Immune dysregulation and glucocorticoid resistance in minority and low income pregnant women

Abstract

Summary Chronic prenatal stress contributes to poor birth outcomes for women and infants. Importantly, poor birth outcomes are most common among minority and low income women. To investigate underlying mechanisms, we tested the hypothesis that chronic stress related to minority or low income status is associated with glucocorticoid resistance as indicated by disruption in the cytokine-glucocorticoid feedback circuit. Home visits were conducted during which 3rd trimester pregnant women completed stress and depression surveys and provided blood for pro- and anti-inflammatory cytokines. Saliva was collected 5 times the preceding day for diurnal cortisol levels. For statistical analyses, women were grouped 3 ways, by race, income, and the presence or absence of either of those risk factors; this last group was labeled high or low general risk. Immune regulation was evaluated by evidence of a functioning negative feedback relationship between cytokines and cortisol. Of 96 participants, 18 were minority, 22 of low income, and 29 either minority or low income (high general risk). Pearson partial correlation identified a significant negative relationship between cortisol area under the curve (AUC) and pro- to anti-inflammatory cytokine ratios in the low general risk women (i.e., Caucasian, higher income) including IFNγ/IL10 (r = −0.73, p < 0.0001), IL6/IL10 (r = 0.38, p = 0.01), IL1β/IL10 (r = −0.44, p = −0.004) and TNFα/IL10 (r = −0.41; p = 0.005); no such correlations existed in the high general risk women (i.e., minority, low income) for (IFNγ/IL10: r = −0.25, p = 0.43; IL6/IL10:r = 0.12, p = 0.70; IL1 β/IL10: r = 0.05, p = 0.87; TNFα/IL10: r = 0.10; p = 0.75), suggestive of glucocorticoid resistance. Cortisol levels throughout the day also were higher in minority and high general risk groups (p < 0.05). Without cytokine glucocorticoid feedback, a pregnant woman’s ability to regulate inflammation is limited, potentially contributing to adverse maternal and infant outcomes.

Relationships among psychosocial factors, biomarkers, preeclampsia, and preterm birth in African American women: A pilot

“…Cortisol did not relate to any cytokine levels. Corwin et al (2013) found a negative relationship between cortisol and pro-to antiinflammatory cytokine ratios in pregnant non-Hispanic white women and women with higher income. However, there was no correlation between cortisol and cytokine levels for pregnant minority women and women with low income.…”

DNA methylation provides insight into intergenerational risk for preterm birth in African Americans

“…In general, African American women have higher levels of inflammation when compared to Caucasian women, and chronic inflammation has been presented as a potential mechanism through which disparities in the rates of PTB and other chronic conditions occur. 11,17,24,38,44,57,60 For example, Liu and colleagues examined DNA methylation of 8 imprinted genes in umbilical cord blood samples for association with PTB and infection status. 26 Though they did not find any association with PTB, they reported that pleiomorphic adenoma gene-like 1 (PLAGL1) DNA methylation associates with chorioamnionitis.…”

Modulation of prenatal stress via docosahexaenoic acid supplementation: implications for child mental health

“…72 In a study in which both cortisol and proinflammatory cytokines were measured during pregnancy, minority race and low-income status were characterized by high levels of cortisol without a compensatory decrease in cytokines, suggesting impaired feedback between the neuroendocrine and immune systems. 73 Thus, race and socioeconomic status appear to impact both the diurnal rhythm and feedback loop of the stress response system as well as the interface between the HPA axis and other systems critical for maintaining health, such as immune functioning. These data provide further support for the hypothesis that health disparities among racial minorities and families living in poverty may be due, in part, to differential exposure to prenatal stress.…”