Maternal inflammation during pregnancy and offspring psychiatric symptoms in childhood: Timing and sex matter.


Journal

Journal of psychiatric research
ISSN: 1879-1379
Titre abrégé: J Psychiatr Res
Pays: England
ID NLM: 0376331

Informations de publication

Date de publication:
04 2019
Historique:
received: 29 08 2018
revised: 21 11 2018
accepted: 07 01 2019
pubmed: 29 1 2019
medline: 18 6 2020
entrez: 29 1 2019
Statut: ppublish

Résumé

Maternal infection during pregnancy has been associated with increased risk of offspring psychopathology, including depression. As most infections do not cross the placenta, maternal immune responses to infection have been considered as potentially contributing to this relationship. This study examined whether gestational timing of maternal inflammation during pregnancy is associated with offspring internalizing and/or externalizing symptoms during childhood and, further, whether fetal sex moderated this relationship. Participants were 737 pregnant women and their offspring who were continuously followed through late childhood. Archived first and second trimester sera were analyzed for markers of inflammation [interleukin 8 (IL-8), IL-6, IL-1 receptor antagonist (IL-1ra), and soluble tumor necrosis factor receptor-II (sTNF-RII)]. When offspring were aged 9-11, mothers completed a questionnaire assessing psychological symptoms. Multivariate regression analyses indicated that elevated IL-8 in the first trimester was associated with significantly higher levels of externalizing symptoms in offspring. Higher IL-1ra in the second trimester was associated with higher offspring internalizing symptoms. Further, second trimester IL-1ra was associated with increased internalizing symptoms in females only. These findings demonstrate that elevated maternal inflammation during pregnancy is associated with the emergence of separate psychological phenotypes and that timing of exposure and fetal sex matter for offspring outcomes. Given that internalizing and externalizing symptoms in childhood increase risk for a variety of mental disorders later in development, these findings potentially have major implications for early intervention and prevention work.

Identifiants

pubmed: 30690329
pii: S0022-3956(18)31033-1
doi: 10.1016/j.jpsychires.2019.01.009
pmc: PMC6644717
mid: NIHMS1519698
pii:
doi:

Substances chimiques

Cytokines 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

96-103

Subventions

Organisme : NIMH NIH HHS
ID : R01 MH096478
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH101168
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier Ltd. All rights reserved.

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Auteurs

Naoise Mac Giollabhui (N)

Department of Psychology, Temple University, Philadelphia, PA, USA.

Elizabeth C Breen (EC)

Cousins Center for Psychoneuroimmunology, Dept. of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, USA.

Shannon K Murphy (SK)

Department of Psychology, Temple University, Philadelphia, PA, USA.

Seth D Maxwell (SD)

Department of Psychology, Temple University, Philadelphia, PA, USA.

Barbara A Cohn (BA)

Child Health and Development Studies, Public Health Institute, Oakland, CA, USA.

Nickilou Y Krigbaum (NY)

Child Health and Development Studies, Public Health Institute, Oakland, CA, USA.

Piera M Cirillo (PM)

Child Health and Development Studies, Public Health Institute, Oakland, CA, USA.

Christian Perez (C)

Cousins Center for Psychoneuroimmunology, Dept. of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, USA.

Lauren B Alloy (LB)

Department of Psychology, Temple University, Philadelphia, PA, USA.

Deborah A G Drabick (DAG)

Department of Psychology, Temple University, Philadelphia, PA, USA.

Lauren M Ellman (LM)

Department of Psychology, Temple University, Philadelphia, PA, USA. Electronic address: ellman@temple.edu.

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