Psychosocial stress and associations with inflammation in mid-gestation maternal, fetal, and placental tissue.

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.