Maternal exposure to combustion generated PM inhibits pulmonary Th1 maturation and concomitantly enhances postnatal asthma development in offspring
Open accessAbstract
BACKGROUND: Epidemiological studies suggest that maternal exposure to environmental hazards, such as particulate matter, is associated with increased incidence of asthma in childhood. We hypothesized that maternal exposure to combustion derived ultrafine particles containing persistent free radicals (MCP230) disrupts the development of the infant immune system and results in aberrant immune responses to allergens and enhances asthma severity. METHODS: Pregnant C57/BL6 mice received MCP230 or saline by oropharyngeal aspiration on gestational days 10 and 17. Three days after the second administration, blood was collected from MCP230 or saline treated dams and 8-isoprostanes in the serum were measured to assess maternal oxidative stress. Pulmonary T cell populations were assayed in the infant mice at six days, three and six weeks of postnatal age. When the infant mice matured to adults (i.e. six weeks of age), an asthma model was established with ovalbumin (OVA). Airway inflammation, mucus production and airway hyperresponsiveness were then examined. RESULTS: Maternal exposure to MCP230 induced systemic oxidative stress. The development of pulmonary T helper (Th1/Th2/Th17) and T regulatory (Treg) cells were inhibited in the infant offspring from MCP230-exposed dams. As the offspring matured, the development of Th2 and Treg cells recovered and eventually became equivalent to that of offspring from non-exposed dams. However, Th1 and Th17 cells remained attenuated through 6 weeks of age. Following OVA sensitization and challenge, mice from MCP230-exposed dams exhibited greater airway hyperresponsiveness, eosinophilia and pulmonary Th2 responses compared to offspring from non-exposed dams. CONCLUSIONS: Our data suggest that maternal exposure to MCP230 enhances postnatal asthma development in mice, which might be related to the inhibition of pulmonary Th1 maturation and systemic oxidative stress in the dams.
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Pulmonary Th1 cells remained suppressed up to 6 weeks after gestational PM0.1 exposure, leading to enhancement of postnatal allergic responses to OVA evidenced by increased AHR, eosinophilia, and pulmonary Th2 responses.
“Pulmonary Th1 cells remained suppressed up to 6 weeks, leading to enhancement of postnatal allergic responses to OVA evidenced by increased AHR, eosinophilia, and pulmonary Th2 responses.”
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 [104]
The Abstract (Results; page unavailable) reports that pulmonary Th1 cells remained attenuated through six weeks and that offspring of MCP230-exposed dams had greater airway hyperresponsiveness, eosinophilia, and pulmonary Th2 responses after OVA challenge. The Discussion (page unavailable) says suppressed Th1 responses *might predispose* offspring to Th2-dominated responses; it does not establish that Th1 suppression caused the enhanced allergic responses. (LLM, conf=0.87)
Experimental — accuracy not yet measuredGestational exposure to combustion-derived PM0.1 inhibited offspring pulmonary T cell development, with suppression of Th1, Th2, Th17, and Tregs at 6 days of age.
“In support of the hypothesis that prenatal PM alters immune development and predisposes offspring toward asthma, Wang et al. [104] showed gestational exposure to combustion-derived PM0.1 inhibited offspring pulmonary T cell development, with suppression of Th1, Th2, Th17, and Tregs at 6 days of age.”
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 [104]
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- Authors
- Wang, P., You, D., Saravia, J., Shen, H., & Cormier, S. A.
- Affiliations
- University of Tennessee Health Science Center (US)
- State Key Laboratory of Respiratory Disease (CN)
- Corresponding author
- Cormier, Stephania A
- Venue
- Particle and Fibre Toxicology
- Published
- 2013-07-16
- Volume
- 10
- Issue
- 1
- Pages
- 29-29
- ISSN
- 1743-8977 (ISSN-L)
- PMC
- PMC3717277
- OpenAlex
- W2139227362
- Cited by
- 58
- References
- 31
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 4 · 2023: 5 · 2022: 3 · 2021: 10 · 2020: 5 · 2019: 4 · 2018: 5 · 2017: 6 · 2016: 4 · 2015: 6 · 2014: 2
- FWCI
- 2.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Particle and Fibre Toxicology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Civil War Book Review (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Allergy and Infectious Diseases (R01AI090059)
- National Institute of Environmental Health Sciences (P42ES013648, R01ES015050)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Air Quality and Health Impacts
- Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
- Keywords
- maternal exposure, ultrafine particles, persistent free radicals, Th1 cells, Th17 cells, regulatory T cells, Th2 cells, oxidative stress, 8-isoprostane, airway hyperresponsiveness, ovalbumin sensitization, airway inflammation, mucus production, offspring immune development, prenatal environmental exposure
- MeSH terms
- Age Factors, Animals, Asthma, Female, Gestational Age, Lung, Mice, Inbred C57BL, Ovalbumin, Pregnancy, Prenatal Exposure Delayed Effects, Pulmonary Eosinophilia, Severity of Illness Index, Dinoprost, Cytokines, Bronchial Hyperreactivity, Oxidative Stress, Th1 Cells, Th2 Cells, Maternal Exposure, Inflammation Mediators, Inhalation Exposure, T-Lymphocytes, Regulatory, Particulate Matter, Th17 Cells
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