TY - JOUR
T1 - Sex-specific association between prenatal life stress exposure and infant pro-inflammatory cytokine levels during acute respiratory infection
AU - Brunwasser, Steven M.
AU - Slavich, George M.
AU - Newcomb, Dawn C.
AU - Gebretsadik, Tebeb
AU - Turi, Kedir N.
AU - Stone, Cosby
AU - Anderson, Larry J.
AU - Hartert, Tina V.
N1 - Funding Information:
This work was supported by The National Institute of Allergy and Infectious Diseases , U.S.A. [ U19 AI 095227 , K24 AI 077930 ]; The Agency for Healthcare Research and Quality , U.S.A. [ K12 HS022990 ]; The National Institute of Mental Health , U.S.A. [ T32 MH018921 , K08 MH103443 ]; and The National Center for Advancing Translational Sciences , U.S.A. [ UL1 TR002243 ]. GMS was supported by a Society in Science—Branco Weiss Fellowship, NARSAD Young Investigator Grant #23958 from the Brain & Behavior Research Foundation, and National Institutes of Health grant K08 MH103443.
Publisher Copyright:
© 2018 Elsevier Inc.
PY - 2019/2
Y1 - 2019/2
N2 - Background: Prenatal 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. Method: To 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. Results: Our 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. Conclusion: These 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.
AB - Background: Prenatal 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. Method: To 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. Results: Our 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. Conclusion: These 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.
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U2 - 10.1016/j.bbi.2018.12.002
DO - 10.1016/j.bbi.2018.12.002
M3 - Article
C2 - 30550928
AN - SCOPUS:85058521128
SN - 0889-1591
VL - 76
SP - 275
EP - 279
JO - Brain, Behavior, and Immunity
JF - Brain, Behavior, and Immunity
ER -