Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epitheliumReport as inadecuate




Acute cigarette smoke exposure activates apoptotic and inflammatory programs but a second stimulus is required to induce epithelial to mesenchymal transition in COPD epithelium - Download this document for free, or read online. Document in PDF available to download.

Respiratory Research

, 18:82

First Online: 03 May 2017Received: 28 June 2016Accepted: 27 April 2017DOI: 10.1186-s12931-017-0565-2

Cite this article as: Murray, L.A., Dunmore, R., Camelo, A. et al. Respir Res 2017 18: 82. doi:10.1186-s12931-017-0565-2

Abstract

BackgroundSmoking 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.

ResultsApoptosis 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.

ConclusionsCollectively, 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.

KeywordsTGFβ1 Poly I:C Remodelling Apoptosis Electronic supplementary materialThe online version of this article doi:10.1186-s12931-017-0565-2 contains supplementary material, which is available to authorized users.





Author: Lynne A. Murray - Rebecca Dunmore - Ana Camelo - Carla A. Da Silva - Malin J. Gustavsson - David M. Habiel - Tillie L 

Source: https://link.springer.com/







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