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Prenatal Maternal Depression and Neonatal Immune Responses

Hahn, Jill, ScD, MS; Gold, Diane R., MD, MPH; Coull, Brent A., PhD; McCormick, Marie C., MD, ScD; Finn, Patricia W., MD; Perkins, David L., MD, PhD; Rich-Edwards, Janet W., ScD, MPH; Rifas Shiman, Sheryl L., MPH; Oken, Emily, MD, MPH; Kubzansky, Laura D., PhD, MPH

doi: 10.1097/PSY.0000000000000686
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Objective The aim of the study was to examine the association of lifetime maternal depression with regulation of immune responses in the infant, measured by cytokine levels and lymphocyte proliferation (LP) in cord blood mononuclear cells collected at delivery.

Methods We studied women recruited in early pregnancy into the Project Viva longitudinal cohort who had cord blood assayed after delivery (N = 463). Women reported about depressive symptoms in midpregnancy (Edinburgh Postnatal Depression Scale) and depression history by questionnaire. Immune responses were assayed by an index of LP, and concentrations of five cytokines (interleukin [IL]-6, IL-10, IL-13, tumor necrosis tumor necrosis factor factor α, and interferon γ) after incubation of cord blood mononuclear cells either in medium alone or stimulated with phytohemagglutinin (PHA), cockroach extract, or house dust mite extract. We examined associations of maternal depression with these sets of cytokine measures using multivariable linear or tobit regression analyses.

Results After adjustment for confounders (mother's age, race/ethnicity, education, household income, season of birth, and child sex), levels of IL-10 after stimulation with cockroach or dust mite allergen were lower in cord blood from ever versus never depressed women, and a similar trend was evident in IL-10 stimulated with PHA (percentage difference: cockroach extract = −41.4, p = .027; house dust mite extract = 1–36.0, p = .071; PHA = −24.2, p = .333). No significant differences were seen in levels of other cytokines or LP.

Conclusions Maternal depression is associated with offspring immune responses at birth, which may have implications for later life atopic risk or immune function.

From the Department of Social and Behavioral Sciences (Hahn, McCormick, Kubzansky), The Harvard T.H. Chan School of Public Health; Channing Laboratory (Gold), Brigham and Women's Hospital, Boston; Department of Environmental Health (Gold), Biostatistics (Coull), and Environment Health (Coull), Harvard T.H. Chan School of Public Health, Boston, Massachusetts; Division of Pulmonary, Critical Care, Sleep, and Allergy (Finn), Department of Medicine; Department of Microbiology and Immunology (Finn); Division of Nephrology (Perkins), Department of Medicine; Department of Surgery (Perkins); and Department of Bioengineering (Perkins), University of Illinois at Chicago; Channing Division of Network Medicine (Rich-Edwards), Department of Medicine, Connors Center for Women's Health and Gender Biology, Brigham and Women's Hospital and Harvard Medical School; Department of Epidemiology (Rich-Edwards), Harvard School of Public Health; and Division of Chronic Disease Research Across the Lifecourse (Rifas Shiman, Oken), Department of Population Medicine, Harvard Medical School and Harvard Pilgrim Health Care Institute, Boston Massachusetts.

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Address correspondence to Jill Hahn, ScD, MS, Department of Social and Behavioral Sciences, The Harvard T.H. Chan School of Public Health, Landmark 437, 401 Park Dr, Boston, MA 02215. E-mail: jhahn@hsph.harvard.edu

Received for publication January 11, 2018; revision received January 24, 2019.

Copyright © 2019 by American Psychosomatic Society
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