Sternthal Michelle Judith, Enlow Michelle Bosquet, Cohen Sheldon, Canner Marina Jacobson, Staudenmayer John, Tsang Kathy, Wright Rosalind J
Department of Environmental and Occupational Medicine and Epidemiology, Harvard School of Public Health, Boston, Mass 02215, USA.
J Allergy Clin Immunol. 2009 Nov;124(5):954-60. doi: 10.1016/j.jaci.2009.07.030. Epub 2009 Sep 12.
Prenatal stress affects immunocompetence in offspring, although the underlying mechanisms are not well understood.
We sought to examine associations between maternal lifetime interpersonal trauma (IPT) and cord blood total IgE levels in a sample of urban newborns (n = 478).
Maternal IPT during childhood and adolescence (birth to 17 years), adulthood (18 years to index pregnancy), and the index pregnancy were ascertained by using the Revised Conflict Tactics Scale at 28.4 +/- 7.9 weeks' gestation. Cord blood IgE levels were derived by using a fluoroenzyme immunoassay. We examined effects of maternal IPT on increased cord blood IgE levels (upper quartile, 1.08 IU/mL) by using logistic regression, adjusting for confounders and mediating variables.
Maternal trauma was categorized as unexposed (n = 285 [60%]), early (childhood and/or teenage years only, n = 107 [22%]), late (adulthood and/or index pregnancy only, n = 29 [6%]), and chronic (early and late, n = 57 [12%]) exposure. Relative to no IPT, early (odds ratio [OR], 1.78; 95% CI, 1.05-3.00) and chronic maternal IPT (OR, 2.25; 95% CI, 1.19-4.24) were independently associated with increased IgE levels in unadjusted analyses. When adjusting for standard controls, including maternal age and race, season of birth, child's sex, and childhood and current socioeconomic status, early effects became nonsignificant (OR, 1.48; 95% CI, 0.85-2.58). Chronic exposure remained significant in fully adjusted models, including standard controls, current negative life events, allergen exposure, and potential pathway variables (maternal atopy, prenatal smoking, and birth weight; OR, 2.18; 95% CI, 1.06-4.50).
These data link chronic trauma over the mother's life course with increased IgE levels in infants at birth. Research examining associations between maternal trauma and indicators of offspring's atopic risk might be particularly relevant in inner-city high-risk populations.
产前应激会影响后代的免疫能力,但其潜在机制尚未完全明确。
我们试图在一个城市新生儿样本(n = 478)中研究母亲一生的人际创伤(IPT)与脐带血总IgE水平之间的关联。
在妊娠28.4±7.9周时,使用修订后的冲突策略量表确定母亲在童年和青少年期(出生至17岁)、成年期(18岁至本次妊娠)以及本次妊娠期间的IPT情况。通过荧光酶免疫测定法检测脐带血IgE水平。我们使用逻辑回归分析母亲IPT对脐带血IgE水平升高(上四分位数,1.08 IU/mL)的影响,并对混杂因素和中介变量进行了调整。
母亲的创伤被分为未暴露(n = 285 [60%])、早期(仅童年和/或青少年期,n = 107 [22%])、晚期(仅成年期和/或本次妊娠,n = 29 [6%])和慢性(早期和晚期,n = 57 [12%])暴露。在未经调整的分析中,相对于无IPT,早期(比值比[OR],1.78;95%可信区间[CI],1.05 - 3.00)和慢性母亲IPT(OR,2.25;95% CI,1.19 - 4.24)与IgE水平升高独立相关。在调整了包括母亲年龄和种族、出生季节、孩子性别以及童年和当前社会经济状况等标准对照因素后,早期影响变得不显著(OR,1.48;95% CI,0.85 - 2.58)。在包括标准对照因素、当前负面生活事件、过敏原暴露以及潜在途径变量(母亲特应性、产前吸烟和出生体重)的完全调整模型中,慢性暴露仍然显著(OR,2.18;95% CI,1.06 - 4.50)。
这些数据将母亲一生中的慢性创伤与婴儿出生时IgE水平升高联系起来。在城市高危人群中,研究母亲创伤与后代特应性风险指标之间的关联可能尤为重要。