Evidence map›Paper›PMID 30550928›Full record

ArticleBrain, behavior, and immunity2019

Sex-specific association between prenatal life stress exposure and infant pro-inflammatory cytokine levels during acute respiratory infection.

Steven M Brunwasser, George M Slavich, Dawn C Newcomb, Tebeb Gebretsadik, Kedir N Turi, Cosby Stone, Larry J Anderson, Tina V Hartert

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 6 citations in OpenAlex.

  1. Sex Differences in Asthma Pathogenesis.Immunological reviews · 2026
    Review
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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

8 authors at 3 institutions in 1 country.

Steven M BrunwasserDepartment of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2650, USA. Electronic address: steven.brunwasser@vumc.org.
George M SlavichCousins Center for Psychoneuroimmunology and Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, CA, USA.
Dawn C NewcombDepartment of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2650, USA.
Tebeb GebretsadikDepartment of Biostatistics, Vanderbilt University Medical Center, Nashville, TN, USA.
Kedir N TuriDepartment of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2650, USA.
Cosby StoneDepartment of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2650, USA.
Larry J AndersonDepartment of Pediatrics, Division of Infectious Diseases, Emory University Medical Center, Atlanta, GA, USA.
Tina V HartertDepartment of Medicine, Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, TN 37232-2650, USA.
Vanderbilt University Medical Center · USUniversity Medical Center · USUniversity of California, Los Angeles · US

Funding

Vanderbilt Institute for Clinical and Translational Research (VICTR) -Identifying correlates of functional immunity in SARS-CoV-2 convalescent plasmaUL1TR002243 · NCATS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Paul A. Harris, Wesley H Self · 2017 to 2026
$130.7M
Viral and Host Determinants of Infant and Childhood Allergy and AsthmaU19AI095227 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Tina V Hartert · 2011 to 2026
$34.9M
Building Interdisciplinary Research Careers in Women's HealthK12HD043483 · NICHD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARTMANN, KATHERINE E, MAJOR, AMY S · 2002 to 2023
$10.3M
Clinical and Translational Training Program in Pulmonary MedicineT32HL087738 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Lorraine B Ware · 2007 to 2026
$7.0M
LIFE-SPAN DEVELOPMENT OF NORMAL AND ABNORMAL BEHAVIORT32MH018921 · NIMH · VANDERBILT UNIVERSITY · PI HUMPHREYS, KATHRYN LEIGH · 1989 to 2024
$6.7M
Role of Gender in TH17-Mediated Inflammation in Severe AsthmaR01HL122554 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI NEWCOMB, DAWN C · 2015 to 2024
$5.5M
The Vanderbilt PCOR Career Knowledge, Education and Training ProgramK12HS022990 · AHRQ · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PENSON, DAVID F. · 2014 to 2018
$3.3M
Midcareer Investigator Patient-oriented Research Award in Bronchiolitis & AsthmaK24AI077930 · NIAID · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARTERT, TINA V · 2008 to 2017
$1.6M
Neural, Inflammatory, and Genomic Mechanisms Underlying Risk for Depression in AdolescenceK08MH103443 · NIMH · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SLAVICH, GEORGE MICHAEL · 2015 to 2018
$772k
AHRQ HHS K12 HS022990NCATS NIH HHS UL1 TR002243NHLBI NIH HHS R01 HL122554NHLBI NIH HHS T32 HL087738NIAID NIH HHS K24 AI077930NIAID NIH HHS U19 AI095227NICHD NIH HHS K12 HD043483NIMH NIH HHS K08 MH103443NIMH NIH HHS T32 MH018921
6 · The paper itself

Abstract

backgroundPrenatal life stress exposure is linked to dysregulated immune function and chronic inflammatory disease in offspring, but we know little about its effects on infant immune response during viral infection.

methodTo address this issue, we examined associations between prenatal life stress exposure and infant upper-airway inflammatory markers during acute respiratory infection (ARI) using data from a prospective, population-based birth-cohort study (N = 180). Infant inflammation was measured as a continuous latent factor within a structural equation modeling framework using nasal wash concentrations of interleukin-1β, interleukin-6, and tumor necrosis factor-α. We hypothesized that infants exposed to prenatal life stress would have greater levels of nasal inflammation during ARI and increased risk for ARI-related morbidity in early childhood.

resultsOur findings contradicted these hypotheses and provided evidence of sexually dimorphic effects of prenatal stress exposure on infant immune functioning during ARI. Among boys, but not girls, prenatal stress was negatively associated with nasal inflammation and indirectly associated with both lower ARI severity and reduced likelihood of subsequent ARI-related hospitalization in the 2nd and 3rd years of life.

conclusionThese data suggest that prenatal stress exposure may be beneficial for infant boys in the context of respiratory viral infections; however, it will be critical to determine if these benefits are offset by increased risk for chronic inflammatory diseases in later childhood. As the participants in this cohort are being followed longitudinally through age 8, we will be able to evaluate long-term health outcomes in future studies.

Indexed as

Child, PreschoolCohort StudiesCytokinesFemaleHumansInfantInfant, NewbornInflammationInterleukin-1betaInterleukin-6Longitudinal StudiesMalePregnancyPrenatal Exposure Delayed EffectsProspective StudiesRespiratory Tract InfectionsCytokinesInterleukin-1betaInterleukin-6Tumor Necrosis Factor-alphaAcute respiratory infectionEarly childhoodInfancyInflammationInterleukin-1βInterleukin-6Prenatal stressSex differencesStructural equation modelingTumor necrosis factor-α

Identifiers

PMID30550928
PMCPMC6380181
OpenAlexW2905441708

What OpenQuestion holds

Textmetadata
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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.