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Using a Murine Model of Psychosocial Stress in Pregnancy as a Translationally Relevant Paradigm for Psychiatric Disorders in Mothers and Infants
Published on: June 13, 2021
Maternal distress and child neuroendocrine and immune regulation
Jenna L Riis1, Douglas A Granger2, Cynthia S Minkovitz3
1Johns Hopkins Bloomberg School of Public Health, 615 N. Wolfe Street, Baltimore 21205, MD, USA.
Insights
Maternal distress weakens the link between stress hormones and immune responses in children, particularly girls, potentially increasing inflammation risk. Early intervention for mothers is crucial for child health.
Area of Science:
- Neuroendocrinology
- Immunology
- Developmental Psychology
Background:
- Neuroendocrine-immune regulation is vital for health.
- Early-life adversity can disrupt this network via stress response, increasing disease risk.
Purpose of the Study:
- To investigate how maternal psychological well-being influences neuroendocrine-immune relationships in children.
- To examine the moderating role of maternal distress on child cytokine and cortisol levels.
Main Methods:
- Studied 125 mother-child pairs, measuring child saliva for cytokines (IL-1β, IL-6, IL-8, TNF-α) and cortisol.
- Assessed maternal psychological distress via depressive symptoms, anxiety, and parenting stress.
- Utilized multilevel mixed models to analyze relationships.
Main Results:
- Increased maternal distress weakened the inverse relationship between cytokines (IL-1β, IL-6, TNF-α) and cortisol in children.
- These interactions were significant only in girls, not boys.
- Boys showed consistent inverse cytokine-cortisol relations, regardless of maternal distress.
Conclusions:
- Maternal distress alters children's neuroendocrine-immune responses, potentially reducing inflammation sensitivity to cortisol.
- This desensitization may elevate the risk for inflammatory diseases in children.
- Early detection and treatment of maternal distress are recommended to safeguard child health.
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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