Lifetime-dependent effects of bisphenol A on asthma development in an experimental mouse model.

Susanne Petzold,Irina Lehmann,Tobias Polte,Jan C Simon,Marco Averbeck,Christopher Torrens

doi:10.1371/journal.pone.0100468

Susanne Petzold, Irina Lehmann + Show 4 more

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https://doi.org/10.1371/journal.pone.0100468

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Abstract

BackgroundEnvironmental factors are thought to contribute significantly to the increase of asthma prevalence in the last two decades. Bisphenol A (BPA) is a xenoestrogen commonly used in consumer products and the plastic industry. There is evidence and an ongoing discussion that endocrine disruptors like BPA may affect human health and also exert alterations on in the immune system. The aim of this study was to investigate age-dependent effects of BPA on the asthma risk using a murine model to explain the controversial results reported till date.MethodsBALB/c mice were exposed to BPA via the drinking water for different time periods including pregnancy and breastfeeding. To induce an asthma phenotype, mice were sensitized to ovalbumin (OVA), followed by an intrapulmonary allergen challenge.ResultsBPA exposure during pregnancy and breastfeeding had no significant effect on asthma development in the offspring. In contrast, lifelong exposure from birth until the last antigen challenge clearly increased eosinophilic inflammation in the lung, airway hyperreactivity and antigen-specific serum IgE levels in OVA-sensitized adult mice compared to mice without BPA exposure. Surprisingly, BPA intake during the sensitization period significantly reduced the development of allergic asthma. This effect was reversed in the presence of a glucocorticoid receptor antagonist.ConclusionsOur results demonstrate that the impact of BPA on asthma risk is strongly age-dependent and ranges from asthma-promoting to asthma-reducing effects. This could explain the diversity of results from previous studies regarding the observed health impact of BPA.

Highlights

Asthma is a T helper 2 (Th2) cell–mediated immune response to common environmental allergens and is characterized by airway inflammation with pulmonary eosinophilia, airway hyperreactivity (AHR), and increased serum immunoglobulin E (IgE) levels [1]
Demonstrate that only a lifelong Bisphenol A (BPA) exposure starting at birth exacerbated the allergic airway inflammation, whereas maternal exposure showed no effect on the disease outcome in the offspring
OVA-sensitized offspring from three mothers exposed to BPA during gravidity did not develop an exacerbated allergic airway inflammation or an increased AHR compared to sensitized mice from three un-exposed mothers (Fig. 1A–F, offspring n$11)

Summary

Introduction

Asthma is a T helper 2 (Th2) cell–mediated immune response to common environmental allergens and is characterized by airway inflammation with pulmonary eosinophilia, airway hyperreactivity (AHR), and increased serum immunoglobulin E (IgE) levels [1]. Previous data from epidemiological as well as animal studies suggest that BPA may affect the reproductive system, insulin production, mental and motor development, and the immune system [9,10]. The results from epidemiological studies and experimental animal models regarding the potential risk of BPA exposure on airway inflammation are highly diverse. The studies mainly describe an interference with hormone receptors like the estrogen receptor These data are inconsistent and show contrasting results [16,17]. There is evidence and an ongoing discussion that endocrine disruptors like BPA may affect human health and exert alterations on in the immune system. The aim of this study was to investigate age-dependent effects of BPA on the asthma risk using a murine model to explain the controversial results reported till date

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