Bisphenol A (BPA) is a ubiquitous component in the manufacturing of plastic. It is commonly found in food and beverage containers. Because of its broad exposure and evidence that it may act as an estrogen-like molecule, many have studied its potential effects. For example, epidemiological studies have found an association between in utero BPA exposure and onset of childhood asthma. Our previous work suggested BPA treated mice induced asthma-like symptoms in both mothers and their pups. In order to better understand theconsequences of BPA exposure and potential mechanisms, we used a proteomics approach. Using both CD4+ T cells from an in vivo model of BPA exposure and an in vitro epithelial cell model, we identified activation of both innate and adaptive immune signaling following BPA exposure. Furthermore, our proteomic results from our multigenerational mouse model study implicates aberrant immune activation across several generations. We propose the following; BPA can active an innate viral immune response by upregulating a probable palmitoyltransferase ZDHHC1, and its binding partner stimulator of interferon-gamma (STING). It also has additional histone epigenetic perturbations, suggesting a role for epigenetic inheritance of these immune perturbations.

中文翻译：

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双酚 A 激活先天病毒免疫反应途径。


双酚 A (BPA) 是塑料制造中普遍存在的成分。它常见于食品和饮料容器中。由于它的广泛曝光和证据表明它可能充当雌激素样分子，许多人研究了它的潜在影响。例如，流行病学研究发现子宫内 BPA 暴露与儿童哮喘发作之间存在关联。我们之前的研究表明，双酚 A 治疗的小鼠在其母亲和幼崽中都会出现类似哮喘的症状。为了更好地了解 BPA 暴露的后果和潜在机制，我们使用了蛋白质组学方法。使用来自 BPA 暴露体内模型和体外上皮细胞模型的 CD4+ T 细胞，我们确定了 BPA 暴露后先天性和适应性免疫信号的激活。此外，我们的多代小鼠模型研究的蛋白质组学结果暗示了几代之间的异常免疫激活。我们提出以下建议； BPA 可以通过上调可能的棕榈酰转移酶 ZDHHC1 及其干扰素γ (STING) 结合伴侣刺激物来激活先天病毒免疫反应。它还具有额外的组蛋白表观遗传扰动，表明这些免疫扰动的表观遗传的作用。