The role of MAC 1 in diesel exhaust particle‐induced microglial activation and loss of dopaminergic neuron function
Open accessAbstract
Increasing reports support that air pollution causes neuroinflammation and is linked to central nervous system (CNS) disease/damage. Diesel exhaust particles (DEP) are a major component of urban air pollution, which has been linked to microglial activation and Parkinson's disease-like pathology. To begin to address how DEP may exert CNS effects, microglia and neuron-glia cultures were treated with either nanometer-sized DEP (< 0.22 μM; 50 μg/mL), ultrafine carbon black (ufCB, 50 μg/mL), or DEP extracts (eDEP; from 50 μg/mL DEP), and the effect of microglial activation and dopaminergic (DA) neuron function was assessed. All three treatments showed enhanced ameboid microglia morphology, increased H2 O2 production, and decreased DA uptake. Mechanistic inquiry revealed that the scavenger receptor inhibitor fucoidan blocked DEP internalization in microglia, but failed to alter DEP-induced H2 O2 production in microglia. However, pre-treatment with the MAC1/CD11b inhibitor antibody blocked microglial H2 O2 production in response to DEP. MAC1(-/-) mesencephalic neuron-glia cultures were protected from DEP-induced loss of DA neuron function, as measured by DA uptake. These findings support that DEP may activate microglia through multiple mechanisms, where scavenger receptors regulate internalization of DEP and the MAC1 receptor is mandatory for both DEP-induced microglial H2 O2 production and loss of DA neuron function.
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Both in co-culture and in vivo, toxins associated with neurodegeneration cause CR3 stimulation by the DAMP HMGB1, which results in activation of NOX2 and production of O2•-.
“Both in co-culture and in vivo, toxins associated with neurodegeneration, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), LPS and diesel exhaust particles, cause CR3 stimulation by the DAMP, high mobility group box 1 (HMGB1), which results in activation of NOX2 and production of O2•– [101,102,103].”
From ROS Generation in Microglia: Understanding Oxidative Stress and Inflammation in Neurodegenerative Disease (2020) · cites this paper as [102]
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- Lucchini RG Dorman DC Elder A Veronesi B Neurological impacts from inhalation of pollutants and the nose-brain connection Neurotoxicology 2012 33 838 841 22178536 PMC3387329
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“Pharmacological blockade or microglial-specific knockout of TLR4 or CR3 severely attenuates ROS production by NOX2, indicating NOX2 activation is of microglial origin, despite reported expression of NOX2 in neurons [64,102,103].”
BackgroundHou, L., Wang, K., Zhang, C., Sun, F., Che, Y., Zhao, X., Zhang, D., Li, H., & Wang, Q. (2018) · Redox Biology · doi:10.1016/j.redox.2017.09.017 · Cited by 104 · see citing works
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- Authors
- Levesque, S., Taetzsch, T., Lull, M. E., Johnson, J. A., McGraw, C., & Block, M. L.
- Affiliations
- Virginia Commonwealth University (US)
- National Institutes of Health (US)
- Corresponding author
- Block, Michelle L.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2013-04-02
- Volume
- 125
- Issue
- 5
- Pages
- 756-765
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC3660420
- OpenAlex
- W2003622777
- Cited by
- 94
- References
- 66
- Citations by year
- 2026: 4 · 2025: 6 · 2024: 5 · 2023: 5 · 2022: 13 · 2021: 10 · 2020: 6 · 2019: 6 · 2018: 6 · 2017: 9 · 2016: 9 · 2015: 4 · 2014: 7 · 2013: 4
- FWCI
- 4.48
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Fisher Digital Publications (St. John Fisher College) (submittedVersion)
- Funders
- National Institute of Environmental Health Sciences/the National Institute of health (1R01ES016951)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- diesel exhaust particles, microglial activation, dopaminergic neurons, Parkinson's disease, neuroinflammation, air pollution, scavenger receptors, ultrafine carbon black, hydrogen peroxide production, dopamine uptake, fucoidan, receptor internalization, neuron-glia co-culture
- MeSH terms
- Animals, Vehicle Emissions, Cell Line, Cells, Cultured, Female, Male, Mice, Inbred C57BL, Mice, Transgenic, Neural Inhibition, Pregnancy, Rats, Inbred F344, Macrophage-1 Antigen, Microglia, Mice, Rats, Particulate Matter, Mice, 129 Strain, Dopaminergic Neurons
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