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Perinatal bisphenol A exposure beginning before gestation enhances allergen sensitization, but not pulmonary inflammation, in adult mice

Published online by Cambridge University Press:  13 February 2014

E. O’Brien ,
I. L. Bergin ,
D. C. Dolinoy ,
Z. Zaslona ,
R. J. A. Little ,
Y. Tao ,
M. Peters-Golden  and
P. Mancuso
E. O’Brien
Affiliation:
Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA
I. L. Bergin
Affiliation:
Unit for Laboratory Animal Medicine, University of Michigan, Ann Arbor, MI, USA
D. C. Dolinoy
Affiliation:
Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA
Z. Zaslona
Affiliation:
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, School of Medicine, University of Michigan, Ann Arbor, MI, USA
R. J. A. Little
Affiliation:
Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA
Y. Tao
Affiliation:
Department of Biostatistics, School of Public Health, University of Michigan, Ann Arbor, MI, USA
M. Peters-Golden
Affiliation:
Division of Pulmonary and Critical Care Medicine, Department of Internal Medicine, School of Medicine, University of Michigan, Ann Arbor, MI, USA
P. Mancuso*
Affiliation:
Department of Environmental Health Sciences, School of Public Health, University of Michigan, Ann Arbor, MI, USA
*
*Address for correspondence: P. Mancuso, Department of Environmental Health Sciences, School of Public Health, University of Michigan, 1415 Washington Heights, Ann Arbor, MI 48109, USA. (Email pmancuso@umich.edu)
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Abstract

Bisphenol A (BPA), a monomer of polycarbonate plastics and epoxide resin, is a high-production-volume chemical implicated in asthma pathogenesis when exposure occurs to the developing fetus. However, few studies have directly examined the effect of in utero and early-life BPA exposure on the pathogenesis of asthma in adulthood. This study examines the influence of perinatal BPA exposure through maternal diet on allergen sensitization and pulmonary inflammation in adult offspring. Two weeks before mating, BALB/c dams were randomly assigned to a control diet or diets containing 50 ng, 50 μg or 50 mg BPA/kg of rodent chow. Dams remained on the assigned diet throughout gestation and lactation until postnatal day (PND) 21 when offspring were weaned onto the control diet. Twelve-week-old offspring were sensitized to ovalbumin (OVA) and subsequently challenged with aerosolized OVA. Sera, splenocytes, bronchoalveolar lavage fluid and whole lungs were harvested to assess allergen sensitization and pulmonary inflammation after OVA challenge. Serum anti-OVA IgE levels were increased two-fold in offspring exposed to 50 μg and 50 mg BPA/kg diet, compared with control animals. In addition, production of interleukin-13 and interferon-γ were increased in OVA-stimulated splenocytes recovered from BPA-exposed mice. Pulmonary inflammation, as indicated by total and differential leukocyte counts, cytokines, chemokines and pulmonary histopathology inflammatory scores, however, was either not different or was reduced in offspring exposed to BPA. Although these data suggest that perinatal BPA exposure beginning before gestation enhances allergen sensitization by increasing serum IgE and splenocyte cytokine production, a substantial impact of BPA on OVA-induced pulmonary inflammation in adulthood was not observed.

Keywords

allergen sensitizationasthmabisphenol Aovalbuminpulmonary inflammation
Type
Original Article
Information
Journal of Developmental Origins of Health and Disease , Volume 5 , Issue 2 , April 2014 , pp. 121 - 131
Copyright
© Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2014 

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