicine Baltimore Maryland USA
BackLink https://www.ncbi.nlm.nih.gov/pubmed/37759406$$D View this record in MEDLINE/PubMed
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Issue 2
Keywords traumatic brain injury
neuroimmunology
metabolism
microglia
mitochondria
Language English
License 2023 The Authors. Journal of Neurochemistry published by John Wiley & Sons Ltd on behalf of International Society for Neurochemistry.
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No
Brian M. Polster, PhD Department of Anesthesiology and Center for Shock, Trauma and Anesthesiology Research, University of Maryland School of Medicine, 685 W. Baltimore St., MSTF 5-34, Baltimore, MD 21201, USA, bpolster@som.umaryland.edu
"All experiments were conducted in compliance with the ARRIVE guidelines." unless it is a Review or Editorial
NRS: Conceptualization, Writing - Original Draft, Writing - Review & Editing, Funding acquisition. LVP: Writing - Review & Editing, Funding acquisition. BMP: Writing - Review & Editing, Funding acquisition. DJL: Conceptualization, Writing - Original Draft, Writing - Review & Editing, Funding acquisition.
if it is a Review or Editorial, skip complete sentence
Author contribution statement
Author contributions--
NA
if No, include a statement in the "Conflict of interest disclosure" section: "ARRIVE guidelines were not followed for the following reason
ARRIVE guidelines have been followed
(edit phrasing to form a complete sentence as necessary).
Luis Valmor Portela, PhD, Laboratory of Neurotrauma and Biomarkers, Departamento de Bioquímica, ICBS, Universidade Federal do Rio Grande do Sul, UFRGS, Rua Ramiro Barcelos 2600, anexo, Bairro Santana, Porto Alegre, RS, Brasil, roskaportela@gmail.com
if Yes, insert in the "Conflict of interest disclosure" section
ORCID 0000-0001-6113-8466
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0000-0003-0393-3503
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Snippet Traumatic brain injury (TBI) is a devastating neurological disorder caused by a physical impact to the brain that promotes diffuse damage and chronic...
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StartPage 129
SubjectTerms Animals
Anti-Inflammatory Agents
Brain
Brain damage
Brain Injuries, Traumatic - metabolism
Environmental effects
Glycolysis
Head injuries
Immune response
Immune system
Immunosurveillance
Impact damage
Inflammation
Lipid peroxidation
Lipids
Macrophages
Metabolic disorders
Metabolic pathways
Metabolism
Metabolites
Mice
Mice, Inbred C57BL
Microglia
Microglia - metabolism
Mitochondria
Neurochemistry
Neurodegeneration
Neuroinflammatory Diseases
Neurological diseases
Oxidation
Oxidative metabolism
Pain perception
Pentose
Pentose phosphate pathway
Phagocytosis
Phenotypes
Phenotyping
Reactive oxygen species
Stimuli
Traumatic brain injury
Title Fundamental Neurochemistry Review: Microglial immunometabolism in traumatic brain injury
URI https://www.ncbi.nlm.nih.gov/pubmed/37759406
https://www.proquest.com/docview/2875686041
https://www.proquest.com/docview/2870141529
https://pubmed.ncbi.nlm.nih.gov/PMC10655864
Volume 167
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