TY - JOUR
T1 - Maternal early life stress is associated with pro-inflammatory processes during pregnancy
AU - Méndez Leal, Adriana S.
AU - Silvers, Jennifer A.
AU - Carroll, Judith E.
AU - Cole, Steve W.
AU - Ross, Kharah M.
AU - Ramey, Sharon L.
AU - Shalowitz, Madeleine U.
AU - Dunkel Schetter, Christine
N1 - Publisher Copyright:
© 2022 Elsevier Inc.
PY - 2023/3
Y1 - 2023/3
N2 - Early life stress (ELS) is common in the United States and worldwide, and contributes to the development of psychopathology in individuals with these experiences and their offspring. A growing body of research suggests that early life stress may contribute to adverse health partly through modulation of immune (and particularly inflammatory) responses. Therefore, increased maternal prenatal inflammation has been proposed as a mechanistic pathway by which the observed cross-generational effects of parental early life stress on child neuropsychiatric outcomes may be exerted. We examined associations between early life stress and molecular markers of inflammation (specifically pro-inflammatory gene expression and receptor-mediated transcription factor activity) and a commonly studied circulating marker of inflammation (C-Reactive Protein) in a diverse group of women in or near their third trimester of pregnancy, covarying for age, race/ethnicity, BMI, concurrent infection, concurrent perceived stress, and per capita household income. Mothers who experienced higher levels of early life stress had significantly increased pro-inflammatory (NF-κB) and decreased anti-viral (IRF) transcription factor activity. Transcripts that were up or down regulated in mothers with high ELS were preferentially derived from both CD16+ and CD16- monocytes. Early life stress was not associated with elevated CRP. Taken together, these findings provide preliminary evidence for an association between ELS and a pro-inflammatory transcriptional phenotype during pregnancy that may serve as a mechanistic pathway for cross-generational transmission of the effects of early life stress on mental and physical health.
AB - Early life stress (ELS) is common in the United States and worldwide, and contributes to the development of psychopathology in individuals with these experiences and their offspring. A growing body of research suggests that early life stress may contribute to adverse health partly through modulation of immune (and particularly inflammatory) responses. Therefore, increased maternal prenatal inflammation has been proposed as a mechanistic pathway by which the observed cross-generational effects of parental early life stress on child neuropsychiatric outcomes may be exerted. We examined associations between early life stress and molecular markers of inflammation (specifically pro-inflammatory gene expression and receptor-mediated transcription factor activity) and a commonly studied circulating marker of inflammation (C-Reactive Protein) in a diverse group of women in or near their third trimester of pregnancy, covarying for age, race/ethnicity, BMI, concurrent infection, concurrent perceived stress, and per capita household income. Mothers who experienced higher levels of early life stress had significantly increased pro-inflammatory (NF-κB) and decreased anti-viral (IRF) transcription factor activity. Transcripts that were up or down regulated in mothers with high ELS were preferentially derived from both CD16+ and CD16- monocytes. Early life stress was not associated with elevated CRP. Taken together, these findings provide preliminary evidence for an association between ELS and a pro-inflammatory transcriptional phenotype during pregnancy that may serve as a mechanistic pathway for cross-generational transmission of the effects of early life stress on mental and physical health.
KW - C-Reactive Protein
KW - Conserved transcriptional response to adversity
KW - Cross-generational transmission of adversity
KW - Early life stress
KW - Inflammation
KW - Pregnancy
UR - http://www.scopus.com/inward/record.url?scp=85147956928&partnerID=8YFLogxK
U2 - 10.1016/j.bbi.2022.10.012
DO - 10.1016/j.bbi.2022.10.012
M3 - Journal Article
C2 - 36280180
AN - SCOPUS:85147956928
SN - 0889-1591
VL - 109
SP - 285
EP - 291
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
ER -