Health Behavior Branch, Division of Intramural Population Health Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Bethesda, MD 20892;
Department of Social and Behavioral Sciences, Harvard T.H. Chan School of Public Health, Boston, MA 02115.
Proc Natl Acad Sci U S A. 2017 Jun 27;114(26):6728-6733. doi: 10.1073/pnas.1617698114. Epub 2017 Jun 12.
Children raised in economically disadvantaged households face increased risks of poor health in adulthood, suggesting that inequalities in health have early origins. From the child's perspective, exposure to economic hardship may begin as early as conception, potentially via maternal neuroendocrine-immune responses to prenatal stressors, which adversely impact neurodevelopment. Here we investigate whether socioeconomic disadvantage is associated with gestational immune activity and whether such activity is associated with abnormalities among offspring during infancy. We analyzed concentrations of five immune markers (IL-1β, IL-6, IL-8, IL-10, and TNF-α) in maternal serum from 1,494 participants in the New England Family Study in relation to the level of maternal socioeconomic disadvantage and their involvement in offspring neurologic abnormalities at 4 mo and 1 y of age. Median concentrations of IL-8 were lower in the most disadvantaged pregnancies [-1.53 log(pg/mL); 95% CI: -1.81, -1.25]. Offspring of these pregnancies had significantly higher risk of neurologic abnormalities at 4 mo [odds ratio (OR) = 4.61; CI = 2.84, 7.48] and 1 y (OR = 2.05; CI = 1.08, 3.90). This higher risk was accounted for in part by fetal exposure to lower maternal IL-8, which also predicted higher risks of neurologic abnormalities at 4 mo (OR = 7.67; CI = 4.05, 14.49) and 1 y (OR = 2.92; CI = 1.46, 5.87). Findings support the role of maternal immune activity in fetal neurodevelopment, exacerbated in part by socioeconomic disadvantage. This finding reveals a potential pathophysiologic pathway involved in the intergenerational transmission of socioeconomic inequalities in health.
儿童在经济贫困家庭中长大，成年后患健康不良的风险增加，这表明健康不平等具有早期起源。从儿童的角度来看，经济困难的暴露可能早在受孕时就开始了，可能是通过母体神经内分泌免疫对产前应激源的反应，从而对神经发育产生不利影响。在这里，我们研究了社会经济劣势是否与妊娠期免疫活性有关，以及这种活性是否与婴儿期后代的异常有关。我们分析了新英格兰家庭研究中 1494 名参与者的母体血清中五种免疫标志物（IL-1β、IL-6、IL-8、IL-10 和 TNF-α）的浓度与母体社会经济劣势水平及其在 4 个月和 1 岁时参与后代神经异常的关系。在最不利的妊娠中，IL-8 的中位数浓度较低[-1.53log(pg/mL)；95%CI：-1.81，-1.25]。这些妊娠的后代在 4 个月时神经异常的风险显著增加[优势比（OR）=4.61；CI=2.84，7.48]，在 1 岁时也显著增加（OR=2.05；CI=1.08，3.90）。这种较高的风险在一定程度上归因于胎儿暴露于较低的母体 IL-8，这也预示着 4 个月（OR=7.67；CI=4.05，14.49）和 1 岁（OR=2.92；CI=1.46，5.87）时神经异常的风险更高。研究结果支持母体免疫活性在胎儿神经发育中的作用，而社会经济劣势在一定程度上加剧了这一作用。这一发现揭示了一个潜在的病理生理途径，涉及到健康方面的社会经济不平等在代际间的传递。
