- Title
- Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium
- Creator
- Murray, Lynne A.; Dunmore, Rebecca; Camelo, Ana; Da Silva, Carla A.; Gustavsson, Malin J.; Habiel, David M.; Hackett, Tillie L.; Hogaboam, Cory M.; Sleeman, Matthew A.; Knight, Darryl A.
- Relation
- Respiratory Research Vol. 18, Issue 1
- Publisher Link
- http://dx.doi.org/10.1186/s12931-017-0565-2
- Publisher
- BioMed Central
- Resource Type
- journal article
- Date
- 2017
- Description
- Background: Smoking and aberrant epithelial responses are risk factors for lung cancer as well as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis. In these conditions, disease progression is associated with epithelial damage and fragility, airway remodelling and sub-epithelial fibrosis. The aim of this study was to assess the acute effects of cigarette smoke on epithelial cell phenotype and pro-fibrotic responses in vitro and in vivo. Results: Apoptosis was significantly greater in unstimulated cells from COPD patients compared to control, but proliferation and CXCL8 release were not different. Cigarette smoke dose-dependently induced apoptosis, proliferation and CXCL8 release with normal epithelial cells being more responsive than COPD patient derived cells. Cigarette smoke did not induce epithelial-mesenchymal transition. In vivo, cigarette smoke exposure promoted epithelial apoptosis and proliferation. Moreover, mimicking a virus-induced exacerbation by exposing to mice to poly I:C, exaggerated the inflammatory responses, whereas expression of remodelling genes was similar in both. Conclusions: Collectively, these data indicate that cigarette smoke promotes epithelial cell activation and hyperplasia, but a secondary stimulus is required for the remodelling phenotype associated with COPD.
- Subject
- TGFβ1; poly I:C; remodelling; apoptosis
- Identifier
- http://hdl.handle.net/1959.13/1351193
- Identifier
- uon:30666
- Identifier
- ISSN:1465-9921
- Rights
- © The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
- Language
- eng
- Full Text
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