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过敏性哮喘患者免疫和神经元参数与应激感知之间的相关性

Correlation between immune and neuronal parameters and stress perception in allergic asthmatics.

作者信息

Joachim R A, Noga O, Sagach V, Hanf G, Fliege H, Kocalevent R D, Peters E M, Klapp B F

机构信息

Department of Internal Medicine and Psychosomatics, Charité Center for Internal Medicine and Dermatology, Charité-Universitaetsmedizin, Berlin, Germany.

出版信息

Clin Exp Allergy. 2008 Feb;38(2):283-90. doi: 10.1111/j.1365-2222.2007.02899.x. Epub 2007 Dec 7.

DOI:10.1111/j.1365-2222.2007.02899.x
PMID:18070153
Abstract

BACKGROUND

Asthma is a chronic disease defined by airway inflammation, increased airway hyperresponsiveness and episodes of airway obstruction. Although there are abundant clinical and experimental data showing that stress may worsen asthma, the mechanisms linking stress to asthma are not well understood. By inducing a pro-inflammatory cytokine milieu, stress might enhance airway inflammation in bronchial asthma. We therefore investigated the correlation of stress perception and the cytokine profile of circulating lymphocytes in humans.

METHODS

Allergic asthmatic patients and healthy controls were evaluated for perceived level of stress, demographic and lung function data. Whole blood cells were obtained and stimulated by mitogen to assess intracellular IL-4, IFN-gamma and TNF-alpha by flow cytometry. Neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) were measured in serum.

RESULTS

Asthmatic patients showed significantly higher percentages of TNF-alpha-producing T cells than healthy controls. Only in asthmatic patients was stress perception correlated with percentages of TNF-alpha-producing T cells and serum BDNF levels, while forced expiratory volume in 1 s (% predicted) was negatively correlated to BDNF.

CONCLUSION

The results of our study support the hypothesis that stress deteriorates bronchial asthma by inducing a pro-inflammatory cytokine profile in allergic asthmatics. Stress management might provide a supplement therapy of allergic asthma.

摘要

背景

哮喘是一种由气道炎症、气道高反应性增加和气道阻塞发作所定义的慢性疾病。尽管有大量临床和实验数据表明应激可能会使哮喘恶化,但应激与哮喘之间的关联机制尚未完全清楚。通过诱导促炎细胞因子环境,应激可能会增强支气管哮喘中的气道炎症。因此,我们研究了人类应激感知与循环淋巴细胞细胞因子谱之间的相关性。

方法

对过敏性哮喘患者和健康对照者进行应激感知水平、人口统计学和肺功能数据评估。获取全血细胞并用丝裂原刺激,通过流式细胞术评估细胞内白细胞介素-4、干扰素-γ和肿瘤坏死因子-α。测定血清中的神经营养因子神经生长因子(NGF)和脑源性神经营养因子(BDNF)。

结果

哮喘患者产生肿瘤坏死因子-α的T细胞百分比显著高于健康对照者。仅在哮喘患者中,应激感知与产生肿瘤坏死因子-α的T细胞百分比和血清BDNF水平相关,而1秒用力呼气量(预测值%)与BDNF呈负相关。

结论

我们的研究结果支持以下假设,即应激通过在过敏性哮喘患者中诱导促炎细胞因子谱而使支气管哮喘恶化。应激管理可能为过敏性哮喘提供一种补充治疗方法。

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