Neha Sehgal , Lin Li , Dana E. Goin , Jessica Chen , Unurzul Jigmeddagva , Rachel Morello-Frosch , Tracey J. Woodruff , Stephanie L. Gaw , Joshua F. Robinson , Stephanie M. Eick
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引用次数: 0
Abstract
Background
Inflammation has been implicated as an intermediary between psychosocial stress and adverse birth outcomes. However, prior work has mostly relied on maternal inflammation as a proxy for fetal inflammation mid-gestation or measured fetal inflammation in cord blood and placenta obtained at delivery. No studies have examined psychosocial stress in relation to fetal inflammation mid-gestation.
Methods
Twenty cytokines were measured in matched maternal blood, cord blood, and placenta obtained mid-gestation from a socio-demographically diverse group of pregnant participants undergoing elective second-trimester pregnancy terminations (N = 106). Corticotropin-releasing hormone, a proposed biomarker of gestational length, was measured in maternal blood. Perceived stress, and exposure to stressful life events, job strain, and social support were measured via questionnaires. We used linear regression to estimate associations between individual stressors and inflammatory biomarkers in each biomatrix and principal component analysis to assess groups of inflammatory biomarkers.
Results
We observed many matrix-specific associations between psychosocial stressors and inflammatory biomarkers. For example, low versus high social support was associated with significantly decreased levels of maternal blood CCL3 (β=-0.53; 95 % confidence interval [CI]=-0.98,-0.07), CCL4 (β=-0.26; 95 % CI=-0.47,-0.04), IL8 (β=-0.79; 95 % CI=-1.47,-0.11), CXCL9 (β=-0.47; 95 % CI=-0.89,-0.06), IFNγ (β=-2.28; 95 % CI=-3.60,-0.96), IL4 (β=-1.07; 95 % CI=-1.88,-0.26); and cord blood IFNγ (β=-0.83; 95 % CI=-1.52,-0.14). Social support was not associated with placental inflammation.
Conclusions
During mid-pregnancy, psychosocial stress─ particularly low social support─ was associated with maternal blood levels of select cytokines, suggesting a potential pathway linking social stress and inflammation. Our results indicate that the placenta may buffer these inflammatory effects on the fetus.
期刊介绍:
Drawing from a large number of disciplines, Reproductive Toxicology publishes timely, original research on the influence of chemical and physical agents on reproduction. Written by and for obstetricians, pediatricians, embryologists, teratologists, geneticists, toxicologists, andrologists, and others interested in detecting potential reproductive hazards, the journal is a forum for communication among researchers and practitioners. Articles focus on the application of in vitro, animal and clinical research to the practice of clinical medicine.
All aspects of reproduction are within the scope of Reproductive Toxicology, including the formation and maturation of male and female gametes, sexual function, the events surrounding the fusion of gametes and the development of the fertilized ovum, nourishment and transport of the conceptus within the genital tract, implantation, embryogenesis, intrauterine growth, placentation and placental function, parturition, lactation and neonatal survival. Adverse reproductive effects in males will be considered as significant as adverse effects occurring in females. To provide a balanced presentation of approaches, equal emphasis will be given to clinical and animal or in vitro work. Typical end points that will be studied by contributors include infertility, sexual dysfunction, spontaneous abortion, malformations, abnormal histogenesis, stillbirth, intrauterine growth retardation, prematurity, behavioral abnormalities, and perinatal mortality.