- Title
- Airway mechanical compression: its role in asthma pathogenesis and progression
- Creator
- Veerati, Punnam Chander; Mitchel, Jennifer A.; Reid, Andrew T.; Knight, Darryl A.; Bartlett, Nathan W.; Park, Jin-Ah; Grainge, Chris L.
- Relation
- European Respiratory Review Vol. 29, Issue 157, no. 190123
- Publisher Link
- http://dx.doi.org/10.1183/16000617.0123-2019
- Publisher
- European Respiratory Society
- Resource Type
- journal article
- Date
- 2020
- Description
- The lung is a mechanically active organ, but uncontrolled or excessive mechanical forces disrupt normal lung function and can contribute to the development of disease. In asthma, bronchoconstriction leads to airway narrowing and airway wall buckling. A growing body of evidence suggests that pathological mechanical forces induced by airway buckling alone can perpetuate disease processes in asthma. Here, we review the data obtained from a variety of experimental models, including in vitro, ex vivo and in vivo approaches, which have been used to study the impact of mechanical forces in asthma pathogenesis. We review the evidence showing that mechanical compression alters the biological and biophysical properties of the airway epithelium, including activation of the epidermal growth factor receptor pathway, overproduction of asthma-associated mediators, goblet cell hyperplasia, and a phase transition of epithelium from a static jammed phase to a mobile unjammed phase. We also define questions regarding the impact of mechanical forces on the pathology of asthma, with a focus on known triggers of asthma exacerbations such as viral infection.
- Subject
- lung function; asthma; mechanical compression; asthma exacerbations; Sustainable Development Goals; SDG 3; SDG 7
- Identifier
- http://hdl.handle.net/1959.13/1427010
- Identifier
- uon:38505
- Identifier
- ISSN:0905-9180
- Rights
- © ERS 2020. This article is open access and distributed under the terms of the Creative Commons Attribution Non-Commercial Licence 4.0, http://creativecommons.org/licenses/by/4.0/.
- Language
- eng
- Full Text
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