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Sci. STKE, 11 April 2006
Vol. 2006, Issue 330, p. tw121
[DOI: 10.1126/stke.3302006tw121]

EDITORS' CHOICE

ASTHMA Signaling Stress in Asthma

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 β2-adrenergic receptor (β2AR). 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 β2AR in leukocytes. Although the abundance of β2AR and GR mRNA was greater in children with asthma, chronic stress was associated with a decrease in the abundance of β2AR mRNA in asthmatic children and an increase in β2AR 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 β2AR or the GR. However, major life events that occurred in the context of chronic stress exacerbated the effects of chronic stress on the β2AR 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 β2AR and GR expression in asthmatic children were in a direction consistent with decreased sensitivity to glucocorticoids and β2-adrenergic agonists.

G. E. Miller, E. Chen, Life stress and diminished expression of genes encoding glucocorticoid receptor and β2-adrenergic receptor in children with asthma. Proc. Natl. Acad. Sci. U.S.A. 103, 5496-5501 (2006). [Abstract] [Full Text]

Citation: Signaling Stress in Asthma. Sci. STKE 2006, tw121 (2006).



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