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The bronchial epithelium in chronic and severe asthma

The bronchial epithelium in chronic and severe asthma
The bronchial epithelium in chronic and severe asthma
Although patients with severe, steroid-refractory asthma represent a minor proportion of the asthmatic population, they consume a disproportionate amount of healthcare costs and have a greatly impaired quality of life. They respond poorly to conventional anti-inflammatory therapy and frequently exhibit a component of fixed airflow obstruction that has been linked to airway wall remodeling. In addition to its classic barrier function, the bronchial epithelium responds to changes in the external environment by secreting cytoprotective molecules and mediators that signal to cells of the immune system. In asthma, the bronchial epithelium is stressed and damaged, with shedding of the columnar cells into the airway lumen. This damage and ensuing repair responses are proposed to orchestrate airway inflammation and remodeling via activation of myofibroblasts in the underlying lamina reticularis. This allows the two cell types to work as a trophic unit, propagating and amplifying the response at the cell surface into the submucosa. Because wound healing involves inflammation, repair, and remodeling processes, this review considers the evidence that exaggerated inflammation and remodeling of the airways arise as a consequence of abnormal injury and repair responses coordinated by the bronchial epithelium, highlighting, where possible, steroid-insensitive components.
1529-7322
127-133
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38
Davies, Donna E.
7de8fdc7-3640-4e3a-aa91-d0e03f990c38

Davies, Donna E. (2001) The bronchial epithelium in chronic and severe asthma. Current Allergy and Asthma Reports, 1 (2), 127-133.

Record type: Article

Abstract

Although patients with severe, steroid-refractory asthma represent a minor proportion of the asthmatic population, they consume a disproportionate amount of healthcare costs and have a greatly impaired quality of life. They respond poorly to conventional anti-inflammatory therapy and frequently exhibit a component of fixed airflow obstruction that has been linked to airway wall remodeling. In addition to its classic barrier function, the bronchial epithelium responds to changes in the external environment by secreting cytoprotective molecules and mediators that signal to cells of the immune system. In asthma, the bronchial epithelium is stressed and damaged, with shedding of the columnar cells into the airway lumen. This damage and ensuing repair responses are proposed to orchestrate airway inflammation and remodeling via activation of myofibroblasts in the underlying lamina reticularis. This allows the two cell types to work as a trophic unit, propagating and amplifying the response at the cell surface into the submucosa. Because wound healing involves inflammation, repair, and remodeling processes, this review considers the evidence that exaggerated inflammation and remodeling of the airways arise as a consequence of abnormal injury and repair responses coordinated by the bronchial epithelium, highlighting, where possible, steroid-insensitive components.

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Published date: 2001

Identifiers

Local EPrints ID: 27013
URI: https://eprints.soton.ac.uk/id/eprint/27013
ISSN: 1529-7322
PURE UUID: 63cb36cb-748a-4f8c-aafa-84ee6371d88d
ORCID for Donna E. Davies: ORCID iD orcid.org/0000-0002-5117-2991

Catalogue record

Date deposited: 26 Apr 2006
Last modified: 15 Aug 2019 00:58

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