Latina mothers, who have one of the highest fertility rates among ethnic groups in the United States (US), often experience discrimination. Psychosocial influences during pregnancy, such as discrimination stress, promotes inflammation. However, the role of epigenetic markers of inflammation as a mediator between, and predictor of, maternal discrimination stress and neuropsychiatric outcomes has not been extensively studied. The current study investigates the role of DNA methylation at FOXP3 Treg-cell-specific demethylated region (TSDR), as a marker of regulatory T (Treg) cells that are important negative regulators of inflammation, and the promoter of tumour necrosis factor-alpha (TNF-α) gene, an important pro-inflammatory cytokine, in relation to discrimination stress during pregnancy and depression and anxiety symptomatology.

A sample of 148 Latina women residing in the US (mean age 27.6 years) were assessed prenatally at 24–32 weeks’ gestation and 4–6 weeks postnatally for perceived discrimination exposure (Everyday Discrimination Scale, EDS), emotional distress (depression, anxiety, perinatal-specific depression), acculturation, and acculturative stress. DNA methylation levels at the FOXP3 and TNFα promoter regions from blood samples collected at the prenatal stage were assessed by bisulphite pyrosequencing.

Regression analyses showed that prenatal EDS associated with postnatal emotional distress, depression and anxiety symptoms only in those individuals with higher than mean levels of FOXP3 TSDR and TNFα promoter methylation; no such significant associations were found in those with lower than mean levels of methylation for either. We further found that these relationships were mediated by TNFα only in those with high FOXP3 TSDR methylation, implying that immunosuppression via TNFα promoter methylation buffers the impact of discrimination stress on postpartum symptomatology. These results indicate that epigenetic markers of immunosuppression and inflammation play an important role in resilience or sensitivity, respectively, to prenatal stress.

拉丁裔母亲是美国 (US) 种族中生育率最高的国家之一，她们经常遭受歧视。怀孕期间的社会心理影响，例如歧视压力，会促进炎症。然而，炎症的表观遗传标记作为母体歧视压力和神经精神结果之间的中介和预测因子的作用尚未得到广泛研究。目前的研究调查了FOXP3 Treg 细胞特异性去甲基化区域 (TSDR) 的 DNA 甲基化的作用，作为调节性 T (Treg) 细胞的标志物，它是炎症的重要负调节因子，以及肿瘤坏死因子-α 的启动子。肿瘤坏死因子-α) 基因，一种重要的促炎细胞因子，与怀孕期间的歧视压力以及抑郁和焦虑症状有关。

对居住在美国的 148 名拉丁裔女性（平均年龄 27.6 岁）的样本在孕 24-32 周和产后 4-6 周进行产前评估，以了解感知歧视暴露（日常歧视量表，EDS）、情绪困扰（抑郁、焦虑） 、围产期特异性抑郁症）、文化适应和文化适应压力。通过亚硫酸氢盐焦磷酸测序评估产前阶段采集的血样中FOXP3和TNFα启动子区域的 DNA 甲基化水平。

回归分析表明，产前 EDS 与产后情绪困扰、抑郁和焦虑症状仅在那些FOXP3 TSDR 和TNFα启动子甲基化水平高于平均水平的个体中相关；在甲基化水平低于平均水平的人中没有发现这种显着的关联。我们进一步发现，这些关系仅在具有高FOXP3 TSDR 甲基化的患者中由TNFα介导，这意味着通过TNFα进行免疫抑制启动子甲基化缓冲了歧视压力对产后症状的影响。这些结果表明，免疫抑制和炎症的表观遗传标记分别在对产前压力的恢复力或敏感性中发挥重要作用。