{
    "abstract": "Inflammation has been implicated as an intermediary between psychosocial stress and adverse birth outcomes. However, prior work has mostly relied on maternal inflammation as a proxy for fetal inflammation mid-gestation or measured fetal inflammation in cord blood and placenta obtained at delivery. No studies have examined psychosocial stress in relation to fetal inflammation mid-gestation.\nTwenty cytokines were measured in matched maternal blood, cord blood, and placenta obtained mid-gestation from a socio-demographically diverse group of pregnant participants undergoing elective second-trimester pregnancy terminations (N\u202f=\u202f106). Corticotropin-releasing hormone, a proposed biomarker of gestational length, was measured in maternal blood. Perceived stress, and exposure to stressful life events, job strain, and social support were measured via questionnaires. We used linear regression to estimate associations between individual stressors and inflammatory biomarkers in each biomatrix and principal component analysis to assess groups of inflammatory biomarkers.\nWe observed many matrix-specific associations between psychosocial stressors and inflammatory biomarkers. For example, low versus high social support was associated with significantly decreased levels of maternal blood CCL3 (\u03b2=-0.53; 95\u202f% confidence interval [CI]=-0.98,-0.07), CCL4 (\u03b2=-0.26; 95\u202f% CI=-0.47,-0.04), IL8 (\u03b2=-0.79; 95\u202f% CI=-1.47,-0.11), CXCL9 (\u03b2=-0.47; 95\u202f% CI=-0.89,-0.06), IFN\u03b3 (\u03b2=-2.28; 95\u202f% CI=-3.60,-0.96), IL4 (\u03b2=-1.07; 95\u202f% CI=-1.88,-0.26); and cord blood IFN\u03b3 (\u03b2=-0.83; 95\u202f% CI=-1.52,-0.14). Social support was not associated with placental inflammation.\nDuring mid-pregnancy, psychosocial stress\u2500 particularly low social support\u2500 was associated with maternal blood levels of select cytokines, suggesting a potential pathway linking social stress and inflammation. Our results indicate that the placenta may buffer these inflammatory effects on the fetus.",
    "authors": [
        {
            "affiliation": "Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.",
            "firstname": "Neha",
            "initials": "N",
            "lastname": "Sehgal"
        },
        {
            "affiliation": "Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.",
            "firstname": "Lin",
            "initials": "L",
            "lastname": "Li"
        },
        {
            "affiliation": "Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA.",
            "firstname": "Dana E",
            "initials": "DE",
            "lastname": "Goin"
        },
        {
            "affiliation": "Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.",
            "firstname": "Jessica",
            "initials": "J",
            "lastname": "Chen"
        },
        {
            "affiliation": "Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.",
            "firstname": "Unurzul",
            "initials": "U",
            "lastname": "Jigmeddagva"
        },
        {
            "affiliation": "Program on Reproductive Health and the Environment, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA; Department of Environmental Science, Policy and Management and School of Public Health, University of California, Berkeley, CA, USA.",
            "firstname": "Rachel",
            "initials": "R",
            "lastname": "Morello-Frosch"
        },
        {
            "affiliation": "Program on Reproductive Health and the Environment, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.",
            "firstname": "Tracey J",
            "initials": "TJ",
            "lastname": "Woodruff"
        },
        {
            "affiliation": "Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA; Division of Maternal Fetal Medicine, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.",
            "firstname": "Stephanie L",
            "initials": "SL",
            "lastname": "Gaw"
        },
        {
            "affiliation": "Center for Reproductive Sciences, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA; Program on Reproductive Health and the Environment, Department of Obstetrics, Gynecology and Reproductive Sciences, University of California, San Francisco, CA, USA.",
            "firstname": "Joshua F",
            "initials": "JF",
            "lastname": "Robinson"
        },
        {
            "affiliation": "Gangarosa Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA. Electronic address: stephanie.marie.eick@emory.edu.",
            "firstname": "Stephanie M",
            "initials": "SM",
            "lastname": "Eick"
        }
    ],
    "conclusions": null,
    "copyrights": "Copyright \u00a9 2025 Elsevier Inc. All rights reserved.",
    "doi": "10.1016/j.reprotox.2025.108922",
    "journal": "Reproductive toxicology (Elmsford, N.Y.)",
    "keywords": [
        "Chemokines",
        "Cytokines",
        "Fetal health",
        "Inflammation",
        "Interferons",
        "Placenta",
        "Stress"
    ],
    "methods": null,
    "publication_date": "2025-04-21",
    "pubmed_id": "40254104",
    "results": "We observed many matrix-specific associations between psychosocial stressors and inflammatory biomarkers. For example, low versus high social support was associated with significantly decreased levels of maternal blood CCL3 (\u03b2=-0.53; 95\u202f% confidence interval [CI]=-0.98,-0.07), CCL4 (\u03b2=-0.26; 95\u202f% CI=-0.47,-0.04), IL8 (\u03b2=-0.79; 95\u202f% CI=-1.47,-0.11), CXCL9 (\u03b2=-0.47; 95\u202f% CI=-0.89,-0.06), IFN\u03b3 (\u03b2=-2.28; 95\u202f% CI=-3.60,-0.96), IL4 (\u03b2=-1.07; 95\u202f% CI=-1.88,-0.26); and cord blood IFN\u03b3 (\u03b2=-0.83; 95\u202f% CI=-1.52,-0.14). Social support was not associated with placental inflammation.",
    "title": "Psychosocial stress and associations with inflammation in mid-gestation maternal, fetal, and placental tissue.",
    "xml": "<Element 'PubmedArticle' at 0x788502fd7060>"
}