Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10455029 | Brain, Behavior, and Immunity | 2010 | 7 Pages |
Abstract
Although psychosocial stress has been linked to clinical asthma outcomes, controlled, laboratory paradigms that test associations between psychosocial stress and markers of airway inflammation in humans are lacking. There is also little known about how individual background characteristics may affect variability across individuals in asthma-relevant inflammatory and pulmonary responses to stress. The goals of this study were to investigate the effects of a laboratory stress paradigm on markers of airway inflammation and pulmonary function in children with asthma, and to determine why some children are more biologically responsive to stress. 38 children physician-diagnosed with asthma, and 23 healthy control children (M age = 15 years) engaged in a conflict discussion task with a parent. Pulmonary function (FEV1) was measured before and immediately after the task. Airway inflammation (indicated by exhaled nitric oxide, FeNO) was measured before and 45 min after the task (to minimize effects from spirometry). Parents were interviewed about family socioeconomic status (SES: income and occupation). In children with asthma only, there was an inverse association of SES with change in FeNO levels in response to the conflict task, meaning that as SES declined, greater increases in FeNO were observed No changes in FEV1 were found in response to the conflict task. This study suggests that lower SES children with asthma may be more vulnerable to heightened airway inflammation in response to stress.
Related Topics
Life Sciences
Immunology and Microbiology
Immunology
Authors
Edith Chen, Robert C. Strunk, Leonard B. Bacharier, Meanne Chan, Gregory E. Miller,