Airway contractility and remodeling: links to asthma symptoms.

Published

Journal Article (Review)

Respiratory symptoms are largely caused by obstruction of the airways. In asthma, airway narrowing mediated by airway smooth muscle (ASM) contraction contributes significantly to obstruction. The spasmogens produced following exposure to environmental triggers, such as viruses or allergens, are initially responsible for ASM activation. However, the extent of narrowing of the airway lumen due to ASM shortening can be influenced by many factors and it remains a real challenge to decipher the exact role of ASM in causing asthmatic symptoms. Innovative tools, such as the forced oscillation technique, continue to develop and have been proven useful to assess some features of ASM function in vivo. Despite these technologic advances, it is still not clear whether excessive narrowing in asthma is driven by ASM abnormalities, by other alterations in non-muscle factors or simply because of the overexpression of spasmogens. This is because a multitude of forces are acting on the airway wall, and because not only are these forces constantly changing but they are also intricately interconnected. To counteract these limitations, investigators have utilized in vitro and ex vivo systems to assess and compare asthmatic and non-asthmatic ASM contractility. This review describes: 1- some muscle and non-muscle factors that are altered in asthma that may lead to airway narrowing and asthma symptoms; 2- some technologies such as the forced oscillation technique that have the potential to unveil the role of ASM in airway narrowing in vivo; and 3- some data from ex vivo and in vitro methods that probe the possibility that airway hyperresponsiveness is due to the altered environment surrounding the ASM or, alternatively, to a hypercontractile ASM phenotype that can be either innate or acquired.

Full Text

Duke Authors

Cited Authors

  • West, AR; Syyong, HT; Siddiqui, S; Pascoe, CD; Murphy, TM; Maarsingh, H; Deng, L; Maksym, GN; Bossé, Y

Published Date

  • February 2013

Published In

Volume / Issue

  • 26 / 1

Start / End Page

  • 3 - 12

PubMed ID

  • 22989721

Pubmed Central ID

  • 22989721

Electronic International Standard Serial Number (EISSN)

  • 1522-9629

Digital Object Identifier (DOI)

  • 10.1016/j.pupt.2012.08.009

Language

  • eng

Conference Location

  • England