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SIRT1 protects against urban particulate matter-induced airway inflammation

PURPOSE: Particulate matter (PM) has been implicated as a risk factor for airway injury. However, the molecular mechanisms remain largely unclear. The goal of this study was to determine whether sirtuin1 (SIRT1), an anti-inflammatory and antiaging protein, protects against PM-induced airway inflamma...

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Autores principales: Lai, Tianwen, Wen, Xiaoxia, Wu, Dong, Su, Guomei, Gao, Yun, Chen, Cuifen, Wu, Weiquan, Lv, Yingying, Chen, Zhanghui, Lv, Quanchao, Li, Wen, Li, Dongming, Chen, Min, Wu, Bin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689129/
https://www.ncbi.nlm.nih.gov/pubmed/31496673
http://dx.doi.org/10.2147/COPD.S202904
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author Lai, Tianwen
Wen, Xiaoxia
Wu, Dong
Su, Guomei
Gao, Yun
Chen, Cuifen
Wu, Weiquan
Lv, Yingying
Chen, Zhanghui
Lv, Quanchao
Li, Wen
Li, Dongming
Chen, Min
Wu, Bin
author_facet Lai, Tianwen
Wen, Xiaoxia
Wu, Dong
Su, Guomei
Gao, Yun
Chen, Cuifen
Wu, Weiquan
Lv, Yingying
Chen, Zhanghui
Lv, Quanchao
Li, Wen
Li, Dongming
Chen, Min
Wu, Bin
author_sort Lai, Tianwen
collection PubMed
description PURPOSE: Particulate matter (PM) has been implicated as a risk factor for airway injury. However, the molecular mechanisms remain largely unclear. The goal of this study was to determine whether sirtuin1 (SIRT1), an anti-inflammatory and antiaging protein, protects against PM-induced airway inflammation. METHODS: The effect of SIRT1 on PM-induced airway inflammation was assessed by using in vivo models of airway inflammation induced by PM and in vitro culture of human bronchial epithelial (HBE) cells exposed to PM, resveratrol (SIRT1 activator), or both. RESULTS: PM-stimulated HBE cells showed a significant decrease in SIRT1 but a notable increase in inflammatory cytokines. SIRT1 gene silencing further enhanced PM-induced expression of inflammatory cytokines. In contrast, resveratrol, a SIRT1 activator, reduced the expression of these cytokines compared with the control cells. In vivo, SIRT1 expression was significantly decreased in lung tissues of PM-exposed mice. Interestingly, resveratrol treatment reversed the enhanced total cells, neutrophils and inflammatory cytokines in PM-induced mice. Moreover, SIRT1 mediated PM-induced inflammatory cytokines expression at least partly through MAPK pathways. CONCLUSION: These findings suggest that SIRT1 is involved in the pathogenesis of PM-induced airway inflammation and activation of SIRT1 could prevent airway disorders or disease exacerbations induced by airborne particulate pollution.
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spelling pubmed-66891292019-09-06 SIRT1 protects against urban particulate matter-induced airway inflammation Lai, Tianwen Wen, Xiaoxia Wu, Dong Su, Guomei Gao, Yun Chen, Cuifen Wu, Weiquan Lv, Yingying Chen, Zhanghui Lv, Quanchao Li, Wen Li, Dongming Chen, Min Wu, Bin Int J Chron Obstruct Pulmon Dis Original Research PURPOSE: Particulate matter (PM) has been implicated as a risk factor for airway injury. However, the molecular mechanisms remain largely unclear. The goal of this study was to determine whether sirtuin1 (SIRT1), an anti-inflammatory and antiaging protein, protects against PM-induced airway inflammation. METHODS: The effect of SIRT1 on PM-induced airway inflammation was assessed by using in vivo models of airway inflammation induced by PM and in vitro culture of human bronchial epithelial (HBE) cells exposed to PM, resveratrol (SIRT1 activator), or both. RESULTS: PM-stimulated HBE cells showed a significant decrease in SIRT1 but a notable increase in inflammatory cytokines. SIRT1 gene silencing further enhanced PM-induced expression of inflammatory cytokines. In contrast, resveratrol, a SIRT1 activator, reduced the expression of these cytokines compared with the control cells. In vivo, SIRT1 expression was significantly decreased in lung tissues of PM-exposed mice. Interestingly, resveratrol treatment reversed the enhanced total cells, neutrophils and inflammatory cytokines in PM-induced mice. Moreover, SIRT1 mediated PM-induced inflammatory cytokines expression at least partly through MAPK pathways. CONCLUSION: These findings suggest that SIRT1 is involved in the pathogenesis of PM-induced airway inflammation and activation of SIRT1 could prevent airway disorders or disease exacerbations induced by airborne particulate pollution. Dove 2019-08-05 /pmc/articles/PMC6689129/ /pubmed/31496673 http://dx.doi.org/10.2147/COPD.S202904 Text en © 2019 Lai et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php).
spellingShingle Original Research
Lai, Tianwen
Wen, Xiaoxia
Wu, Dong
Su, Guomei
Gao, Yun
Chen, Cuifen
Wu, Weiquan
Lv, Yingying
Chen, Zhanghui
Lv, Quanchao
Li, Wen
Li, Dongming
Chen, Min
Wu, Bin
SIRT1 protects against urban particulate matter-induced airway inflammation
title SIRT1 protects against urban particulate matter-induced airway inflammation
title_full SIRT1 protects against urban particulate matter-induced airway inflammation
title_fullStr SIRT1 protects against urban particulate matter-induced airway inflammation
title_full_unstemmed SIRT1 protects against urban particulate matter-induced airway inflammation
title_short SIRT1 protects against urban particulate matter-induced airway inflammation
title_sort sirt1 protects against urban particulate matter-induced airway inflammation
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6689129/
https://www.ncbi.nlm.nih.gov/pubmed/31496673
http://dx.doi.org/10.2147/COPD.S202904
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