Pulmonary, Allergy and Critical Care Division, Department of Medicine, University of Pennsylvania, Philadelphia, Pa 19104-3403, USA.
J Allergy Clin Immunol. 2010 Mar;125(3):550-8. doi: 10.1016/j.jaci.2009.11.005. Epub 2010 Feb 11.
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.
心理社会压力改变了对传染性和全身性疾病的易感性，并可能通过神经和激素途径调节免疫细胞功能，从而增强哮喘中的气道炎症。压力会激活下丘脑-垂体-肾上腺轴。内源性糖皮质激素的释放，可能会在改变气道免疫平衡方面发挥突出作用。尽管皮质类固醇和儿茶酚胺的血浆水平很高，但慢性心理社会压力会引发哮喘恶化。动物研究表明，社会压力会引起皮质类固醇不敏感，这部分可能是由于糖皮质激素受体表达和/或功能受损所致。这种机制可能会促进和放大气道炎症对感染、过敏原或刺激物的反应。这篇综述讨论了慢性心理社会压力导致的皮质类固醇反应状态改变的证据。阐明应激诱导的糖皮质激素反应性和免疫平衡受损的机制，可以确定改善哮喘管理的新的治疗靶点。
