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 articlepeer-review

49 Scopus citations


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
Issue number2
StatePublished - Jan 15 2019
Externally publishedYes


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

ASJC Scopus subject areas

  • Biological Psychiatry


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