Jenna L Riis1, Douglas A Granger2, Cynthia S Minkovitz3, Karen Bandeen-Roche4, Janet A DiPietro5, Sara B Johnson6. 1. Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA. Electronic address: jriis1@jhu.edu. 2. Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA; Institute for Interdisciplinary Salivary Bioscience Research Arizona State University, 550 E. Orange Street, Tempe 85287-3604, AZ, USA; Johns Hopkins University School of Nursing, 525 North Wolfe Street, Baltimore 21205, MD, USA. Electronic address: Douglas.Granger@asu.edu. 3. Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA; Johns Hopkins School of Medicine, 1800 Orleans Street, Baltimore 21287, MD, USA. Electronic address: cmink@jhu.edu. 4. Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA. Electronic address: kbandee1@jhu.edu. 5. Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA. Electronic address: jdipiet1@jhu.edu. 6. Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA; Institute for Interdisciplinary Salivary Bioscience Research Arizona State University, 550 E. Orange Street, Tempe 85287-3604, AZ, USA; Johns Hopkins School of Medicine, 1800 Orleans Street, Baltimore 21287, MD, USA. Electronic address: sjohnson@jhu.edu.
Abstract
RATIONALE: Neuroendocrine-immune regulation is essential for maintaining health. Early-life adversity may cause dysregulation in the neuroendocrine-immune network through repeated activation of the stress response, thereby increasing disease risk. OBJECTIVE: This paper examined the extent to which maternal psychological well-being moderates neuroendocrine-immune relations in children. METHODS: We used data from a laboratory-based study of mothers and their five-year old children (n = 125 mother-child pairs) conducted from 2011 to 2013 in Baltimore, Maryland. Child saliva was assayed for markers of immune function (i.e., cytokines: interleukin [IL]-1β, IL-6, IL-8, tumor necrosis factor alpha [TNF-α]) and hypothalamic-pituitary-adrenal activity (i.e., cortisol). A composite score for depressive symptoms, anxiety, and parenting stress characterized maternal psychological distress. Multilevel mixed models examined the relationship between maternal psychological well-being and child neuroendocrine-immune relations. RESULTS: Significant cytokine × maternal distress interactions indicated that as maternal distress increased, expected inverse cytokine-cortisol relations within children became weaker for IL-1β, IL-6, and TNF-α. Sex-stratified models revealed that these interactions were only significant among girls. Among boys, there were inverse cytokine-cortisol relations for all cytokines, and, while in the same direction as observed among girls, the cytokine × maternal distress interactions were non-significant. CONCLUSION: The findings suggest that maternal distress is associated with child neuroendocrine-immune relations in saliva and may alter the sensitivity of inflammatory immune processes to cortisol's inhibitory effects. This desensitization may place the child at risk for inflammatory diseases. The findings support efforts for the early detection and treatment of at-risk mothers to protect maternal and child health and well-being.
RATIONALE: Neuroendocrine-immune regulation is essential for maintaining health. Early-life adversity may cause dysregulation in the neuroendocrine-immune network through repeated activation of the stress response, thereby increasing disease risk. OBJECTIVE: This paper examined the extent to which maternal psychological well-being moderates neuroendocrine-immune relations in children. METHODS: We used data from a laboratory-based study of mothers and their five-year old children (n = 125 mother-child pairs) conducted from 2011 to 2013 in Baltimore, Maryland. Child saliva was assayed for markers of immune function (i.e., cytokines: interleukin [IL]-1β, IL-6, IL-8, tumor necrosis factor alpha [TNF-α]) and hypothalamic-pituitary-adrenal activity (i.e., cortisol). A composite score for depressive symptoms, anxiety, and parenting stress characterized maternal psychological distress. Multilevel mixed models examined the relationship between maternal psychological well-being and child neuroendocrine-immune relations. RESULTS: Significant cytokine × maternal distress interactions indicated that as maternal distress increased, expected inverse cytokine-cortisol relations within children became weaker for IL-1β, IL-6, and TNF-α. Sex-stratified models revealed that these interactions were only significant among girls. Among boys, there were inverse cytokine-cortisol relations for all cytokines, and, while in the same direction as observed among girls, the cytokine × maternal distress interactions were non-significant. CONCLUSION: The findings suggest that maternal distress is associated with child neuroendocrine-immune relations in saliva and may alter the sensitivity of inflammatory immune processes to cortisol's inhibitory effects. This desensitization may place the child at risk for inflammatory diseases. The findings support efforts for the early detection and treatment of at-risk mothers to protect maternal and child health and well-being.
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