Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs

Abstract Recent clinical studies have suggested that inhalation of incense smoke (IS) may result in impaired lung function and asthma. However, there is little experimental evidence to link IS with airway hyperresponsiveness (AHR) and bronchial epithelial barrier function. Using mouse and cell cultu...

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Autores principales:	Norio Yamamoto, Keiko Kan-o, Miyoko Tatsuta, Yumiko Ishii, Tomohiro Ogawa, Seiji Shinozaki, Satoru Fukuyama, Yoichi Nakanishi, Koichiro Matsumoto
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/664a47ed5dde424bb255ed50971b71cf
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spelling	oai:doaj.org-article:664a47ed5dde424bb255ed50971b71cf2021-12-02T18:17:53ZIncense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs10.1038/s41598-021-86745-72045-2322https://doaj.org/article/664a47ed5dde424bb255ed50971b71cf2021-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-86745-7https://doaj.org/toc/2045-2322Abstract Recent clinical studies have suggested that inhalation of incense smoke (IS) may result in impaired lung function and asthma. However, there is little experimental evidence to link IS with airway hyperresponsiveness (AHR) and bronchial epithelial barrier function. Using mouse and cell culture models, we evaluated the effects of IS exposure on AHR, expression of multiple epithelial tight junction (TJ)- and adherens junction-associated mRNAs and proteins in the lungs, and the barrier function of bronchial epithelial cells assessed by transepithelial electronic resistance (TEER). Exposure of BALB/c mice to IS increased AHR and inflammatory macrophage recruitment to BALF; reduced claudin-1, -2, -3, -7, -10b, -12, -15, and -18, occludin, zonula occludens-1 [ZO-1], and E-cadherin mRNA expression; and caused discontinuity of claudin-2 and ZO-1 protein immunostaining in lung tissue. IS extract dose-dependently decreased TEER and increased reactive oxygen species production in bronchial epithelial cell cultures. Treatment with N-acetyl-l-cysteine, but not glucocorticosteroids or long-acting β2-agonists, prevented the detrimental effects of IS. IS exposure can be problematic for respiratory health, as evidenced by AHR, increased recruitment of inflammatory macrophages and disruption of TJ proteins in the lung, and damage to epithelial barrier function. However, antioxidants may be useful for the treatment of IS-induced airway dysfunction.Norio YamamotoKeiko Kan-oMiyoko TatsutaYumiko IshiiTomohiro OgawaSeiji ShinozakiSatoru FukuyamaYoichi NakanishiKoichiro MatsumotoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-14 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Norio Yamamoto Keiko Kan-o Miyoko Tatsuta Yumiko Ishii Tomohiro Ogawa Seiji Shinozaki Satoru Fukuyama Yoichi Nakanishi Koichiro Matsumoto Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
description	Abstract Recent clinical studies have suggested that inhalation of incense smoke (IS) may result in impaired lung function and asthma. However, there is little experimental evidence to link IS with airway hyperresponsiveness (AHR) and bronchial epithelial barrier function. Using mouse and cell culture models, we evaluated the effects of IS exposure on AHR, expression of multiple epithelial tight junction (TJ)- and adherens junction-associated mRNAs and proteins in the lungs, and the barrier function of bronchial epithelial cells assessed by transepithelial electronic resistance (TEER). Exposure of BALB/c mice to IS increased AHR and inflammatory macrophage recruitment to BALF; reduced claudin-1, -2, -3, -7, -10b, -12, -15, and -18, occludin, zonula occludens-1 [ZO-1], and E-cadherin mRNA expression; and caused discontinuity of claudin-2 and ZO-1 protein immunostaining in lung tissue. IS extract dose-dependently decreased TEER and increased reactive oxygen species production in bronchial epithelial cell cultures. Treatment with N-acetyl-l-cysteine, but not glucocorticosteroids or long-acting β2-agonists, prevented the detrimental effects of IS. IS exposure can be problematic for respiratory health, as evidenced by AHR, increased recruitment of inflammatory macrophages and disruption of TJ proteins in the lung, and damage to epithelial barrier function. However, antioxidants may be useful for the treatment of IS-induced airway dysfunction.
format	article
author	Norio Yamamoto Keiko Kan-o Miyoko Tatsuta Yumiko Ishii Tomohiro Ogawa Seiji Shinozaki Satoru Fukuyama Yoichi Nakanishi Koichiro Matsumoto
author_facet	Norio Yamamoto Keiko Kan-o Miyoko Tatsuta Yumiko Ishii Tomohiro Ogawa Seiji Shinozaki Satoru Fukuyama Yoichi Nakanishi Koichiro Matsumoto
author_sort	Norio Yamamoto
title	Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
title_short	Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
title_full	Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
title_fullStr	Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
title_full_unstemmed	Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
title_sort	incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/664a47ed5dde424bb255ed50971b71cf
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Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs

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