Stress, Race, and Immune Adaptation Across Pregnancy: Predictors of Preterm Birth

怀孕期间的压力、种族和免疫适应：早产的预测因素

基本信息

批准号：
8294406
负责人：
Lisa Michelle Christian
金额：
$ 22.88万
依托单位：
OHIO STATE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2011
资助国家：
美国
起止时间：
2011-07-04 至 2014-06-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8294406
关键词：
Accounting Address Adult African American American Antibodies Attenuated Australia Biological Birth Rate Canada Case Study Cells Cellular Immunity Cellular Stress Cervical Ripening Chronic stress Conflict (Psychology)Data Developed Countries Employee Strikes Enzyme-Linked Immunosorbent Assay Epstein-Barr Virus latency Europe European Exhibits Exposure to Family Fetal Development Health Health Services Health behavior Human Herpesvirus 4 Immune Immune system Immunosuppression Impairment In Vitro Infection Inflammatory Inflammatory Response Knowledge Lead Length Link Literature Low Birth Weight Infant Measurement Measures Mediating Membrane Meta-Analysis Methodology Minority Outcome Pathologic Processes Perinatal Physiological Play Pregnancy Pregnancy Outcome Pregnancy Trimesters Pregnant Women Premature Birth Premature Labor Process Production Psychological Stress Psychosocial Stress Race Research Risk Role Rupture Socioeconomic Status Stress Testing United States Virus Woman attenuation base cost cytokine design immune function inflammatory marker novel perinatal health therapy design

项目摘要

Preterm delivery, an increasingly frequent occurrence in the United States, is associated with significant family burden and an estimated societal cost of at least $26 billion per year. Psychosocial stress and related physiological sequelae may contribute to preterm birth in general, as well as racial disparities in preterm birth. It is well-established that among nonpregnant adults, chronic stress promotes immune dysregulation. Importantly, immune function changes substantially to support healthy pregnancy, with mild elevations in circulating inflammatory cytokines, attenuation of inflammatory responses, and impairment of cell-mediated immunity. However very limited research has examined the extent to which measures of psychosocial stress or race predict differential immune adaptation longitudinally across pregnancy. Chronic stress can directly stimulate the production of proinflammatory cytokines and prime the immune system to respond in an exaggerated manner upon exposure to biological challenges. Excessive elevations in maternal circulating inflammatory markers and a tendency toward inflammatory responding have been associated with adverse perinatal health outcomes, including preterm birth. In addition, stress can suppress cellular immune function. Typically kept in a latent state by cell-mediated immunity, Epstein-Barr Virus (EBV) may reactivate under conditions of immunosuppression, including stress. Thus, EBV latency provides a measure of cellular immune function. Due to suppression of cell-mediated immunity, EBV is more likely to be reactivated during pregnancy than nonpregnancy. Further, EBV reactivation has been associated with shorter gestation and lower birth weight, although it is not known if this plays a causal role or serves as a marker of a pathological process. Despite unique implications for health, limited data are available regarding effect of race or stress on immune parameters during pregnancy. The current study will build upon and address important gaps in the literature by examining immune parameters among 80 pregnant women (40 African-American and 40 European-American) longitudinally across pregnancy. This research will a) provide more comprehensive information about immune adaptation during pregnancy by examining circulating cytokine levels, in vitro stimulated cytokine production, and cellular immune function (i.e., EBV reactivation) longitudinally during each trimester of pregnancy, b) examine effects of stress and race on such adaptation and, c) provide preliminary data regarding whether differential immune profiles predict increased risk of preterm birth. Thus, this research is designed to ultimately lead to the identification of women at greater risk for negative perinatal outcomes and elucidation of mechanisms underlying increased risk, providing a basis for individualized health care services.

早产在美国越来越频繁地发生，与显着的家庭负担和估计每年至少 260 亿美元的社会成本。社会心理压力及相关一般而言，生理后遗症以及早产的种族差异可能会导致早产。众所周知，在未怀孕的成年人中，慢性压力会导致免疫失调。重要的是，免疫功能发生显着变化以支持健康怀孕，其中免疫功能轻度升高循环炎症细胞因子、炎症反应减弱和细胞介导的损伤免疫。然而，非常有限的研究探讨了社会心理压力或心理压力测量的程度。种族预测整个怀孕期间纵向的差异免疫适应。慢性压力可以直接刺激促炎细胞因子的产生并启动免疫系统在暴露于生物挑战时以夸张的方式做出反应。过多的母体循环炎症标志物的升高和炎症反应的趋势与不良的围产期健康结局有关，包括早产。此外，压力还可以抑制细胞免疫功能。 Epstein-Barr 通常通过细胞介导的免疫保持潜伏状态病毒 (EBV) 可能在免疫抑制条件下（包括压力）重新激活。因此，EBV潜伏期提供细胞免疫功能的测量。由于抑制细胞介导的免疫，EBV更容易与非怀孕期间相比，在怀孕期间更有可能重新激活。此外，EBV 重新激活与妊娠期较短和出生体重较低，尽管尚不清楚这是否起着因果作用或作为一个因素病理过程的标志。尽管对健康有独特的影响，但有关方面的可用数据有限种族或压力对怀孕期间免疫参数的影响。当前的研究将通过检查免疫来建立并解决文献中的重要空白 80 名孕妇（40 名非洲裔美国人和 40 名欧洲裔美国人）的纵向参数整个怀孕期间。这项研究将a）提供有关免疫适应的更全面的信息怀孕期间通过检查循环细胞因子水平、体外刺激的细胞因子产生和细胞因子在怀孕的每个三个月期间纵向免疫功能（即 EBV 重新激活），b) 检查效果压力和种族对这种适应的影响，c) 提供关于是否差异免疫的初步数据概况预测早产风险增加。因此，这项研究旨在最终导致确定围产期不良结果风险较高的妇女并阐明机制潜在增加的风险，为个性化医疗保健服务提供基础。