Racial discrimination and leukocyte glucocorticoid sensitivity: Implications for birth timing.
Racial discrimination and leukocyte glucocorticoid sensitivity: Implications for birth timing.
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DOI：
10.1016/j.socscimed.2018.08.010
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发表时间：
2018-11
期刊：
影响因子：
--
通讯作者：
Anderson CM
中科院分区：
文献类型：
--
作者：
Gillespie SL;Anderson CM
心理压力引起的皮质醇升高似乎有助于早产。然而，一些研究表明，种族歧视相关压力的生物学后果是独特的，可能涉及糖皮质激素敏感性降低的发展，尽管皮质醇水平正常化。在这项研究中，我们研究了种族歧视对产妇皮质醇输出，白细胞糖皮质激素敏感性，皮质醇水平和出生时间之间的对应程度在非洲裔美国人队列的影响。在妊娠28至32周时入组了一个总体健康的前瞻性队列（n=91）。给予歧视经历量表，收集全血，定量测定血浆皮质醇水平、细胞因子水平和白细胞计数，以检查内源性反馈模式。在报告内化反应的妇女中，中间三分位数的种族歧视与母亲皮质醇水平高于底部三分位数相关（B*=0.68，p=0.001）。白细胞糖皮质激素敏感性降低见于种族歧视发生频率较高的人群，表现为母体皮质醇水平与血浆IL-8水平、单核细胞计数和淋巴细胞计数之间的对应性降低（ps≤0.043）。母亲皮质醇水平与出生时间之间的关联因三分位数的差异而不同（p值≤0.005），在没有种族歧视的妇女中，皮质醇水平较高可预测早产（B*=-0.59，p<0.001），但不存在种族歧视（ps≥0.497）。我们提供了新的证据表明，糖皮质激素敏感性下降，在越来越多的频率暴露于种族歧视。我们的研究结果表明，早产的生物学可能取决于种族歧视的暴露，有利于途径依赖于糖皮质激素诱导的白细胞组织监视增加与糖皮质激素耐药相关的炎症畸变在增加暴露水平。迫切需要精确的产前护理方法来防治早产，特别是在非裔美国妇女中，其努力取决于进一步的研究，研究导致该综合征的途径取决于个人暴露的总体情况。
Psychological stress-induced cortisol elevations appear to contribute to preterm birth. Yet, some studies suggest that the biological ramifications of racial discrimination-associated stress are unique and may involve development of decreased glucocorticoid sensitivity despite normalized cortisol levels. In this study, we examined the effects of racial discrimination on maternal cortisol output, leukocyte glucocorticoid sensitivity, and the degree of correspondence between cortisol levels and birth timing in an African American cohort. A generally healthy prospective cohort was enrolled at 28 to 32 weeks gestation (n=91). The Experiences of Discrimination scale was administered, whole blood collected, and plasma cortisol levels, cytokine levels, and leukocyte counts quantified for examination of patterns of endogenous feedback. Racial discrimination in the mid-tertile was associated with greater maternal cortisol levels than the bottom tertile among women reporting internalizing responses (b*=0.68, p=0.001). Decreased leukocyte glucocorticoid sensitivity was witnessed at greater frequencies of experiences of racial discrimination, as evidenced by decreased correspondence between maternal cortisol levels and plasma IL-8 levels, monocyte counts, and lymphocyte counts (ps≤0.043). The association between maternal cortisol levels and birth timing differed by discrimination tertile (p values≤0.005), with greater cortisol levels predictive of earlier birth among women without (b*=−0.59, p<0.001) but not with racial discrimination (ps≥0.497). We provide novel evidence of decreased glucocorticoid sensitivity at increasing frequency of exposure to racial discrimination. Our findings suggest that the biology of preterm birth may depend upon racial discriminatory exposures, favoring pathways dependent upon glucocorticoid-induced increases in leukocyte tissue surveillance versus glucocorticoid resistance-associated inflammatory aberrations at increasing levels of exposure. Precision approaches to prenatal care are sorely needed to combat preterm birth, particularly among African American women, with efforts dependent upon further research examining the pathways contributing to the syndrome dependent upon the totality of an individual’s exposures.
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