Opposing effects of short- and long-term stress on airway inflammation
Opposing effects of short- and long-term stress on airway inflammation
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DOI：
10.1164/rccm.200307-979oc
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发表时间：
2004-01-15
影响因子：
24.7
通讯作者：
Vliagoftis, H
中科院分区：
文献类型：
--
作者：
Forsythe, P;Ebeling, C;Vliagoftis, H
20%至35%的哮喘受试者在压力期间会发生哮喘急性发作。这些加重的生物学机制尚不清楚，心理因素在哮喘病理生理学中的作用仍有争议。我们研究了心理应激调节哮喘小鼠模型气道炎症和气道高反应性（AHR）的能力。每天将动物暴露于应激源，持续3天（短期应激）或7天（长期应激）。过敏原激发后，通过体积描记法评估AHR，并计数支气管肺泡灌洗液细胞作为炎症的量度。短期应激后，与未应激的动物相比，炎症细胞数量减少，而白细胞介素（IL）-6，IL-9和IL-13的水平增加。在应激前给予皮质类固醇受体拮抗剂可防止炎症细胞数量减少。相反，连续7天应激的动物显示炎性细胞数量显著增加，这与糖皮质激素反应无关，但细胞因子水平没有变化。AHR在应激动物中没有改变。我们的研究结果表明，长期反复暴露于压力下会产生与短期压力不同的机制，并会加剧气道的慢性炎症反应。
Between 20% and 35% of subjects with asthma experience asthma exacerbations during periods of stress. The biological mechanisms underlying these exacerbations are not clearly understood, and the role of psychologic factors in the pathophysiology of asthma remains controversial. We investigated the ability of psychologic stress to modulate airway inflammation and airway hyperresponsiveness (AHR) 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. After allergen challenge, AHR was assessed through plethysmography, and bronchoalveolar lavage cells were counted as a measure of inflammation. After short-term stress, inflammatory cell number was decreased compared with unstressed animals, whereas levels of interleukin (IL)-6, IL-9, and IL-13 were increased. Administration of a corticosteroid receptor antagonist, before 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. AHR 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.