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Erdosteine effects cell barriers causing decreased inflammation and increased pulmonary function in asthmatic mice exposed to nanoparticulate pollution

Objectives: Erdosteine, an oral mucoactive anti-oxidant molecule, interferes with the pathological processes seen in respiratory disorders including thickened or increased mucus production, increased oxidative stress, and chronic inflammation; however, its efficacy as an asthma therapy remains to be...

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Published in:European journal of inflammation 2023-04, Vol.21
Main Authors: An, Min-Hyeok, Lee, Pureun-Haneul, Choi, Seon-Muk, Hwang, DaYeon, Park, Shinhee, Baek, Ae-Rin, Jang, An-Soo
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container_title European journal of inflammation
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Lee, Pureun-Haneul
Choi, Seon-Muk
Hwang, DaYeon
Park, Shinhee
Baek, Ae-Rin
Jang, An-Soo
description Objectives: Erdosteine, an oral mucoactive anti-oxidant molecule, interferes with the pathological processes seen in respiratory disorders including thickened or increased mucus production, increased oxidative stress, and chronic inflammation; however, its efficacy as an asthma therapy remains to be fully clarified. Therefore, the aim of this study was to assess the effects of erdosteine on epithelial barrier function in asthma. Methods: To investigate the effects of erdosteine on cell barrier expression in a mouse model of asthma, BALB/c mice (n = 8 per group; total of 40 mice) were exposed to saline (Sham), ovalbumin (OVA), or OVA plus TiO2 inhalation (200 μg/m3; OVA + TiO2). The mice were then treated with erdosteine orally (OVA + TiO2 + Erdos) or intraperitoneal dexamethasone (OVA + TiO2 + Dex). Bronchoalveolar lavage and histology were performed. Enhanced pause was used as an indicator of pulmonary function, and samples were collected. The effect of erdosteine on cell barrier expression was assessed by immunoblotting and immunohistochemical analyses. Results: OVA + TiO2 + erdosteine mice exhibited decreased inflammation, and mucous gland hyperplasia, and increased pulmonary function compared with OVA + TiO2 mice. Levels of claudin (CLDN)-4 and nectin-4 protein were higher in lung tissue from OVA + TiO2 mice than Sham and OVA mice, and were reduced by erdosteine treatment. In contrast, CLDN14 and CLDN18 protein levels were lower in lung tissue from OVA + TiO2 mice than those from control mice, but were increased by treatment with erdosteine. Conclusion: Cell barriers are involved in airway inflammation in asthma patients, and erdosteine reduces airway inflammation by changing the cell barrier.
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Therefore, the aim of this study was to assess the effects of erdosteine on epithelial barrier function in asthma. Methods: To investigate the effects of erdosteine on cell barrier expression in a mouse model of asthma, BALB/c mice (n = 8 per group; total of 40 mice) were exposed to saline (Sham), ovalbumin (OVA), or OVA plus TiO2 inhalation (200 μg/m3; OVA + TiO2). The mice were then treated with erdosteine orally (OVA + TiO2 + Erdos) or intraperitoneal dexamethasone (OVA + TiO2 + Dex). Bronchoalveolar lavage and histology were performed. Enhanced pause was used as an indicator of pulmonary function, and samples were collected. The effect of erdosteine on cell barrier expression was assessed by immunoblotting and immunohistochemical analyses. Results: OVA + TiO2 + erdosteine mice exhibited decreased inflammation, and mucous gland hyperplasia, and increased pulmonary function compared with OVA + TiO2 mice. Levels of claudin (CLDN)-4 and nectin-4 protein were higher in lung tissue from OVA + TiO2 mice than Sham and OVA mice, and were reduced by erdosteine treatment. In contrast, CLDN14 and CLDN18 protein levels were lower in lung tissue from OVA + TiO2 mice than those from control mice, but were increased by treatment with erdosteine. Conclusion: Cell barriers are involved in airway inflammation in asthma patients, and erdosteine reduces airway inflammation by changing the cell barrier.</description><identifier>ISSN: 1721-727X</identifier><identifier>EISSN: 2058-7392</identifier><identifier>DOI: 10.1177/1721727X231172836</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Antioxidants ; Asthma ; Inflammation ; Nanoparticles ; Oxidative stress</subject><ispartof>European journal of inflammation, 2023-04, Vol.21</ispartof><rights>The Author(s) 2023</rights><rights>The Author(s) 2023. This work is licensed under the Creative Commons Attribution – Non-Commercial License https://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c373t-6ddf7066c072c34dd8d68bb9a513ef16de53522c8ea0985ccc393fb1e69ded6c3</cites><orcidid>0000-0001-5343-023X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1177/1721727X231172836$$EPDF$$P50$$Gsage$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2920205815?