Abstract

BackgroundMultiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring. However, the effects of prenatal environmental exposures on adult offspring have not been well-studied. We hypothesized that combined prenatal exposure to Aspergillus fumigatus (A. fumigatus) allergen and diesel exhaust particles will be associated with altered IgE production, airway inflammation, airway hyperreactivity (AHR), and airway remodeling of adult offspring.MethodsFollowing sensitization via the airway route to A. fumigatus and mating, pregnant BALB/c mice were exposed to additional A. fumigatus and/or diesel exhaust particles. At age 9-10 weeks, their offspring were sensitized and challenged with A. fumigatus.ResultsWe found that adult offspring from mice that were exposed to A. fumigatus or diesel exhaust particles during pregnancy experienced decreases in IgE production. Adult offspring of mice that were exposed to both A. fumigatus and diesel exhaust particles during pregnancy experienced decreases in airway eosinophilia.ConclusionThese results suggest that, in this model, allergen and/or diesel administration during pregnancy may be associated with protection from developing systemic and airway allergic immune responses in the adult offspring.

Highlights

  • Multiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring

  • Ig induction in offspring after three, five and six doses of A. fumigatus Adult offspring from mothers who received A. fumigatus or diesel exhaust particles (DEP) alone, or A. fumigatus and DEP together, developed lower levels of total IgE when assessed after the fifth dose of A. fumigatus compared to offspring from mothers treated with saline only prior to mating (p < 0.0001 analysis of variance (ANOVA), Figure 3a)

  • IgE levels from offspring from mice exposed to DEP alone were lower than those from offspring from mice exposed to A. fumigatus alone (p < 0.05 Tukey HSD test)

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Summary

Introduction

Multiple studies have suggested that prenatal exposure to either allergens or air pollution may increase the risk for the development of allergic immune responses in young offspring. We hypothesized that combined prenatal exposure to Aspergillus fumigatus (A. fumigatus) allergen and diesel exhaust particles will be associated with altered IgE production, airway inflammation, airway hyperreactivity (AHR), and airway remodeling of adult offspring. Epidemiological studies and murine models suggest that prenatal environmental exposures can enhance the risk for developing asthma in the offspring [1,2]. Prenatal exposure to residual oil fly ash was associated with increased airway hyperresponsiveness, allergic inflammation, and elevated immunoglobulin (Ig) E and IgG1 in the ovalbumin (OVA) sensitized offspring by age 16-37 days [2]. Prenatal exposure to farms, sources of endotoxin exposure, was associated as well with childhood protection from

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