Published ahead of print on November 6, 2003, doi:10.1164/rccm.200307-979OC Am. J. Respir. Crit. Care Med., Volume 169, Number 2, January 2004, 220-226 A more recent version of this article appeared on January 15, 2004
Submitted on July 22, 2003 Opposing effects of short and long term stress on airway inflammationPaul Forsythe1,1 Medicine, University of Alberta, Edmonton, Alberta, Canada, 2 Immunology Research Group, University of Saskatchewan, Saskatoon, Saskatchewan, Canada * To whom correspondence should be addressed. E-mail: hari{at}ualberta.ca.
Between 20 and 35 % of asthmatics experience asthma exacerbations during periods of stress. The biological mechanisms underlying these exacerbations are not clearly understood and the role of psychological factors in the pathophysiology of asthma remains controversial. We investigated the ability of psychological stress to modulate airway inflammation and airway hyperresponsiveness to methacholine in a murine model of asthma. Animals were exposed to a stressor daily for 3 (short-term stress) or 7 (long-term stress) days. Following allergen challenge, airway hyperresponsiveness was assessed through plethysmography and bronchoalveolar lavage cells were counted as a measure of inflammation. Following short-term stress, inflammatory cell number was decreased compared to unstressed animals while levels of IL-6, 9 and 13 were increased. Administration of a corticosteroid receptor antagonist, prior to stress, prevented the decrease in inflammatory cell numbers. In contrast animals stressed for 7 consecutive days showed a significant increase in inflammatory cell numbers, which was independent of the glucocorticoid response, but no change in cytokine levels. Airway hyperresponsiveness was not altered in stressed animals. Our results indicate that repeated exposure to stress over the long term engages different mechanisms than short-term stress and can exacerbate the chronic inflammatory responses of the airway. Key words: Stress, inflammation, asthma, mouse
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