Journal
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY
Volume 125, Issue 3, Pages 550-558Publisher
MOSBY-ELSEVIER
DOI: 10.1016/j.jaci.2009.11.005
Keywords
Airway inflammation; psychosocial stress corticosteroids; innate immune system
Categories
Funding
- NIH [R01A1055593, R01HL076646]
- Mind, Body, Brain, and Health Initiative
- Sepracor
- NIH-NHLBI
- AstraZeneca
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Psychosocial stress alters susceptibility to infectious and systemic illnesses and may enhance airway inflammation in asthma by modulating immune cell function through neural and hormonal pathways. Stress activates the hypothalamic-pituitary-adrenal axis. Release of endogenous glucocorticoids, as a consequence, may play a prominent role in altering the airway immune homeostasis. Despite substantial corticosteroid and catecholamine plasma levels, chronic psychosocial stress evokes asthma exacerbations. Animal studies suggest that social stress induces corticosteroid insensitivity that in part may be a result of impaired glucocorticoid receptor expression and/or function. Such mechanisms likely promote and amplify airway inflammation in response to infections, allergen, or irritant exposure. This review discusses evidence of an altered corticosteroid responsive state as a consequence of chronic psychosocial stress. Elucidation of the mechanisms of stress-induced impairment of glucocorticoid responsiveness and immune homeostasis may identify novel therapeutic targets that could improve asthma management. (J Allergy Clin Immunol 2010;125:550-8.)
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