ArticleEnvironmental health perspectives2017
Maternal Exposure of BALB/c Mice to Indoor NO2 and Allergic Asthma Syndrome in Offspring at Adulthood with Evaluation of DNA Methylation Associated Th2 Polarization.
Article in Environmental health perspectives, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 35 citations in OpenAlex.
- Investigation analysis of the acute asthma risk factor and phenotype based on relational analysis with outdoor air pollutants in Xi'an, China.Environmental geochemistry and health · 2024Article
- Deficiency of interleukin-6 receptor ameliorates PMEcotoxicology and environmental safety · 2022Article
- Article
- Ten-eleven translocation 2 modulates allergic inflammation by 5-hydroxymethylcytosine remodeling of immunologic pathways.Human molecular genetics · 2021Article
- Increased airway epithelial cell-derived exosomes activate macrophage-mediated allergic inflammation via CD100 shedding.Journal of cellular and molecular medicine · 2021Article
- Short-term exposure to ambient air pollution and hospital visits for IgE-mediated allergy: A time-stratified case-crossover study in southern China from 2012 to 2019.EClinicalMedicine · 2021Article
- A review of epigenetic changes in asthma: methylation and acetylation.Clinical epigenetics · 2021Review
- [Establishment of an ovalbumin-induced bronchial asthma model in mice with intrauterine growth retardation].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2019Article
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8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundFetal stress has been proposed to be associated with diseases in both children and adults. Epidemiological studies suggest that maternal exposure to nitrogen dioxide (NO2) contributes to increased morbidity and mortality of offspring with allergic asthma later in life.
objectivesWe aimed to test whether maternal NO2 exposure causes allergic asthma-related consequences in offspring absent any subsequent lung provocation and whether this exposure enhances the likelihood of developing allergic asthma or the intensity of developed allergic airway disease following postnatal allergic sensitization and challenge. In addition, if such consequences and enhancements occurred, we sought to determine the mechanism(s) of these responses.
methodsPregnant BALB/c mice were exposed to either NO2 (2.5 ppm, 5 h/day) or air daily throughout the gestation period. Offspring were sacrificed on postnatal days (PNDs) 1, 7, 14, 21, and 42, and remaining offspring were sensitized by ovalbumin (OVA) injection followed by OVA aerosol challenge during postnatal wk 7-9. We analyzed the lung histopathology, inflammatory cell infiltration, airway hyper-responsiveness (AHR), immune responses, and gene methylation under different treatment conditions.
resultsMaternal exposure to NO2 caused a striking increase in inflammatory cell infiltration and the release of type 2 cytokines in the lungs of offspring at PNDs 1 and 7; however, these alterations were reversed during postnatal development. Following OVA sensitization and challenge, the exposure enhanced the levels of allergic asthma-characterized OVA-immunoglobulin (Ig) E, AHR, and airway inflammation in adult offspring. Importantly, differentiation of T-helper (Th) 2 cells and demethylation of the interleukin-4 (
conclusionsMaternal exposure to indoor environmental NO2 causes allergic asthma-related consequences in offspring absent any subsequent lung provocation and potentiates the symptoms of allergic asthma in adult offspring following postnatal allergic sensitization and challenge; this response is associated with the Th2-based immune response and DNA methylation of the
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