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FASEB J. 2014 Nov;28(11):4893-900. doi: 10.1096/fj.14-255380. Epub 2014 Aug 1.

Food intolerance at adulthood after perinatal exposure to the endocrine disruptor bisphenol A.

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Department of Neurogastroenterology and Nutrition and
Department of Intestinal Development, Xenobiotics, and Immunotoxicology, Institut National de la Recherche Agronomique (INRA), Unité Mixte de Recherche (UMR) 1331 Toxalim, Research Centre in Food Toxicology, Toulouse, France.
Department of Neurogastroenterology and Nutrition and.


The food contaminant bisphenol A (BPA) is pointed out as a risk factor in development of food allergy and food intolerance, two adverse food reactions increasing worldwide. We evaluated the consequences of perinatal exposure to low doses of BPA on immune-specific response to the food antigen ovalbumin (OVA) at adulthood. Perinatal exposure to BPA (0.5, 5, or 50 μg/kg/d) from 15th day of gravidity to pups weaning resulted in an increase of anti-OVA IgG titers at all BPA dosages in OVA-tolerized rats, and at 5 μg/kg/d in OVA-immunized rats compared to control rats treated with vehicle. In BPA-treated and OVA-tolerized rats, increased anti-OVA IgG titers were associated with higher IFNγ secretion by the spleen. This result is in accordance with the increase of activated CD4(+)CD44(high)CD62L(low) T lymphocytes observed in spleen of BPA-exposed rats compared to controls. Finally, when BPA-treated OVA-tolerized rats were orally challenged with OVA, colonic inflammation occurred, with neutrophil infiltration, increased IFNγ, and decreased TGFβ. We show that perinatal exposure to BPA altered oral tolerance and immunization to dietary antigens (OVA). In summary, the naive immune system of neonate is vulnerable to low doses of BPA that trigger food intolerance later in life.


humoral and cellular response; immune system; oral challenge; systemic immunization

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