BACKGROUND Prenatal exposure to environmental adversities, including maternal overweight/obesity, diabetes/hypertensive disorders, or mood/anxiety disorders, increases the risk for adverse neurodevelopmental outcomes in children. However, the underlying biological mechanisms remain elusive. We tested whether maternal antenatal inflammation was associated with the number of neurodevelopmental delay areas in children and whether it mediated the association between exposure to any prenatal environmental adversity and child neurodevelopmental delay. METHODS Mother-child dyads (N = 418) from the PREDO (Prediction and Prevention of Preeclampsia and Intrauterine Growth Restriction) study were followed up to 10.8 years. We analyzed maternal plasma high-sensitivity C-reactive protein and glycoprotein acetyls at 3 consecutive antenatal time points, measured maternal body mass index in early pregnancy, extracted data on diabetes/hypertensive disorders in pregnancy from medical records, and extracted data on mood/anxiety disorders until childbirth from the Care Register for Health Care. To estimate the number of neurodevelopmental delay areas in children across cognitive, motor, and social functioning, we pooled data from the Care Register for Health Care on psychological development disorders with mother-reported Ages and Stages Questionnaire data on developmental milestones. RESULTS Higher levels of maternal high-sensitivity C-reactive protein and glycoprotein acetyls at and across all 3 antenatal time points were associated with 1.30- to 2.36-fold (p values < .02) increased relative risk for higher number of areas of child neurodevelopmental delay. Higher maternal inflammation across the 3 time points also mediated the effect of any prenatal environmental adversity on child neurodevelopmental delay. CONCLUSIONS Higher levels of maternal inflammation, especially when persisting throughout pregnancy, increase a child's risk of neurodevelopmental delay and mediate the effect of prenatal environmental adversity on child neurodevelopmental delay.

中文翻译：

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持续高水平的母体产前炎症与产前环境逆境对后代神经发育延迟的影响有关并介导

背景 产前暴露于环境逆境，包括母亲超重/肥胖、糖尿病/高血压疾病或情绪/焦虑症，会增加儿童不良神经发育结果的风险。然而，潜在的生物学机制仍然难以捉摸。我们测试了母亲产前炎症是否与儿童神经发育迟缓区域的数量相关，以及它是否介导了暴露于任何产前环境逆境与儿童神经发育迟缓之间的关联。方法 来自 PREDO（先兆子痫和宫内生长受限的预测和预防）研究的母子二人组 (N = 418) 随访至 10.8 年。我们在连续 3 个产前时间点分析了母体血浆高敏 C 反应蛋白和糖蛋白乙酰基，测量怀孕早期的母亲体重指数，从医疗记录中提取有关怀孕期间糖尿病/高血压疾病的数据，并从医疗保健护理登记册中提取有关分娩前情绪/焦虑障碍的数据。为了估计儿童在认知、运动和社会功能方面神经发育迟缓区域的数量，我们将来自卫生保健护理登记册的关于心理发育障碍的数据与母亲报告的关于发​​育里程碑的年龄和阶段问卷数据进行了汇总。结果 在所有 3 个产前时间点和跨越所有 3 个产前时间点，母体高敏 C 反应蛋白和糖蛋白乙酰的水平较高与 1.30 至 2.36 倍（p 值 < 0.02）增加儿童神经发育区域数量较多的相对风险延迟。3 个时间点内较高的母体炎症也介导了任何产前环境逆境对儿童神经发育延迟的影响。结论 母体炎症水平较高，尤其是在整个妊娠期间持续存在时，会增加儿童神经发育迟缓的风险，并介导产前环境逆境对儿童神经发育迟缓的影响。