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,21966,25753,27853,27924,27925,37012,44590,44945,45333</link.rule.ids></links><search><creatorcontrib>An, Min-Hyeok</creatorcontrib><creatorcontrib>Lee, Pureun-Haneul</creatorcontrib><creatorcontrib>Choi, Seon-Muk</creatorcontrib><creatorcontrib>Hwang, DaYeon</creatorcontrib><creatorcontrib>Park, Shinhee</creatorcontrib><creatorcontrib>Baek, Ae-Rin</creatorcontrib><creatorcontrib>Jang, An-Soo</creatorcontrib><title>Erdosteine effects cell barriers causing decreased inflammation and increased pulmonary function in asthmatic mice exposed to nanoparticulate pollution</title><title>European journal of inflammation</title><description>Objectives: Erdosteine, an oral mucoactive anti-oxidant molecule, interferes with the pathological processes seen in respiratory disorders including thickened or increased mucus production, increased oxidative stress, and chronic inflammation; however, its efficacy as an asthma therapy remains to be fully clarified. Therefore, the aim of this study was to assess the effects of erdosteine on epithelial barrier function in asthma. Methods: To investigate the effects of erdosteine on cell barrier expression in a mouse model of asthma, BALB/c mice (n = 8 per group; total of 40 mice) were exposed to saline (Sham), ovalbumin (OVA), or OVA plus TiO2 inhalation (200 μg/m3; OVA + TiO2). The mice were then treated with erdosteine orally (OVA + TiO2 + Erdos) or intraperitoneal dexamethasone (OVA + TiO2 + Dex). Bronchoalveolar lavage and histology were performed. Enhanced pause was used as an indicator of pulmonary function, and samples were collected. The effect of erdosteine on cell barrier expression was assessed by immunoblotting and immunohistochemical analyses. Results: OVA + TiO2 + erdosteine mice exhibited decreased inflammation, and mucous gland hyperplasia, and increased pulmonary function compared with OVA + TiO2 mice. Levels of claudin (CLDN)-4 and nectin-4 protein were higher in lung tissue from OVA + TiO2 mice than Sham and OVA mice, and were reduced by erdosteine treatment. In contrast, CLDN14 and CLDN18 protein levels were lower in lung tissue from OVA + TiO2 mice than those from control mice, but were increased by treatment with erdosteine. 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Therefore, the aim of this study was to assess the effects of erdosteine on epithelial barrier function in asthma. Methods: To investigate the effects of erdosteine on cell barrier expression in a mouse model of asthma, BALB/c mice (n = 8 per group; total of 40 mice) were exposed to saline (Sham), ovalbumin (OVA), or OVA plus TiO2 inhalation (200 μg/m3; OVA + TiO2). The mice were then treated with erdosteine orally (OVA + TiO2 + Erdos) or intraperitoneal dexamethasone (OVA + TiO2 + Dex). Bronchoalveolar lavage and histology were performed. Enhanced pause was used as an indicator of pulmonary function, and samples were collected. The effect of erdosteine on cell barrier expression was assessed by immunoblotting and immunohistochemical analyses. Results: OVA + TiO2 + erdosteine mice exhibited decreased inflammation, and mucous gland hyperplasia, and increased pulmonary function compared with OVA + TiO2 mice. Levels of claudin (CLDN)-4 and nectin-4 protein were higher in lung tissue from OVA + TiO2 mice than Sham and OVA mice, and were reduced by erdosteine treatment. In contrast, CLDN14 and CLDN18 protein levels were lower in lung tissue from OVA + TiO2 mice than those from control mice, but were increased by treatment with erdosteine. Conclusion: Cell barriers are involved in airway inflammation in asthma patients, and erdosteine reduces airway inflammation by changing the cell barrier.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><doi>10.1177/1721727X231172836</doi><orcidid>https://orcid.org/0000-0001-5343-023X</orcidid><oa>free_for_read</oa></addata></record>
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subjects Antioxidants
Asthma
Inflammation
Nanoparticles
Oxidative stress
title Erdosteine effects cell barriers causing decreased inflammation and increased pulmonary function in asthmatic mice exposed to nanoparticulate pollution
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