Abnormal differentiation of regulatory T cells and Th17 cells induced by perinatal bisphenol A exposure in female offspring mice

Background Bisphenol A (BPA) is an environmental estrogen widely exposed to human beings, and there are more studies on its reproductive toxicity, endocrine disruption and neurobehavioral disorders. Recent few studies have found that BPA has immunotoxicity, and its mechanism is not clear. Therefore, the effects of BPA on immune system have attracted extensive attention. The aim of this study was to investigate the effect and mechanism of perinatal exposure to BPA on regulatory T cells (Treg) and Th17 cells in female offspring mice. Methods Twenty-one pregnant C57BL/6 mice were randomly divided into three groups: a control group, low-dose BPA (0.2 mu g/mL) and high-dose BPA (2.0 mu g/mL) exposure group. All received BPA exposure via drinking water from gestational day 6 to the end of lactation. Female offspring were fed a normal diet and drinking water for 1 month. The percentages of Treg and Th17 cells, the levels of Foxp3 and ROR gamma t protein and IL-17 and TGF-beta from spleen tissue or blood were measured in female offspring. Results The percentage of Treg cells and levels of Foxp3 protein decreased, while the percentage of Th17 cells and levels of ROR gamma t protein increased, which showed a dose-effect relationship. The levels of serum TGF-beta were significantly lower and the levels of serum IL-17 were statistically higher in BPA-exposed female offspring compared with controls (P < 0.05 or P < 0.01). But there were no statistical difference in the levels of serum TGF-beta and IL-17 between 0.2 mu g/mL and 2.0 mu g/mL BPA groups (P > 0.05). Conclusion BPA exposure during pregnancy and lactation could cause abnormal differentiation and function of Treg and Th17 cells in female offspring mice, which was associated with down-regulated Foxp3 and up-regulated ROR gamma t protein, respectively. Our findings indicated that BPA exposure during early development may play an important role in the development of autoimmune diseases later.