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支气管反应性与非吸烟者呼出的一氧化氮(FE(NO))增加和吸烟者 FE(NO)降低有关。

Bronchial responsiveness is related to increased exhaled NO (FE(NO)) in non-smokers and decreased FE(NO) in smokers.

机构信息

Department of Medical Sciences: Clinical Physiology, Uppsala University, Uppsala, Sweden.

出版信息

PLoS One. 2012;7(4):e35725. doi: 10.1371/journal.pone.0035725. Epub 2012 Apr 26.

Abstract

RATIONALE

Both atopy and smoking are known to be associated with increased bronchial responsiveness. Fraction of nitric oxide (NO) in the exhaled air (FE(NO)), a marker of airways inflammation, is decreased by smoking and increased by atopy. NO has also a physiological bronchodilating and bronchoprotective role.

OBJECTIVES

To investigate how the relation between FE(NO) and bronchial responsiveness is modulated by atopy and smoking habits.

METHODS

Exhaled NO measurements and methacholine challenge were performed in 468 subjects from the random sample of three European Community Respiratory Health Survey II centers: Turin (Italy), Gothenburg and Uppsala (both Sweden). Atopy status was defined by using specific IgE measurements while smoking status was questionnaire-assessed.

MAIN RESULTS

Increased bronchial responsiveness was associated with increased FE(NO) levels in non-smokers (p = 0.02) and decreased FE(NO) levels in current smokers (p = 0.03). The negative association between bronchial responsiveness and FE(NO) was seen only in the group smoking less <10 cigarettes/day (p = 0.008). Increased bronchial responsiveness was associated with increased FE(NO) in atopic subjects (p = 0.04) while no significant association was found in non-atopic participants. The reported interaction between FE(NO) and smoking and atopy, respectively were maintained after adjusting for possible confounders (p-values<0.05).

CONCLUSIONS

The present study highlights the interactions of the relationship between FE(NO) and bronchial responsiveness with smoking and atopy, suggesting different mechanisms behind atopy- and smoking-related increases of bronchial responsiveness.

摘要

背景

已知特应性和吸烟与支气管高反应性增加有关。呼出气中一氧化氮(NO)的分数(FE(NO)),气道炎症的标志物,可被吸烟减少,可被特应性增加。NO 也具有生理性的支气管舒张和支气管保护作用。

目的

研究特应性和吸烟习惯如何调节 FE(NO)与支气管高反应性之间的关系。

方法

从三个欧洲共同体呼吸健康调查 II 中心的随机样本中,对 468 名受试者进行呼出气 NO 测量和乙酰甲胆碱挑战:都灵(意大利)、哥德堡和乌普萨拉(瑞典)。特应性状态通过使用特异性 IgE 测量来定义,而吸烟状态通过问卷调查来评估。

主要结果

在不吸烟者中,支气管高反应性与 FE(NO)水平升高相关(p=0.02),而在当前吸烟者中,FE(NO)水平降低(p=0.03)。在每天吸烟少于<10 支的吸烟者中,FE(NO)与支气管高反应性之间的负相关仅见于该组(p=0.008)。在特应性受试者中,支气管高反应性与 FE(NO)升高相关(p=0.04),而在非特应性参与者中未发现显著相关性。在调整了可能的混杂因素后,FE(NO)与吸烟和特应性之间的交互作用仍然存在(p 值<0.05)。

结论

本研究强调了 FE(NO)与支气管高反应性之间关系与吸烟和特应性之间的相互作用,提示了特应性和吸烟相关的支气管高反应性增加背后的不同机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ae52/3338521/5746c828a25e/pone.0035725.g001.jpg

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