Radical-Containing Ultrafine Particulate Matter Initiates Epithelial-to-Mesenchymal Transitions in Airway Epithelial Cells
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Environmentally persistent free radicals (EPFRs) in combustion-generated particulate matter (PM) are capable of inducing pulmonary pathologies and contributing to the development of environmental asthma. In vivo exposure of infant rats to EPFRs demonstrates their ability to induce airway hyperresponsiveness to methacholine, a hallmark of asthma. However, the mechanisms by which combustion-derived EPFRs elicit in vivo responses remain elusive. In this study, we used a chemically defined EPFR consisting of approximately 0.2 μm amorphrous silica containing 3% cupric oxide with the organic pollutant 1,2-dichlorobenzene (DCB-230). DCB-230 possesses similar radical content to urban-collected EPFRs but offers several advantages, including lack of contaminants and chemical uniformity. DCB-230 was readily taken up by BEAS-2B and at high doses (200 μg/cm2) caused substantial necrosis. At low doses (20 μg/cm2), DCB-230 particles caused lysosomal membrane permeabilization, oxidative stress, and lipid peroxidation within 24 hours of exposure. During this period, BEAS-2B underwent epithelial-to-mesenchymal transition (EMT), including loss of epithelial cell morphology, decreased E-cadherin expression, and increased α–smooth muscle actin (α-SMA) and collagen I production. Similar results were observed in neonatal air–liquid interface culture (i.e., disruption of epithelial integrity and EMT). Acute exposure of infant mice to DCB-230 resulted in EMT, as confirmed by lineage tracing studies and evidenced by coexpression of epithelial E-cadherin and mesenchymal α-SMA proteins in airway cells and increased SNAI1 expression in the lungs. EMT in neonatal mouse lungs after EPFR exposure may provide an explanation for epidemiological evidence supporting PM exposure and increased risk of asthma.
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The EMT phenotype was also characterized in a mouse model of neonatal exposure to radical-containing ultrafine particles.
“This phenotype was also characterized in a mouse model of neonatal exposure to radical-containing ultrafine particles [72].”
From Air pollution and children’s health—a review of adverse effects associated with prenatal exposure from fine to ultrafine particulate matter (2021) · cites this paper as [72]
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- Authors
- Thevenot, P. T., Saravia, J., Jin, N., Giaimo, J. D., Chustz, R. E., Mahne, S., Kelley, M. A., Hebert, V. Y., Dellinger, B., Dugas, T. R., DeMayo, F. J., & Cormier, S. A.
- Affiliations
- Louisiana State University (US)
- Louisiana State University Health Sciences Center New Orleans (US)
- Baylor College of Medicine (US)
- Louisiana State University Health Sciences Center Shreveport (US)
- Corresponding author
- Cormier, Stephania A.
- ORCID
- Venue
- American Journal of Respiratory Cell and Molecular Biology
- Publisher
- Oxford University Press (OUP)
- Published
- 2013-02-01
- Volume
- 48
- Issue
- 2
- Pages
- 188-197
- ISSN
- 1044-1549 (ISSN-L)
- 1535-4989
- PMC
- PMC3604062
- OpenAlex
- W2016382510
- Cited by
- 110
- References
- 55
- Citations by year
- 2026: 2 · 2025: 4 · 2024: 12 · 2023: 10 · 2022: 4 · 2021: 13 · 2020: 16 · 2019: 11 · 2018: 4 · 2017: 8 · 2016: 9 · 2015: 3 · 2014: 8 · 2013: 5 · 2012: 1
- FWCI
- 6.13
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- American Journal of Respiratory Cell and Molecular Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Civil War Book Review (submittedVersion)
- Funders
- Louisiana State University
- National Institute on Alcohol Abuse and Alcoholism (AA007577, T32AA007577)
- National Institute of Environmental Health Sciences (P42ES013648, R01ES015050)
- Topics
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Keywords
- ultrafine particles, epithelial-mesenchymal transition, airway epithelial cells, 1,2-dichlorobenzene, cupric oxide, silica particles, airway hyperresponsiveness, asthma, lysosomal membrane permeabilization, oxidative stress, lipid peroxidation, E-cadherin, alpha-smooth muscle actin, SNAI1, neonatal lung development, air-liquid interface culture, BEAS-2B cells
- MeSH terms
- Air Pollutants, Animals, Animals, Newborn, Cell Line, Cell Membrane Permeability, Dose-Response Relationship, Drug, Epithelial Cells, Particle Size, Oxidative Stress, Mice, Bronchioles, Epithelial-Mesenchymal Transition
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