Exposure to combustion generated environmentally persistent free radicals enhances severity of influenza virus infection
Open accessAbstract
BACKGROUND: Exposures to elevated levels of particulate matter (PM) enhance severity of influenza virus infection in infants. The biological mechanism responsible for this phenomenon is unknown. The recent identification of environmentally persistent free radicals (EPFRs) associated with PM from a variety of combustion sources suggests its role in the enhancement of influenza disease severity. METHODS: Neonatal mice (< seven days of age) were exposed to DCB230 (combustion derived PM with a chemisorbed EPFR), DCB50 (non-EPFR PM sample), or air for 30 minutes/day for seven consecutive days. Four days post-exposure, neonates were infected with influenza intranasally at 1.25 TCID50/neonate. Neonates were assessed for morbidity (% weight gain, peak pulmonary viral load, and viral clearance) and percent survival. Lungs were isolated and assessed for oxidative stress (8-isoprostanes and glutathione levels), adaptive immune response to influenza, and regulatory T cells (Tregs). The role of the EPFR was also assessed by use of transgenic mice expressing human superoxide dismutase 2. RESULTS: Neonates exposed to EPFRs had significantly enhanced morbidity and decreased survival following influenza infection. Increased oxidative stress was also observed in EPFR exposed neonates. This correlated with increased pulmonary Tregs and dampened protective T cell responses to influenza infection. Reduction of EPFR-induced oxidative stress attenuated these effects. CONCLUSIONS: Neonatal exposure to EPFR containing PM resulted in pulmonary oxidative stress and enhanced influenza disease severity. EPFR-induced oxidative stress resulted in increased presence of Tregs in the lungs and subsequent suppression of adaptive immune response to influenza.
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Neonates exposed to PM0.1 early in life were more susceptible to severe influenza infection.
“Moreover, the initial immune suppression is relevant to respiratory infection risk, which investigators went on to show neonates exposed to PM0.1 early in life were more susceptible to severe influenza infection [74].”
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 [74]
The Discussion (page unavailable) reports that neonatal mice exposed to EPFR-containing particles had more severe influenza, including greater morbidity and lower survival. However, Methods > Combustion derived PM (page unavailable) specifies particles with a mean aerodynamic diameter of 0.2 μm, not PM0.1; the finding also concerns mice, not human neonates. (LLM, conf=0.90)
Experimental — accuracy not yet measuredEarly life PM0.1 exposure is associated with increased risk of both asthma and respiratory infection.
“Successive research from this group supports the role of early life PM0.1 exposure and increased risk of both asthma and respiratory infection risk.”
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 [74]
The Discussion reports that prenatal exposure to EPFR-containing particles increased asthma risk in offspring in the group's prior work, and that neonatal exposure worsened influenza outcomes in this study. But the Methods specify particles with a mean diameter of 0.2 µm, not PM0.1, and the study measured severity after deliberate infection rather than the risk of acquiring a respiratory infection (no page numbers available). (LLM, conf=0.90)
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- Authors
- Lee, G. I., Saravia, J., You, D., Shrestha, B., Jaligama, S., Hebert, V. Y., Dugas, T. R., & Cormier, S. A.
- Affiliations
- University of Tennessee Health Science Center (US)
- Louisiana State University Health Sciences Center Shreveport (US)
- Corresponding author
- Cormier, Stephania A
- Venue
- Particle and Fibre Toxicology
- Published
- 2014-10-30
- Volume
- 11
- Issue
- 1
- Pages
- 57-57
- ISSN
- 1743-8977 (ISSN-L)
- PMC
- PMC4222384
- OpenAlex
- W2102366014
- Cited by
- 119
- References
- 47
- Citations by year
- 2026: 1 · 2025: 7 · 2024: 14 · 2023: 17 · 2022: 16 · 2021: 23 · 2020: 13 · 2019: 8 · 2018: 6 · 2017: 4 · 2016: 5 · 2015: 5
- FWCI
- 3.07
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Particle and Fibre Toxicology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Civil War Book Review (submittedVersion)
- Funders
- National Institute of Allergy and Infectious Diseases (R01AI090059)
- 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 › Epidemiology › Influenza Virus Research Studies
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Keywords
- environmentally persistent free radicals, particulate matter, influenza, disease severity, neonatal mice, oxidative stress, regulatory T cells, adaptive immune response, manganese superoxide dismutase, air pollution
- MeSH terms
- Superoxide Dismutase 2, Animals, Animals, Newborn, Free Radicals, Glutathione, Humans, Lung, Mice, Inbred C57BL, Mice, Transgenic, Orthomyxoviridae Infections, Superoxide Dismutase, Time Factors, Dinoprost, Oxidative Stress, Risk Assessment, Viral Load, Inhalation Exposure, T-Lymphocytes, Regulatory, Mice, Particulate Matter, Influenza A Virus, H1N1 Subtype, Adaptive Immunity
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