Inhibition of endotoxin‐induced perinatal asthma protection by pollutants in an experimental mouse model
Abstract
Background One of the most promising strategies to face the increasing asthma prevalence and to prevent disease development might be an early contact with microbial compounds. However, little is known about an interaction between an early-life contact to microbial compounds leading to asthma protection in the offspring and a co-exposure to allergy-promoting pollutants. Methods Pregnant BALB/c mice were repeatedly exposed to aerosolized endotoxin (lipopolysaccharide, LPS). The offspring was further exposed to aerosolized LPS before allergen sensitization with ovalbumin (OVA). Some of the mice were co-exposed to mycotoxins or diesel exhaust particles (DEP) during pregnancy. The 6-week-old offspring was immunized with OVA and analyzed in a murine asthma model. Results While the offspring of naïve mothers developed an asthma-like phenotype, the offspring of mice perinatally exposed to LPS was significantly protected. Co-exposure of mice to mycotoxins or DEP during pregnancy inhibited the LPS-induced protection leading to the development of eosinophilic airway inflammation, airway hyperactivity, and increased antigen-specific IgE levels in the offspring. Furthermore, the asthma-preventive effect of perinatal LPS exposure was IFN-gamma dependent. Additionally, the IFN-gamma promoter of CD4+ T cells in the LPS-exposed offspring revealed a significant protection against loss of histone 4 acetylation, which was abolished after prenatal co-exposure to pollutants. Prenatal treatment of…
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LPS protected against OVA-induced pulmonary inflammation and airway hyperresponsiveness, but in offspring prenatally exposed to DEPs, LPS failed to confer protection.
“LPS protected against OVA-induced pulmonary inflammation and AHR; however, in offspring prenatally exposed to DEPs, LPS failed to confer protection.”
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 [103]
Maternal supplementation with N-acetylcysteine reversed the effects of prenatal DEP exposure, suggesting maternal dietary supplementation may prevent DEP-induced oxidative stress and downstream consequences in offspring.
“Maternal supplementation with the antioxidant N-acetylcysteine reversed these effects suggesting that maternal dietary supplementation may serve as a preventive intervention to combat DEP-induced oxidative stress and downstream consequences in offspring.”
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 [103]
The protection by LPS was dependent on epigenetic regulation of IFNγ expression.
“Investigators showed the protection was dependent on the epigenetic regulation of IFNγ expression.”
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 [103]
Maternal treatment with the antioxidant N-acetyl cysteine (NAC) reversed the IFN-γ-dependent asthma risk in offspring, thereby re-conferring protection.
“This effect was dependent on IFN-γ, and maternal treatment with the antioxidant N-acetyl cysteine (NAC) reversed the IFN-γ-dependent asthma risk in offspring, thereby re-conferring protection.”
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 [103]
Protection conferred from endotoxin (LPS) on offspring OVA-induced asthma was erased if dams were co-exposed to diesel exhaust PM during pregnancy.
“Using elegant study design, Repreich et al. [103] demonstrated protection conferred from endotoxin (LPS) on offspring OVA-induced asthma was erased if dams were co-exposed to diesel exhaust PM during pregnancy.”
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 [103]
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Johnson, N. M., Hoffmann, A. R., Behlen, J. C., Lau, C., Pendleton, D., Harvey, N., Shore, R., Li, Y., Chen, J., Tian, Y., et al. (2021) · Environmental Health and Preventive Medicine · doi:10.1186/s12199-021-00995-5 · Cited by 339 · see citing works
“[103] demonstrated protection conferred from endotoxin (LPS) on offspring OVAinduced asthma was erased if dams were co-exposed to diesel exhaust PM during pregnancy.”
BackgroundInfluentialThe gut microbiota and its role in the development of allergic disease: A wider perspective
West, C. E., Jenmalm, M. C., & Prescott, S. L. (2015) · Clinical & Experimental Allergy · doi:10.1111/cea.12332 · Cited by 223 · see citing works
In utero ultrafine particulate matter exposure causes offspring pulmonary immunosuppression
Rychlik, K. A., Secrest, J. R., Lau, C., Pulczinski, J., Zamora, M. L., Leal, J., Langley, R., Myatt, L. G., Raju, M., Chang, R. C.-A., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1816103116 · Cited by 98 · see citing works
- Authors
- Reiprich, M., Rudzok, S., Schütze, N., Simon, J. C., Lehmann, I., Trump, S., & Polte, T.
- Affiliations
- Helmholtz Centre for Environmental Research (DE)
- University Hospital Leipzig (DE)
- Corresponding author
- Polte, T.
- Venue
- Allergy
- Publisher
- Wiley
- Published
- 2013-02-15
- Volume
- 68
- Issue
- 4
- Pages
- 481-489
- ISSN
- 0105-4538 (ISSN-L)
- 1398-9995
- OpenAlex
- W1973460381
- Cited by
- 31
- References
- 2
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 1 · 2023: 1 · 2021: 4 · 2020: 5 · 2019: 3 · 2017: 3 · 2016: 1 · 2015: 2 · 2014: 3 · 2013: 4 · 2012: 1
- FWCI
- 2.31
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Allergy (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Asthma and respiratory diseases
- Health Sciences › Medicine › Immunology and Allergy › Allergic Rhinitis and Sensitization
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Occupational exposure and asthma
- Keywords
- endotoxin, lipopolysaccharide, prenatal exposure, mycotoxins, diesel exhaust particles, air pollution, ovalbumin sensitization, allergic asthma, eosinophilic airway inflammation, IgE, interferon-gamma, CD4+ T cells, N-acetylcysteine, antioxidants, maternal exposure
- MeSH terms
- Acetylation, Acetylcysteine, Air Pollutants, Allergens, Animals, Antibodies, Monoclonal, Antioxidants, Asthma, Disease Models, Animal, Endotoxins, Female, Histones, Interferon-gamma, Lipopolysaccharides, Mycotoxins, Ovalbumin, Pregnancy, Prenatal Exposure Delayed Effects, Promoter Regions, Genetic, Maternal Exposure, Antibodies, Blocking, Epigenesis, Genetic, Mice
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