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

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....

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Bibliographic Details
Published in:	Respiratory research Vol. 18; no. 1; p. 82
Main Authors:	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
Format:	Journal Article
Language:	English
Published:	England BioMed Central 03-05-2017 BMC
Subjects:	Aberration Acute effects Airway management Animals Antigens Apoptosis Apoptosis - drug effects Cancer Cell activation Cell growth Cell proliferation Chronic obstructive pulmonary disease Cigarette smoke Cigarettes Cytokines Epithelial cells Epithelial-Mesenchymal Transition - drug effects Epithelium Experiments Exposure Fibrosis Fragility Gene expression Genotype & phenotype Health risks Humans Hyperplasia In vitro methods and tests Inflammation Kinases Lung cancer Lung diseases Mesenchyme Mice Mice, Inbred C57BL Mimicry Obstructive lung disease Poly I:C Polyinosinic:polycytidylic acid Pulmonary Disease, Chronic Obstructive - chemically induced Pulmonary Disease, Chronic Obstructive - pathology Pulmonary Disease, Chronic Obstructive - physiopathology Pulmonary Fibrosis - chemically induced Pulmonary Fibrosis - pathology Pulmonary Fibrosis - physiopathology Remodelling Respiratory Mucosa - drug effects Respiratory Mucosa - pathology Respiratory Mucosa - physiopathology Respiratory tract Risk analysis Risk factors Smoke Smoke - adverse effects Smoking TGFβ1 Tobacco Products - poisoning Viruses Remodelling TGFβ1 Poly I:C Apoptosis
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Summary:	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. 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. 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.
Bibliography:	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23
ISSN:	1465-993X 1465-9921 1465-993X 1465-9921
DOI:	10.1186/s12931-017-0565-2