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The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice
PM(2.5) is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM(2.5) inhalation. Pro-inflammatory cytokine IL-1β generated from effected cells usually plays a crucial role in many kinds of lung...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343586/ https://www.ncbi.nlm.nih.gov/pubmed/28276511 http://dx.doi.org/10.1038/srep44256 |
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author | Wang, Hetong Song, Laiyu Ju, Wenhui Wang, Xuguang Dong, Lu Zhang, Yining Ya, Ping Yang, Chun Li, Fasheng |
author_facet | Wang, Hetong Song, Laiyu Ju, Wenhui Wang, Xuguang Dong, Lu Zhang, Yining Ya, Ping Yang, Chun Li, Fasheng |
author_sort | Wang, Hetong |
collection | PubMed |
description | PM(2.5) is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM(2.5) inhalation. Pro-inflammatory cytokine IL-1β generated from effected cells usually plays a crucial role in many kinds of lung inflammatory reactions. The exacerbation of Th immune responses are identified in some PM(2.5) related diseases. To elucidate the underlying mechanism of PM(2.5)-induced acute lung inflammation, we exposed Balb/c mice to PM(2.5) intratracheally and established a mice model. Acute lung inflammation and increased IL-1β expression was observed after PM(2.5) instillation. Regulatory factors of IL-1β (TLR4/MyD88 signaling pathway and NLRP3 inflammasome) participated in this lung inflammatory response as well. Treatment with compound essential oils (CEOs) substantially attenuated PM(2.5)-induced acute lung inflammation. The decreased IL-1β and Th immune responses after CEOs treatment were significant. PM(2.5) may increase the secretion of IL-1β through TLR4/MyD88 and NLRP3 pathway resulting in murine airway inflammation. CEOs could attenuate the lung inflammation by reducing IL-1β and Th immune responses in this model. This study describes a potentially important mechanism of PM(2.5)-induced acute lung inflammation and that may bring about novel therapies for the inflammatory diseases associated with PM(2.5) inhalation. |
format | Online Article Text |
id | pubmed-5343586 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-53435862017-03-14 The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice Wang, Hetong Song, Laiyu Ju, Wenhui Wang, Xuguang Dong, Lu Zhang, Yining Ya, Ping Yang, Chun Li, Fasheng Sci Rep Article PM(2.5) is the main particulate air pollutant whose aerodynamic diameter is less than 2.5 micron. The inflammation of various respiratory diseases are associated with PM(2.5) inhalation. Pro-inflammatory cytokine IL-1β generated from effected cells usually plays a crucial role in many kinds of lung inflammatory reactions. The exacerbation of Th immune responses are identified in some PM(2.5) related diseases. To elucidate the underlying mechanism of PM(2.5)-induced acute lung inflammation, we exposed Balb/c mice to PM(2.5) intratracheally and established a mice model. Acute lung inflammation and increased IL-1β expression was observed after PM(2.5) instillation. Regulatory factors of IL-1β (TLR4/MyD88 signaling pathway and NLRP3 inflammasome) participated in this lung inflammatory response as well. Treatment with compound essential oils (CEOs) substantially attenuated PM(2.5)-induced acute lung inflammation. The decreased IL-1β and Th immune responses after CEOs treatment were significant. PM(2.5) may increase the secretion of IL-1β through TLR4/MyD88 and NLRP3 pathway resulting in murine airway inflammation. CEOs could attenuate the lung inflammation by reducing IL-1β and Th immune responses in this model. This study describes a potentially important mechanism of PM(2.5)-induced acute lung inflammation and that may bring about novel therapies for the inflammatory diseases associated with PM(2.5) inhalation. Nature Publishing Group 2017-03-09 /pmc/articles/PMC5343586/ /pubmed/28276511 http://dx.doi.org/10.1038/srep44256 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Wang, Hetong Song, Laiyu Ju, Wenhui Wang, Xuguang Dong, Lu Zhang, Yining Ya, Ping Yang, Chun Li, Fasheng The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice |
title | The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice |
title_full | The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice |
title_fullStr | The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice |
title_full_unstemmed | The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice |
title_short | The acute airway inflammation induced by PM(2.5) exposure and the treatment of essential oils in Balb/c mice |
title_sort | acute airway inflammation induced by pm(2.5) exposure and the treatment of essential oils in balb/c mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5343586/ https://www.ncbi.nlm.nih.gov/pubmed/28276511 http://dx.doi.org/10.1038/srep44256 |
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