Stress-related Neuroendocrine-Immune Function and Asthma in Young Children

• In Event: Poster Session 02
  In Poster Session: PS 02 Topic - Biological Processes: Psychophysiology

Abstract

Background
Asthma is the leading childhood chronic disease in the U.S. affecting 8.4% of children. Asthma disproportionately affects non-white and lower socioeconomic status children with higher disease rates and more severe consequences from asthma found among these groups compared to non-Hispanic white children. These disparities may be related to disproportionate exposures to environmental (e.g., pollutants), as well psychosocial triggers (e.g., stress). Acute stress activates the hypothalamic-pituitary-adrenal (HPA) axis and coordinated activity within the immune system. Chronic stress, especially during developmentally-sensitive periods, has been shown to modulate this cross-system coordination in neuroendocrine-immune (NEI) function which may increase the risk of inflammation-related diseases such as asthma.

To further our understanding of NEI function and stress-reactivity in children with asthma, we examined salivary measures of inflammatory and HPA activation in 5-year old children across a series of laboratory-based stressor tasks. We examined asthma-related differences in: 1) inflammatory cytokine levels and stress-reactivity, and 2) NEI function across the stressor tasks. Given variability in NEI function by sex, we examined these effects separately for male and female children. We hypothesized that children with asthma would have significantly higher levels of inflammatory cytokines across the stressor tasks compared to those without asthma and show stress-related NEI dysregulation.

Methods
Data from a sub-sample of child participants of the Fetus to Five study were examined [N=83, 48% female, 92% Black/African American, Mage(SD)=5.50(0.28) years]. During a 90-minute study visit, children participated in four age-appropriate, laboratory-based, stressor tasks and provided four saliva samples. Mothers completed the Asthma Predictive Index and sociodemographic surveys. Saliva samples were analyzed for indices of oral inflammation (IL-1β, IL-6, IL-8, TNF-a) and HPA activation (cortisol). Separate multilevel mixed models were conducted for each cytokine to assess stress-reactivity in cytokine levels as well as variability in this response by asthma status. An interaction term between cortisol and asthma status was added to these models to assess whether NEI relations varied by asthma status. All models were stratified by sex and adjusted for mother-reported indices of child oral health, as well as conceptually and/or statistically important covariates.

Results
There were no significant differences in overall cytokine levels between children with (n=25) and without asthma. Boys with asthma showed a steeper decline in TNF-a levels across the stressor tasks than boys without asthma (b=-0.23, SE=0.08, p=.004). For both boys and girls, the relation between cortisol and IL-8 varied by asthma status with more negative NEI relations found among children with asthma (b=-2.59 to -6.39, SE=1.31 to 2.92, ps ≤ .05), and among girls, relations between IL-6 and cortisol also showed similar moderation effects by asthma status (b=-9.91, SE=4.02, p=.014).

Discussion
The findings offer insight into potential stress-related NEI dysfunction associated with asthma. Further research is needed to confirm these findings among larger and more diverse samples. Additional studies are also needed to assess the nature, development, and environmental sensitivity of NEI function, and evaluate associations between NEI function measured in saliva and later-life health and disease risk.

Authors

• Olivia M Silke, University of California - Irvine
  Presenting Author

• Hedyeh Ahmadi, University of California - Irvine
  Non-Presenting Author

• Sara B. Johnson, Johns Hopkins School of Medicine
  Non-Presenting Author

• Douglas A. Granger, Institute for Interdisciplinary Salivary Bioscience Research, University of California, Irvine
  Non-Presenting Author

• Jenna L. Riis, Institute for Interdisciplinary Salivary Bioscience Research, University of California, Irvine
  Non-Presenting Author