TY - JOUR
T1 - Prenatal maternal distress and immune cell epigenetic profiles at 3-months of age
AU - Letourneau, Nicole
AU - Ntanda, Henry
AU - Jong, Victor L.
AU - Mahinpey, Newsha
AU - Giesbrecht, Gerald
AU - Ross, Kharah M.
N1 - Publisher Copyright:
© 2021 Wiley Periodicals LLC
PY - 2021/7
Y1 - 2021/7
N2 - Background: Prenatal maternal distress predicts altered offspring immune outcomes, potentially via altered epigenetics. The role of different kinds of prenatal maternal distress on DNA methylation profiles is not understood. Methods: A sample of 117 women (APrON cohort) were followed from pregnancy to the postpartum period. Maternal distress (depressive symptoms, pregnancy-specific anxiety, stressful life events) were assessed mid-pregnancy, late-pregnancy, and 3-months postpartum. DNA methylation profiles were obtained from 3-month-old blood samples. Principal component analysis identified two epigenetic components, characterized as Immune Signaling and DNA Transcription through gene network analysis. Covariates were maternal demographics, pre-pregnancy body mass index, child sex, birth gestational age, and postpartum maternal distress. Penalized regression (LASSO) models were used. Results: Late-pregnancy stressful life events, b = 0.006, early-pregnancy depressive symptoms, b = 0.027, late-pregnancy depressive symptoms, b = 0.014, and pregnancy-specific anxiety during late pregnancy, b = −0.631, were predictive of the Immune Signaling component, suggesting that these aspects of maternal distress could affect methylation in offspring immune signaling pathways. Only early-pregnancy depressive symptoms was predictive of the DNA Transcription component, b = −0.0004, suggesting that this aspect of maternal distress is implicated in methylation of offspring DNA transcription pathways. Conclusions: Exposure timing and kind of prenatal maternal distress could matter in the prediction of infant immune epigenetic profiles.
AB - Background: Prenatal maternal distress predicts altered offspring immune outcomes, potentially via altered epigenetics. The role of different kinds of prenatal maternal distress on DNA methylation profiles is not understood. Methods: A sample of 117 women (APrON cohort) were followed from pregnancy to the postpartum period. Maternal distress (depressive symptoms, pregnancy-specific anxiety, stressful life events) were assessed mid-pregnancy, late-pregnancy, and 3-months postpartum. DNA methylation profiles were obtained from 3-month-old blood samples. Principal component analysis identified two epigenetic components, characterized as Immune Signaling and DNA Transcription through gene network analysis. Covariates were maternal demographics, pre-pregnancy body mass index, child sex, birth gestational age, and postpartum maternal distress. Penalized regression (LASSO) models were used. Results: Late-pregnancy stressful life events, b = 0.006, early-pregnancy depressive symptoms, b = 0.027, late-pregnancy depressive symptoms, b = 0.014, and pregnancy-specific anxiety during late pregnancy, b = −0.631, were predictive of the Immune Signaling component, suggesting that these aspects of maternal distress could affect methylation in offspring immune signaling pathways. Only early-pregnancy depressive symptoms was predictive of the DNA Transcription component, b = −0.0004, suggesting that this aspect of maternal distress is implicated in methylation of offspring DNA transcription pathways. Conclusions: Exposure timing and kind of prenatal maternal distress could matter in the prediction of infant immune epigenetic profiles.
KW - APrON Study
KW - depressive symptoms
KW - epigenetics
KW - fetal programming hypothesis
KW - gene network analysis
KW - pregnancy-specific anxiety
KW - principal component analysis
KW - stress
UR - http://www.scopus.com/inward/record.url?scp=85100959015&partnerID=8YFLogxK
U2 - 10.1002/dev.22103
DO - 10.1002/dev.22103
M3 - Journal Article
C2 - 33569773
AN - SCOPUS:85100959015
SN - 0012-1630
VL - 63
SP - 973
EP - 984
JO - Developmental Psychobiology
JF - Developmental Psychobiology
IS - 5
ER -