Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk

Liisa Hantsoo, Sara Kornfield, Montserrat C. Anguera, C. Neill Epperson

Research output: Contribution to journalReview article

Abstract

During pregnancy, programming of the fetal central nervous system establishes vulnerabilities for emergence of neuropsychiatric phenotypes later in life. Psychosocial influences during pregnancy, such as stressful life events and chronic stress, correlate with offspring neuropsychiatric disorders and inflammation, respectively. Stress promotes inflammation, but the role of inflammation as a mediator between maternal psychosocial stress and offspring neuropsychiatric outcomes has not been extensively studied in humans. This review summarizes clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy. We propose that inflammation is a mediator in the relationship between psychosocial stress and offspring neuropsychiatric outcomes, potentially influenced by poor maternal glucocorticoid–immune coordination. We present relevant experimental animal research supporting this hypothesis. We conclude that clinical and preclinical research supports the premise that stress-induced maternal immune activation contributes in part to prenatal programming of risk. Programming of risk is likely due to a combination of vulnerabilities, including multiple or repeated inflammatory events; timing of such events; poor maternal regulation of inflammation; genetic vulnerability; and lifestyle contributors.

Original languageEnglish (US)
Pages (from-to)97-106
Number of pages10
JournalBiological psychiatry
Volume85
Issue number2
DOIs
StatePublished - Jan 15 2019
Externally publishedYes

Fingerprint

Mothers
Inflammation
Pregnancy
Embryonic and Fetal Development
Fetal Development
Life Style
Central Nervous System
Phenotype
Research

Keywords

  • Cytokines
  • Cytokine–glucocorticoid feedback
  • Hypothalamic pituitary adrenal
  • Pregnancy
  • Stress
  • Transgenerational

ASJC Scopus subject areas

  • Biological Psychiatry

Cite this

Inflammation : A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk. / Hantsoo, Liisa; Kornfield, Sara; Anguera, Montserrat C.; Epperson, C. Neill.

In: Biological psychiatry, Vol. 85, No. 2, 15.01.2019, p. 97-106.

Research output: Contribution to journalReview article

Hantsoo, Liisa ; Kornfield, Sara ; Anguera, Montserrat C. ; Epperson, C. Neill. / Inflammation : A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk. In: Biological psychiatry. 2019 ; Vol. 85, No. 2. pp. 97-106.
@article{07c8566ff25b494a800888b0dd4679f6,
title = "Inflammation: A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk",
abstract = "During pregnancy, programming of the fetal central nervous system establishes vulnerabilities for emergence of neuropsychiatric phenotypes later in life. Psychosocial influences during pregnancy, such as stressful life events and chronic stress, correlate with offspring neuropsychiatric disorders and inflammation, respectively. Stress promotes inflammation, but the role of inflammation as a mediator between maternal psychosocial stress and offspring neuropsychiatric outcomes has not been extensively studied in humans. This review summarizes clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy. We propose that inflammation is a mediator in the relationship between psychosocial stress and offspring neuropsychiatric outcomes, potentially influenced by poor maternal glucocorticoid–immune coordination. We present relevant experimental animal research supporting this hypothesis. We conclude that clinical and preclinical research supports the premise that stress-induced maternal immune activation contributes in part to prenatal programming of risk. Programming of risk is likely due to a combination of vulnerabilities, including multiple or repeated inflammatory events; timing of such events; poor maternal regulation of inflammation; genetic vulnerability; and lifestyle contributors.",
keywords = "Cytokines, Cytokine–glucocorticoid feedback, Hypothalamic pituitary adrenal, Pregnancy, Stress, Transgenerational",
author = "Liisa Hantsoo and Sara Kornfield and Anguera, {Montserrat C.} and Epperson, {C. Neill}",
year = "2019",
month = "1",
day = "15",
doi = "10.1016/j.biopsych.2018.08.018",
language = "English (US)",
volume = "85",
pages = "97--106",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier USA",
number = "2",

}

TY - JOUR

T1 - Inflammation

T2 - A Proposed Intermediary Between Maternal Stress and Offspring Neuropsychiatric Risk

AU - Hantsoo, Liisa

AU - Kornfield, Sara

AU - Anguera, Montserrat C.

AU - Epperson, C. Neill

PY - 2019/1/15

Y1 - 2019/1/15

N2 - During pregnancy, programming of the fetal central nervous system establishes vulnerabilities for emergence of neuropsychiatric phenotypes later in life. Psychosocial influences during pregnancy, such as stressful life events and chronic stress, correlate with offspring neuropsychiatric disorders and inflammation, respectively. Stress promotes inflammation, but the role of inflammation as a mediator between maternal psychosocial stress and offspring neuropsychiatric outcomes has not been extensively studied in humans. This review summarizes clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy. We propose that inflammation is a mediator in the relationship between psychosocial stress and offspring neuropsychiatric outcomes, potentially influenced by poor maternal glucocorticoid–immune coordination. We present relevant experimental animal research supporting this hypothesis. We conclude that clinical and preclinical research supports the premise that stress-induced maternal immune activation contributes in part to prenatal programming of risk. Programming of risk is likely due to a combination of vulnerabilities, including multiple or repeated inflammatory events; timing of such events; poor maternal regulation of inflammation; genetic vulnerability; and lifestyle contributors.

AB - During pregnancy, programming of the fetal central nervous system establishes vulnerabilities for emergence of neuropsychiatric phenotypes later in life. Psychosocial influences during pregnancy, such as stressful life events and chronic stress, correlate with offspring neuropsychiatric disorders and inflammation, respectively. Stress promotes inflammation, but the role of inflammation as a mediator between maternal psychosocial stress and offspring neuropsychiatric outcomes has not been extensively studied in humans. This review summarizes clinical evidence linking specific types of stress to maternal inflammatory load during pregnancy. We propose that inflammation is a mediator in the relationship between psychosocial stress and offspring neuropsychiatric outcomes, potentially influenced by poor maternal glucocorticoid–immune coordination. We present relevant experimental animal research supporting this hypothesis. We conclude that clinical and preclinical research supports the premise that stress-induced maternal immune activation contributes in part to prenatal programming of risk. Programming of risk is likely due to a combination of vulnerabilities, including multiple or repeated inflammatory events; timing of such events; poor maternal regulation of inflammation; genetic vulnerability; and lifestyle contributors.

KW - Cytokines

KW - Cytokine–glucocorticoid feedback

KW - Hypothalamic pituitary adrenal

KW - Pregnancy

KW - Stress

KW - Transgenerational

UR - http://www.scopus.com/inward/record.url?scp=85054467461&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85054467461&partnerID=8YFLogxK

U2 - 10.1016/j.biopsych.2018.08.018

DO - 10.1016/j.biopsych.2018.08.018

M3 - Review article

C2 - 30314641

AN - SCOPUS:85054467461

VL - 85

SP - 97

EP - 106

JO - Biological Psychiatry

JF - Biological Psychiatry

SN - 0006-3223

IS - 2

ER -