哮喘加重期的应激与炎症
Stress and inflammation in exacerbations of asthma.
作者信息
Chen Edith, Miller Gregory E
机构信息
University of British Columbia, Department of Psychology, 2136 West Mall, Vancouver, BC, Canada V6T 1Z4.
出版信息
Brain Behav Immun. 2007 Nov;21(8):993-9. doi: 10.1016/j.bbi.2007.03.009. Epub 2007 May 9.
Abstract
In this mini-review, we outline a model depicting the immunologic mechanisms by which psychological stress can exacerbate clinical symptoms in patients with asthma. This model highlights the importance of both social and physical exposures in the exacerbation of asthma symptoms. The basic premise of the model is that psychological stress operates by altering the magnitude of the airway inflammatory response that irritants, allergens, and infections bring about in persons with asthma. The biological pathways for how stress amplifies the immune response to asthma triggers include the hypothalamic-pituitary-adrenal (HPA) axis, the sympathetic-adrenal-medullary (SAM) axis, and the sympathetic (SNS) and parasympathetic (PNS) arms of the autonomic nervous system. Empirical evidence for this model is reviewed, and conclusions and future research directions are discussed.
摘要
在本综述中，我们概述了一个模型，该模型描述了心理压力可加重哮喘患者临床症状的免疫机制。该模型强调了社会暴露和身体暴露在哮喘症状加重中的重要性。该模型的基本前提是，心理压力通过改变气道炎症反应的程度来发挥作用，而刺激物、过敏原和感染会在哮喘患者中引发这种炎症反应。压力如何放大对哮喘触发因素的免疫反应的生物学途径包括下丘脑-垂体-肾上腺（HPA）轴、交感-肾上腺-髓质（SAM）轴以及自主神经系统的交感（SNS）和副交感（PNS）分支。本文回顾了该模型的实证证据，并讨论了结论和未来的研究方向。
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