Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway

Abstract Wildfire smoke induces acute pulmonary distress and is of particular concern to risk groups such as the sick and elderly. Wood smoke (WS) contains many of the same toxic compounds as those found in cigarette smoke (CS) including polycyclic aromatic hydrocarbons, carbon monoxide, and free ra...

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Autores principales: Matthew R. Zeglinski, Christopher T. Turner, Rui Zeng, Carley Schwartz, Stephanie Santacruz, Megan A. Pawluk, Hongyan Zhao, Arthur W. H. Chan, Christopher Carlsten, David J. Granville
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Publicado: Nature Portfolio 2019
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spelling oai:doaj.org-article:1b6c2b4dbf5d4315845a64aa81cc98692021-12-02T15:08:47ZSoluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway10.1038/s41598-019-46400-82045-2322https://doaj.org/article/1b6c2b4dbf5d4315845a64aa81cc98692019-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-019-46400-8https://doaj.org/toc/2045-2322Abstract Wildfire smoke induces acute pulmonary distress and is of particular concern to risk groups such as the sick and elderly. Wood smoke (WS) contains many of the same toxic compounds as those found in cigarette smoke (CS) including polycyclic aromatic hydrocarbons, carbon monoxide, and free radicals. CS is a well-established risk factor for respiratory diseases such as asthma and COPD. Limited studies investigating the biological effects of WS on the airway epithelium have been performed. Using a cell culture-based model, we assessed the effects of a WS-infused solution on alveolar epithelial barrier function, cell migration, and survival. The average geometric mean of particles in the WS was 178 nm. GC/MS analysis of the WS solution identified phenolic and cellulosic compounds. WS exposure resulted in a significant reduction in barrier function, which peaked after 24 hours of continuous exposure. The junctional protein E-cadherin showed a prominent reduction in response to increasing concentrations of WS. Furthermore, WS significantly repressed cell migration following injury to the cell monolayer. There was no difference in cell viability following WS exposure. Mechanistically, WS exposure induced activation of the p44/42, but not p38, MAPK signaling pathway, and inhibition of p44/42 phosphorylation prevented the disruption of barrier function and loss of E-cadherin staining. Thus, WS may contribute to the breakdown of alveolar structure and function through a p44/42 MAPK-dependent pathway and may lead to the development and/or exacerbation of respiratory pathologies with chronic exposure.Matthew R. ZeglinskiChristopher T. TurnerRui ZengCarley SchwartzStephanie SantacruzMegan A. PawlukHongyan ZhaoArthur W. H. ChanChristopher CarlstenDavid J. GranvilleNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 9, Iss 1, Pp 1-13 (2019)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Matthew R. Zeglinski
Christopher T. Turner
Rui Zeng
Carley Schwartz
Stephanie Santacruz
Megan A. Pawluk
Hongyan Zhao
Arthur W. H. Chan
Christopher Carlsten
David J. Granville
Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
description Abstract Wildfire smoke induces acute pulmonary distress and is of particular concern to risk groups such as the sick and elderly. Wood smoke (WS) contains many of the same toxic compounds as those found in cigarette smoke (CS) including polycyclic aromatic hydrocarbons, carbon monoxide, and free radicals. CS is a well-established risk factor for respiratory diseases such as asthma and COPD. Limited studies investigating the biological effects of WS on the airway epithelium have been performed. Using a cell culture-based model, we assessed the effects of a WS-infused solution on alveolar epithelial barrier function, cell migration, and survival. The average geometric mean of particles in the WS was 178 nm. GC/MS analysis of the WS solution identified phenolic and cellulosic compounds. WS exposure resulted in a significant reduction in barrier function, which peaked after 24 hours of continuous exposure. The junctional protein E-cadherin showed a prominent reduction in response to increasing concentrations of WS. Furthermore, WS significantly repressed cell migration following injury to the cell monolayer. There was no difference in cell viability following WS exposure. Mechanistically, WS exposure induced activation of the p44/42, but not p38, MAPK signaling pathway, and inhibition of p44/42 phosphorylation prevented the disruption of barrier function and loss of E-cadherin staining. Thus, WS may contribute to the breakdown of alveolar structure and function through a p44/42 MAPK-dependent pathway and may lead to the development and/or exacerbation of respiratory pathologies with chronic exposure.
format article
author Matthew R. Zeglinski
Christopher T. Turner
Rui Zeng
Carley Schwartz
Stephanie Santacruz
Megan A. Pawluk
Hongyan Zhao
Arthur W. H. Chan
Christopher Carlsten
David J. Granville
author_facet Matthew R. Zeglinski
Christopher T. Turner
Rui Zeng
Carley Schwartz
Stephanie Santacruz
Megan A. Pawluk
Hongyan Zhao
Arthur W. H. Chan
Christopher Carlsten
David J. Granville
author_sort Matthew R. Zeglinski
title Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
title_short Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
title_full Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
title_fullStr Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
title_full_unstemmed Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway
title_sort soluble wood smoke extract promotes barrier dysfunction in alveolar epithelial cells through a mapk signaling pathway
publisher Nature Portfolio
publishDate 2019
url https://doaj.org/article/1b6c2b4dbf5d4315845a64aa81cc9869
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