Abstract
Stress and anxiety significantly impact the hypothalamic–pituitary axis, and in pregnancy, the subsequent maternal–fetal response can lead to poor outcomes. The objective of this study was to assess the association between psychosocial measures of pregnancy-specific anxiety and physiologic inflammatory responses. Specifically, to determine the effectiveness of the Mentors Offering Maternal Support (M-O-M-STM) program to reduce psychosocial anxiety and associated inflammatory response. In conjunction with measures of pregnancy-specific anxiety and depression, serum biomarkers (IL-2, IL-6, IL-10, IL1-B, TNF-α, CRH, CRP, and cortisol) were analyzed for each trimester throughout pregnancy. Results demonstrated that women receiving the M-O-M-STM intervention had longitudinally sustained lower TNF-α/IL-10 ratios than the control group, and it was significantly associated with psychosocial measures of anxiety, specifically for fears of labor and spouse/partner relationships. Additionally, the anxiety of spouse/partner relationships was significantly associated with IL-6/IL-10 ratios. The findings highlight the important counter-regulatory relationship between anti- and pro-inflammatory cytokines and provide insight into the distinct physiologic responses to pregnancy-specific anxiety with early prenatal intervention.
Highlights
Maternal adaptive responses to psychosocial stress and anxiety during pregnancy are inherently complex and critical in maintaining a unique immune-privileged environment that influences birth outcomes
Consistent with previous literature reports [8], our results found that IL-6 and TNF-α were significantly important in their association with pregnancy anxiety and function as drivers of inflammation
Our results suggest that the protective, balancing effect of pro- and anti-inflammatory cytokines in pregnancy is negatively affected by increased maternal pregnancy-specific anxiety
Summary
Maternal adaptive responses to psychosocial stress and anxiety during pregnancy are inherently complex and critical in maintaining a unique immune-privileged environment that influences birth outcomes. The hypothalamic–pituitary–adrenal (HPA) axis stress response and the subsequent production of glucocorticoids is delicately balanced throughout the pregnancy to ensure healthy outcomes [1]. As the placenta is a stresssensitive organ, any modulation of corticotrophin-releasing hormone (CRH) may augment labor [2]. Normal, or decreased levels of CRH concentration have been associated with preterm, term, or post-term labor, respectively. In addition to changes in stress response, the normal immune response in pregnant mothers progressively shifts from a cell-mediated, pro-inflammatory, Th1 response to a humoral, anti-inflammatory, Th2 response [3]. The balance between Th1 and Th2 response and the interaction of the associated pro- and anti-inflammatory cytokines, TNF-α, IL-1β, IL-6, and IL-10, are important in the development and maintenance of a normal pregnancy [4,5]
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