Evidence map›Paper›PMID 30314641›Full record

ReviewBiological psychiatry2019

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

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

Abstract readReview
In one paragraph

Review in Biological psychiatry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 3 pooled it
12.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

124 citing papers in PubMed, 3 syntheses or guidelines pooled it, 271 citations in OpenAlex.

  1. Pooled it
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  12. Cortisol Stress Response is Associated with Iron Status in Pregnancy.medRxiv : the preprint server for health sciences · 2026
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64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Liisa HantsooDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. Electronic address: liisahantsoo@pennmedicine.upenn.edu.
Sara KornfieldDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
Montserrat C AngueraDepartment of Biomedical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
C Neill EppersonDepartment of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; Department of Obstetrics and Gynecology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; Penn PROMOTES Research on Sex and Gender in Health, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania.
University of Pennsylvania · US

Funding

Prepubertal Stress, Windows of Risk & Sex Bias for Affective DisturbanceP50MH099910 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI EPPERSON, C. NEILL · 2012 to 2017
$6.5M
Training in Sex and Gender Differences Research to Improve Women's HealthK12HD085848 · NICHD · UNIVERSITY OF PENNSYLVANIA · PI OQUENDO, MARIA A · 2015 to 2019
$2.2M
Psychophysiology, Neurosteroids, and Stress in Premenstrual Dysphoric Disorder (PMDD)K23MH107831 · NIMH · UNIVERSITY OF PENNSYLVANIA · PI HANTSOO, LIISA VICTORIA · 2016 to 2020
$905k
PTSD AND PREGNANCY: PSYCHOPHYSIOLOGY, RESPONSE TO TREATMENT & PREGNANCY OUTCOMEK23MH102360 · NIMH · WASHINGTON UNIVERSITY · PI KORNFIELD, SARA L. · 2014 to 2018
$675k
Expression of X-linked autoimmunity genes in B cells during female-biased autoimmunityR21AI124084 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI ANGUERA, MONTSERRAT C · 2017 to 2018
$443k
NIAID NIH HHS R21 AI124084NICHD NIH HHS K12 HD085848NIMH NIH HHS K23 MH102360NIMH NIH HHS K23 MH107831NIMH NIH HHS P50 MH099910
6 · The paper itself

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.

Indexed as

AnimalsFemaleHumansImmune SystemInflammationMental DisordersPregnancyPrenatal Exposure Delayed EffectsStress, PsychologicalCytokine–glucocorticoid feedbackCytokinesHypothalamic pituitary adrenalPregnancyStressTransgenerational

Identifiers

PMID30314641
PMCPMC6309506
OpenAlexW2890036014

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.