Features of Microglia and Neuroinflammation Relevant to Environmental Exposure and Neurotoxicity
Abstract
Microglia are resident cells of the brain involved in regulatory processes critical for development, maintenance of the neural environment, injury and repair. They belong to the monocytic-macrophage lineage and serve as brain immune cells to orchestrate innate immune responses; however, they are distinct from other tissue macrophages due to their relatively quiescent phenotype and tight regulation by the CNS microenvironment. Microglia actively survey the surrounding parenchyma and respond rapidly to changes such that any disruption to neural architecture or function can contribute to the loss in regulation of the microglia phenotype. In many models of neurodegeneration and neurotoxicity, early events of synaptic degeneration and neuronal loss are accompanied by an inflammatory response including activation of microglia, perivascular monocytes, and recruitment of leukocytes. In culture, microglia have been shown to be capable of releasing several potentially cytotoxic substances, such as reactive oxygen intermediates, nitric oxide, proteases, arachidonic acid derivatives, excitatory amino acids, and cytokines; however, they also produce various neurotrophic factors and quench damage from free radicals and excitotoxins. As the primary source for pro-inflammatory cytokines, microglia are implicated as pivotal mediators of neuroinflammation and can induce or modulate a broad spectrum of cellular responses. Neuroinflammation should be considered as amore »
- Authors:
-
- Oak Ridge Institute for Science and Education (ORISE), at the US Environmental Protection Agency (EPA), Arlington, VA (United States)
- National Institutes of Health, Research Triangle Park, NC (United States)
- Publication Date:
- Research Org.:
- Oak Ridge Institute for Science and Education (ORISE), Oak Ridge, TN (United States)
- Sponsoring Org.:
- USDOE Office of Science (SC), Biological and Environmental Research (BER); National Institutes of Health (NIH); US Environmental Protection Agency (EPA)
- OSTI Identifier:
- 1628353
- Grant/Contract Number:
- SC0014664; 1Z01ES101623; ES021164
- Resource Type:
- Accepted Manuscript
- Journal Name:
- International Journal of Environmental Research and Public Health
- Additional Journal Information:
- Journal Volume: 8; Journal Issue: 7; Journal ID: ISSN 1660-4601
- Publisher:
- MDPI
- Country of Publication:
- United States
- Language:
- English
- Subject:
- 60 APPLIED LIFE SCIENCES; neuroinflammation; microglia; neurotoxicity; neurodegeneration; cytokines; environmental exposure
Citation Formats
Kraft, Andrew D., and Harry, G. Jean. Features of Microglia and Neuroinflammation Relevant to Environmental Exposure and Neurotoxicity. United States: N. p., 2011.
Web. doi:10.3390/ijerph8072980.
Kraft, Andrew D., & Harry, G. Jean. Features of Microglia and Neuroinflammation Relevant to Environmental Exposure and Neurotoxicity. United States. https://doi.org/10.3390/ijerph8072980
Kraft, Andrew D., and Harry, G. Jean. Wed .
"Features of Microglia and Neuroinflammation Relevant to Environmental Exposure and Neurotoxicity". United States. https://doi.org/10.3390/ijerph8072980. https://www.osti.gov/servlets/purl/1628353.
@article{osti_1628353,
title = {Features of Microglia and Neuroinflammation Relevant to Environmental Exposure and Neurotoxicity},
author = {Kraft, Andrew D. and Harry, G. Jean},
abstractNote = {Microglia are resident cells of the brain involved in regulatory processes critical for development, maintenance of the neural environment, injury and repair. They belong to the monocytic-macrophage lineage and serve as brain immune cells to orchestrate innate immune responses; however, they are distinct from other tissue macrophages due to their relatively quiescent phenotype and tight regulation by the CNS microenvironment. Microglia actively survey the surrounding parenchyma and respond rapidly to changes such that any disruption to neural architecture or function can contribute to the loss in regulation of the microglia phenotype. In many models of neurodegeneration and neurotoxicity, early events of synaptic degeneration and neuronal loss are accompanied by an inflammatory response including activation of microglia, perivascular monocytes, and recruitment of leukocytes. In culture, microglia have been shown to be capable of releasing several potentially cytotoxic substances, such as reactive oxygen intermediates, nitric oxide, proteases, arachidonic acid derivatives, excitatory amino acids, and cytokines; however, they also produce various neurotrophic factors and quench damage from free radicals and excitotoxins. As the primary source for pro-inflammatory cytokines, microglia are implicated as pivotal mediators of neuroinflammation and can induce or modulate a broad spectrum of cellular responses. Neuroinflammation should be considered as a balanced network of processes whereby subtle modifications can shift the cells toward disparate outcomes. For any evaluation of neuroinflammation and microglial responses, within the framework of neurotoxicity or degeneration, one key question in determining the consequence of neuroinflammation is whether the response is an initiating event or the consequence of tissue damage. As examples of environmental exposure-related neuroinflammation in the literature, we provide an evaluation of data on manganese and diesel exhaust particles.},
doi = {10.3390/ijerph8072980},
journal = {International Journal of Environmental Research and Public Health},
number = 7,
volume = 8,
place = {United States},
year = {Wed Jul 20 00:00:00 EDT 2011},
month = {Wed Jul 20 00:00:00 EDT 2011}
}
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- Ye, Minsook; Lee, Seul gi; Chung, Eun Sook
- Evidence-Based Complementary and Alternative Medicine, Vol. 2014
Coordinated Gene Expression of Neuroinflammatory and Cell Signaling Markers in Dorsolateral Prefrontal Cortex during Human Brain Development and Aging
journal, October 2014
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Oxidative Stress and Microglial Cells in Parkinson's Disease
journal, January 2012
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Ecological implications of individuality in the context of the concept of adaptive strategy
journal, December 1966
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Zinc Oxide Nanoparticle Induces Microglial Death by NADPH-Oxidase-Independent Reactive Oxygen Species as well as Energy Depletion
journal, October 2016
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Histone Deacetylase Inhibitor Trichostatin A Ameliorated Endotoxin-Induced Neuroinflammation and Cognitive Dysfunction
journal, January 2015
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Adenosine A2A Receptor Deficiency Up-Regulates Cystatin F Expression in White Matter Lesions Induced by Chronic Cerebral Hypoperfusion
journal, December 2012
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Non-toxic engineered carbon nanodiamond concentrations induce oxidative/nitrosative stress, imbalance of energy metabolism, and mitochondrial dysfunction in microglial and alveolar basal epithelial cells
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Microglia amplify inflammatory activation of astrocytes in manganese neurotoxicity
journal, May 2017
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Neurotoxicants Are in the Air: Convergence of Human, Animal, andIn VitroStudies on the Effects of Air Pollution on the Brain
journal, January 2014
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Dexmedetomidine inhibits the lipopolysaccharide‐stimulated inflammatory response in microglia through the pathway involving TLR4 and NF‐κB
journal, August 2019
- Zhou, Xue‐Yue; Liu, Jing; Xu, Zhi‐Peng
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