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Cigarette smoke represses the innate immune response to asbestos
Both cigarette smoke (CS) and asbestos cause lung inflammation and lung cancer, and at high asbestos exposure levels, populations exposed to both of these carcinogens display a synergistic increase in the development of lung cancer. The mechanisms through which these two toxic agents interact to pro...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760433/ https://www.ncbi.nlm.nih.gov/pubmed/26660560 http://dx.doi.org/10.14814/phy2.12652 |
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author | Morris, Gilbert F. Danchuk, Svitlana Wang, Yu Xu, Beibei Rando, Roy J. Brody, Arnold R. Shan, Bin Sullivan, Deborah E. |
author_facet | Morris, Gilbert F. Danchuk, Svitlana Wang, Yu Xu, Beibei Rando, Roy J. Brody, Arnold R. Shan, Bin Sullivan, Deborah E. |
author_sort | Morris, Gilbert F. |
collection | PubMed |
description | Both cigarette smoke (CS) and asbestos cause lung inflammation and lung cancer, and at high asbestos exposure levels, populations exposed to both of these carcinogens display a synergistic increase in the development of lung cancer. The mechanisms through which these two toxic agents interact to promote lung tumorigenesis are poorly understood. Here, we begin to dissect the inflammatory signals induced by asbestos in combination with CS using a rodent inhalation model and in vitro cell culture. Wild‐type C57BL/6 mice were exposed to room air as a control, CS, and/or asbestos (4 days per week to CS and 1 day per week to asbestos for 5 weeks). Bronchoalveolar lavage (BAL) fluid was collected following exposure and analyzed for inflammatory mediators. Asbestos‐exposed mice displayed an increased innate immune response consistent with NLRP3 inflammasome activation. Compared to mice exposed only to asbestos, animals coexposed to CS + asbestos displayed attenuated levels of innate immune mediators and altered inflammatory cell recruitment. Histopathological changes in CS + asbestos‐exposed mice correlated with attenuated fibroproliferative lesion development relative to their counterparts exposed only to asbestos. In vitro experiments using a human monocyte cell line (THP‐1 cells) supported the in vivo results in that coexposure to cigarette smoke extract repressed NLRP3 inflammasome markers in cells treated with asbestos. These observations indicate that CS represses central components of the innate immune response to inhaled asbestos. |
format | Online Article Text |
id | pubmed-4760433 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-47604332016-02-22 Cigarette smoke represses the innate immune response to asbestos Morris, Gilbert F. Danchuk, Svitlana Wang, Yu Xu, Beibei Rando, Roy J. Brody, Arnold R. Shan, Bin Sullivan, Deborah E. Physiol Rep Original Research Both cigarette smoke (CS) and asbestos cause lung inflammation and lung cancer, and at high asbestos exposure levels, populations exposed to both of these carcinogens display a synergistic increase in the development of lung cancer. The mechanisms through which these two toxic agents interact to promote lung tumorigenesis are poorly understood. Here, we begin to dissect the inflammatory signals induced by asbestos in combination with CS using a rodent inhalation model and in vitro cell culture. Wild‐type C57BL/6 mice were exposed to room air as a control, CS, and/or asbestos (4 days per week to CS and 1 day per week to asbestos for 5 weeks). Bronchoalveolar lavage (BAL) fluid was collected following exposure and analyzed for inflammatory mediators. Asbestos‐exposed mice displayed an increased innate immune response consistent with NLRP3 inflammasome activation. Compared to mice exposed only to asbestos, animals coexposed to CS + asbestos displayed attenuated levels of innate immune mediators and altered inflammatory cell recruitment. Histopathological changes in CS + asbestos‐exposed mice correlated with attenuated fibroproliferative lesion development relative to their counterparts exposed only to asbestos. In vitro experiments using a human monocyte cell line (THP‐1 cells) supported the in vivo results in that coexposure to cigarette smoke extract repressed NLRP3 inflammasome markers in cells treated with asbestos. These observations indicate that CS represses central components of the innate immune response to inhaled asbestos. John Wiley and Sons Inc. 2015-12-10 /pmc/articles/PMC4760433/ /pubmed/26660560 http://dx.doi.org/10.14814/phy2.12652 Text en © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. This is an open access article under the terms of the Creative Commons Attribution (http://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Research Morris, Gilbert F. Danchuk, Svitlana Wang, Yu Xu, Beibei Rando, Roy J. Brody, Arnold R. Shan, Bin Sullivan, Deborah E. Cigarette smoke represses the innate immune response to asbestos |
title | Cigarette smoke represses the innate immune response to asbestos |
title_full | Cigarette smoke represses the innate immune response to asbestos |
title_fullStr | Cigarette smoke represses the innate immune response to asbestos |
title_full_unstemmed | Cigarette smoke represses the innate immune response to asbestos |
title_short | Cigarette smoke represses the innate immune response to asbestos |
title_sort | cigarette smoke represses the innate immune response to asbestos |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4760433/ https://www.ncbi.nlm.nih.gov/pubmed/26660560 http://dx.doi.org/10.14814/phy2.12652 |
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