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Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells
BACKGROUND: The use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defe...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068890/ https://www.ncbi.nlm.nih.gov/pubmed/32164736 http://dx.doi.org/10.1186/s12931-020-1317-2 |
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author | Herr, Christian Tsitouras, Konstantinos Niederstraßer, Julia Backes, Christina Beisswenger, Christoph Dong, Li Guillot, Loïc Keller, Andreas Bals, Robert |
author_facet | Herr, Christian Tsitouras, Konstantinos Niederstraßer, Julia Backes, Christina Beisswenger, Christoph Dong, Li Guillot, Loïc Keller, Andreas Bals, Robert |
author_sort | Herr, Christian |
collection | PubMed |
description | BACKGROUND: The use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE). METHODS: We exposed pHBEs and several cell lines to TCIG-smoke or ECIG-vapor. Epithelial host defense and barrier integrity were determined. The transcriptome of airway epithelial cells was compared by gene expression array analysis. Gene interaction networks were constructed and differential gene expression over all groups analyzed. The expression of several candidate genes was validated by qRT-PCR. RESULTS: Bacterial killing, barrier integrity and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples. In contrast, TCIGs negatively affected host defense and reduced barrier integrity in a significant way. Furthermore ECIG-exposure significantly induced IL-8 secretion from Calu-3 cells but had no effect on NCI-H292 or primary cells. The gene expression based on array analysis distinguished TCIG-exposed cells from ECIG and room air-exposed samples. CONCLUSION: The transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use. |
format | Online Article Text |
id | pubmed-7068890 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-70688902020-03-18 Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells Herr, Christian Tsitouras, Konstantinos Niederstraßer, Julia Backes, Christina Beisswenger, Christoph Dong, Li Guillot, Loïc Keller, Andreas Bals, Robert Respir Res Research BACKGROUND: The use of electronic cigarettes (ECIGs) is increasing, but the impact of ECIG-vapor on cellular processes like inflammation or host defense are less understood. The aim of the present study was to compare the acute effects of traditional cigarettes (TCIGs) and ECIG-exposure on host defense, inflammation, and cellular activation of cell lines and primary differentiated human airway epithelial cells (pHBE). METHODS: We exposed pHBEs and several cell lines to TCIG-smoke or ECIG-vapor. Epithelial host defense and barrier integrity were determined. The transcriptome of airway epithelial cells was compared by gene expression array analysis. Gene interaction networks were constructed and differential gene expression over all groups analyzed. The expression of several candidate genes was validated by qRT-PCR. RESULTS: Bacterial killing, barrier integrity and the expression of antimicrobial peptides were not affected by ECIG-vapor compared to control samples. In contrast, TCIGs negatively affected host defense and reduced barrier integrity in a significant way. Furthermore ECIG-exposure significantly induced IL-8 secretion from Calu-3 cells but had no effect on NCI-H292 or primary cells. The gene expression based on array analysis distinguished TCIG-exposed cells from ECIG and room air-exposed samples. CONCLUSION: The transcriptome patterns of host defense and inflammatory genes are significantly distinct between ECIG-exposed and TCIG-treated cells. The overall effects of ECIGs on epithelial cells are less in comparison to TCIG, and ECIG-vapor does not affect host defense. Nevertheless, although acute exposure to ECIG-vapor induces inflammation, and the expression of S100 proteins, long term in vivo data is needed to evaluate the chronic effects of ECIG use. BioMed Central 2020-03-12 2020 /pmc/articles/PMC7068890/ /pubmed/32164736 http://dx.doi.org/10.1186/s12931-020-1317-2 Text en © The Author(s). 2020 Open AccessThis 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. |
spellingShingle | Research Herr, Christian Tsitouras, Konstantinos Niederstraßer, Julia Backes, Christina Beisswenger, Christoph Dong, Li Guillot, Loïc Keller, Andreas Bals, Robert Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
title | Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
title_full | Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
title_fullStr | Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
title_full_unstemmed | Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
title_short | Cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
title_sort | cigarette smoke and electronic cigarettes differentially activate bronchial epithelial cells |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7068890/ https://www.ncbi.nlm.nih.gov/pubmed/32164736 http://dx.doi.org/10.1186/s12931-020-1317-2 |
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