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慢性阻塞性肺疾病中的气道重塑:这不是哮喘!

Airway remodelling in COPD: It's not asthma!

作者信息

Jones Robyn L, Noble Peter B, Elliot John G, James Alan L

机构信息

Department of Pulmonary Physiology and Sleep Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia.

School of Anatomy, Physiology and Human Biology, University of Western Australia, Perth, Western Australia, Australia.

出版信息

Respirology. 2016 Nov;21(8):1347-1356. doi: 10.1111/resp.12841. Epub 2016 Jul 5.

DOI:10.1111/resp.12841
PMID:27381663
Abstract

COPD is defined as airflow limitation that is not reversed by treatment. In asthma, airflow limitation is not only reversible, but also inducible. This is called 'airway hyperresponsiveness' (AHR) and is associated with thickening of the airway wall, predominantly the layer of airway smooth muscle, due to more cells, bigger cells and more extracellular matrix (ECM) in proportion to the increase in smooth muscle. AHR is also observed in COPD if the changes in airflow are expressed as a percent of the baseline lung function. However, the absolute change in baseline lung function that can be induced in COPD is actually less than that seen in normal subjects, suggesting that the airways in COPD are resistant not only to opening, but also to closing. This observation agrees with physiological measures showing increased airway wall stiffness in COPD. Like asthma, airway wall thickness is increased in COPD, including the layer of smooth muscle. Unlike asthma, however, fixed airflow obstruction appears to be characterized by a disproportionate increase in the ECM within the smooth muscle layer. In this review, we summarize the studies of airway matrix deposition in COPD and put forward the proposal that the airway remodelling in COPD is different from that in asthma and call for a systematic analysis of airway matrix deposition in COPD.

摘要

慢性阻塞性肺疾病(COPD)被定义为气流受限,且这种受限不能通过治疗逆转。在哮喘中,气流受限不仅是可逆的,而且是可诱导的。这被称为“气道高反应性”(AHR),并且与气道壁增厚有关,主要是气道平滑肌层增厚,这是由于细胞增多、细胞变大以及与平滑肌增加成比例的更多细胞外基质(ECM)。如果将气流变化表示为基线肺功能的百分比,在COPD中也可观察到AHR。然而,COPD中可诱导的基线肺功能的绝对变化实际上小于正常受试者,这表明COPD中的气道不仅对开放有抵抗,而且对关闭也有抵抗。这一观察结果与显示COPD中气道壁硬度增加的生理测量结果一致。与哮喘一样,COPD中的气道壁厚度增加,包括平滑肌层。然而,与哮喘不同的是,固定性气流阻塞似乎以平滑肌层内ECM的不成比例增加为特征。在本综述中,我们总结了关于COPD气道基质沉积的研究,并提出COPD中的气道重塑不同于哮喘中的气道重塑这一观点,并呼吁对COPD气道基质沉积进行系统分析。

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