Signaling Stress in Asthma

Abstract

The apparent ability of stress to exacerbate childhood asthma provides a conundrum. Stress promotes the secretion of cortisol (which diminishes airway inflammation) and epinephrine (which acts as a bronchodilator). Thus, one might predict that stress should alleviate asthmatic symptoms. Miller and Chen investigated the relationship between life stress and expression of the glucocorticoid receptor (GR) and the β 2 -adrenergic receptor (β 2 AR). They administered an interview designed to assess stress to 38 healthy children and 39 children who had been diagnosed with asthma, collected a sample of blood from each child, and used reverse transcription polymerase chain reaction to quantify the expression of the GR and the β 2 AR in leukocytes. Although the abundance of β 2 AR and GR mRNA was greater in children with asthma, chronic stress was associated with a decrease in the abundance of β 2 AR mRNA in asthmatic children and an increase in β 2 AR abundance in healthy children. No effect of chronic stress alone on GR was apparent, and isolated major life events (acute stressors) within the past 3 or 6 months failed to affect the expression of either the β 2 AR or the GR. However, major life events that occurred in the context of chronic stress exacerbated the effects of chronic stress on the β 2 AR and uncovered a decrease in GR expression in asthmatic children and a more modest increase in GR expression in healthy children. Thus, the effects of stress on β 2 AR and GR expression in asthmatic children were in a direction consistent with decreased sensitivity to glucocorticoids and β 2 -adrenergic agonists. G. E. Miller, E. Chen, Life stress and diminished expression of genes encoding glucocorticoid receptor and β 2 -adrenergic receptor in children with asthma. Proc. Natl. Acad. Sci. U.S.A. 103 , 5496-5501 (2006). [Abstract] [Full Text]