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哮喘中气道平滑肌的重塑:你患的是哪种类型?

Remodelling of airway smooth muscle in asthma: what sort do you have?

作者信息

James A

机构信息

West Australian Sleep Disorders Research Institute, School of Medicine and Pharmacology, University of Western Australia, Nedlands, WA, Australia.

出版信息

Clin Exp Allergy. 2005 Jun;35(6):703-7. doi: 10.1111/j.1365-2222.2005.02270.x.

Abstract

BACKGROUND

Shortening of smooth muscle around airways is the basis of symptoms and abnormal lung function in asthma. The airway wall is increased in thickness in small and large airways asthma, in relation to the clinical severity of asthma and the airway smooth muscle layer is the main contributor to this thickening. The relative contributions of more airway smooth muscle cells, bigger cells or more extracellular matrix to the increased thickness of the smooth muscle layer in asthma is not clear and has been examined in only a small number of cases, Studies of the natural history of asthma suggest that the clinical severity of asthma is relatively constant over time, deficits in lung function compared with nonasthmatic subjects occur early in the course of the disease and the decline in lung function with age is increased in asthma.

HYPOTHESIS

The observations from studies of the quantitative pathology and the natural history of asthma might be combined in the hypothesis that the severity of asthma is determined early (in its natural history) and is related mainly to increased volume density of airways smooth muscle cells (hyperplasia) and that later deposition of extracellular matrix from larger, hypertrophic smooth muscle cells results in fixed and increasing deficits in lung function.

SPECULATION

The relative contribution of more smooth muscle cells, bigger cells and extracellular matrix will be determined by unbiased stereological measurements in many cases of asthma of varying severity. The outcomes of such studies will be methods of monitoring and of treatment that will be tailored to the sort of smooth muscle modelling that is present in individual cases.

摘要

背景

气道周围平滑肌缩短是哮喘症状和肺功能异常的基础。在小气道和大气道哮喘中,气道壁厚度增加,这与哮喘的临床严重程度相关,而气道平滑肌层是这种增厚的主要原因。在哮喘中,气道平滑肌层厚度增加是由于更多的气道平滑肌细胞、更大的细胞还是更多的细胞外基质,其相对贡献尚不清楚,且仅在少数病例中进行过研究。哮喘自然史的研究表明,哮喘的临床严重程度随时间相对恒定,与非哮喘受试者相比,肺功能缺陷在疾病早期就已出现,且哮喘患者肺功能随年龄下降的幅度更大。

假设

对哮喘定量病理学和自然史研究的观察结果可结合为以下假设:哮喘的严重程度在早期(其自然史中)就已确定,主要与气道平滑肌细胞体积密度增加(增生)有关,随后来自更大、肥大的平滑肌细胞的细胞外基质沉积导致肺功能固定且不断增加的缺陷。

推测

在许多不同严重程度的哮喘病例中,将通过无偏倚的体视学测量来确定更多平滑肌细胞、更大细胞和细胞外基质的相对贡献。此类研究的结果将是针对个别病例中存在的平滑肌模型类型量身定制的监测和治疗方法。

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