In animal studies, Bauer et al. reported that prenatal and postnatal exposure to BPA enhanced allergic lung inflammation in female but not male offspring of mice. 

A significant decrease in body temperature was observed after a challenge in mice sensitized with native gliadin (NG). There was a significant increase in the plasma level of mMCP-1 in allergic mice compared to CTL mice. The plasma level of mMCP-1 was increased in mice exposed to BPA at 4 µg/kg (FA 4 BPA) and 40 µg/ml (FA 40 BPA) compared to allergic mice (FA). When measuring the level of wheat-specific IgE in the blood of mice after the second challenge, as expected, we observed an increase in specific IgE in FA mice compared to CTL mice.

An increase in acid sulfonic FITC flux in allergic mice and allergic mice exposed to BPA were observed compared to CTL mice as ntestinal paracellular permeability. 

There was a significantly higher level of specific IgG1 in the four groups of FA mice than in the CTL mice. For the level of specific IgA, there was a significant increase for all groups of FA mice compared to CTL mice. In contrast, FA mice displayed a higher level of specific IgG2A than CTL mice. exposure to BPA, especially at a dose of 4 µg/kg and higher, induces a modulation of the humoral response towards a Th2 response highlighted by an increasing rate of IgG1 and IgA and a dampened Th1 response via a decreased rate of IgG2a.

The increase in Th2 cells was more pronounced in FA 4 BPA and higher mice than in FA mice. In contrast, the FA 0.4 BPA group showed levels of Th2 cells similar to those of the FA group. A significant decrease was observed in the Treg frequency in FA mice compared to CTL mice. FA mice displayed a higher frequency of Th17 cells than CTL mice.

The T-cell response is initiated by contact with antigen-presenting cells, especially DCs, which are regulated by plasmacytoid DCs (pDCs) and are largely influenced by the presence of innate cells, such as recently defined innate lymphoid cells (ILCs), which are the counterparts of T cells that contribute to immune responses. ILCs are particularly abundant at mucosal barriers, where they are exposed to allergens. 

There were a significant increase in total CD11c+MHCII+ DCs in all FA mice compared to CTL mice. BPA-exposed mice at doses of 4 and 40 µg/kg also displayed an increase in their gut ILC2s compared to FA and FA 0.4 mice, which was already significantly different from CTL mice. 

Th2 cytokines, including IL-13, IL-4 and IL-5, were increased in FA mice compared to CTL mice. In contrast, the Th1 cytokines IFN-γ and IL-12 as well as IL-10 were increased in FA mice compared to CTL mice. 

The flattening of the rarefaction curve based on the values of observed species indicated that our data volume covered all species of the community in the gut samples in all groups. Moreover, there was a decrease in gut bacterial operational taxonomic units (OTUs) in the FA and FA exposed to BPA mice, suggesting a decrease in species number. Significant decreases in the Shannon index from both the FA and the FA BPA groups were detected compared to the CTL group. Distribution histograms of the taxonomic composition of the six main phyla from the respective groups showed differences among test groups. Either the FA or FA BPA protocol could cause a reduction in the species diversity of the microbial community in the animal gut with an increase in the effect induced by BPA exposure, especially a dose corresponding to the TDI or higher.

BPA can exacerbate allergic markers, increase serum levels of specific IgE and compromise Th2 responses. Moreover, the effect of BPA is linked to the dose used and affects gut physiology and microorganisms.

1. B. Misme-Aucouturier, M. De Carvalho, E. Delage, E. Dijoux, M. Klein, C. Brosseau, M. Bodinier, L. Guzylack-Piriou, G. Bouchaud, Oral exposure to bisphenol A exacerbates allergic inflammation in a mouse model of food allergy. Toxicology 472, 153188 (2022).