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 µg/mL) and high-dose BPA (2.0 µg/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 RORγt protein and IL-17 and TGF-β 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 RORγt protein increased, which showed a dose–effect relationship. The levels of serum TGF-β 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-β and IL-17 between 0.2 µg/mL and 2.0 µg/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 RORγt protein, respectively. Our findings indicated that BPA exposure during early development may play an important role in the development of autoimmune diseases later.

中文翻译：

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围生期双酚A暴露引起的雌性后代小鼠调节性T细胞和Th17细胞的异常分化

背景

双酚A（BPA）是一种广泛暴露于人类的环境雌激素，并且对其生殖毒性，内分泌干扰和神经行为异常有更多的研究。最近很少有研究发现BPA具有免疫毒性，其机制尚不清楚。因此，BPA对免疫系统的影响已引起广泛关注。这项研究的目的是调查围产期BPA暴露对雌性后代小鼠中调节性T细胞（Treg）和Th17细胞的影响和机制。

方法

将21只怀孕的C57BL / 6小鼠随机分为三组：对照组，低剂量BPA（0.2 µg / mL）和高剂量BPA（2.0 µg / mL）暴露组。从妊娠第6天到哺乳期结束，所有的人都通过饮用水接触了BPA。给雌性后代喂食正常饮食和饮用水1个月。测量雌性后代中脾脏或血液中Treg和Th17细胞的百分比，Foxp3和RORγt蛋白的水平以及IL-17和TGF-β的水平。

结果

Treg细胞百分比和Foxp3蛋白水平降低，而Th17细胞百分比和RORγt蛋白水平升高，这显示出剂量-效应关系。与对照相比，BPA暴露的雌性后代的血清TGF-β水平显着降低，而血清IL-17统计学上较高（P  <0.05或P  <0.01）。但是在0.2 µg / mL和2.0 µg / mL BPA组之间，血清TGF-β和IL-17的含量没有统计学差异（P  > 0.05）。

结论

怀孕和哺乳期的BPA暴露可能会导致雌性后代小鼠Treg和Th17细胞异常分化和功能，这分别与Foxp3下调和RORγt蛋白上调有关。我们的发现表明，在早期发育过程中接触BPA可能在后来的自身免疫性疾病的发展中发挥重要作用。