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Cigarette Smoke Modulates Repair and Innate Immunity following Injury to Airway Epithelial Cells
Cigarette smoking is the main risk factor associated with chronic obstructive pulmonary disease (COPD), and contributes to COPD development and progression by causing epithelial injury and inflammation. Whereas it is known that cigarette smoke (CS) may affect the innate immune function of airway epi...
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| Published in: | PloS one 2016-11, Vol.11 (11), p.e0166255-e0166255 |
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| container_issue | 11 |
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| creator | Amatngalim, Gimano D Broekman, Winifred Daniel, Nadia M van der Vlugt, Luciën E P M van Schadewijk, Annemarie Taube, Christian Hiemstra, Pieter S |
| description | Cigarette smoking is the main risk factor associated with chronic obstructive pulmonary disease (COPD), and contributes to COPD development and progression by causing epithelial injury and inflammation. Whereas it is known that cigarette smoke (CS) may affect the innate immune function of airway epithelial cells and epithelial repair, this has so far not been explored in an integrated design using mucociliary differentiated airway epithelial cells. In this study, we examined the effect of whole CS exposure on wound repair and the innate immune activity of mucociliary differentiated primary bronchial epithelial cells, upon injury induced by disruption of epithelial barrier integrity or by mechanical wounding. Upon mechanical injury CS caused a delayed recovery in the epithelial barrier integrity and wound closure. Furthermore CS enhanced innate immune responses, as demonstrated by increased expression of the antimicrobial protein RNase 7. These differential effects on epithelial repair and innate immunity were both mediated by CS-induced oxidative stress. Overall, our findings demonstrate modulation of wound repair and innate immune responses of injured airway epithelial cells that may contribute to COPD development and progression. |
| doi_str_mv | 10.1371/journal.pone.0166255 |
| format | article |
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Whereas it is known that cigarette smoke (CS) may affect the innate immune function of airway epithelial cells and epithelial repair, this has so far not been explored in an integrated design using mucociliary differentiated airway epithelial cells. In this study, we examined the effect of whole CS exposure on wound repair and the innate immune activity of mucociliary differentiated primary bronchial epithelial cells, upon injury induced by disruption of epithelial barrier integrity or by mechanical wounding. Upon mechanical injury CS caused a delayed recovery in the epithelial barrier integrity and wound closure. Furthermore CS enhanced innate immune responses, as demonstrated by increased expression of the antimicrobial protein RNase 7. These differential effects on epithelial repair and innate immunity were both mediated by CS-induced oxidative stress. Overall, our findings demonstrate modulation of wound repair and innate immune responses of injured airway epithelial cells that may contribute to COPD development and progression.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0166255</identifier><identifier>PMID: 27829065</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Biology and Life Sciences ; Blotting, Western ; Bronchi - cytology ; Bronchi - drug effects ; Cell adhesion & migration ; Cells, Cultured ; Chronic obstructive lung disease ; Chronic obstructive pulmonary disease ; Cigarette smoke ; Cigarette smoking ; Epidermal growth factor ; Epithelial cells ; Humans ; Immune response ; Immunity ; Immunity, Innate - drug effects ; Inflammation ; Injuries ; Innate immunity ; Integrity ; Lung cancer ; Lung diseases ; MAP Kinase Signaling System - physiology ; Medicine and Health Sciences ; Microscopy, Fluorescence ; Mucous membrane ; Obstructive lung disease ; Oxidative stress ; Oxidative Stress - drug effects ; Pathogens ; Real-Time Polymerase Chain Reaction ; Receptor, Epidermal Growth Factor - physiology ; Repair ; Respiratory Mucosa - drug effects ; Respiratory Mucosa - immunology ; Respiratory tract ; Ribonuclease ; Ribonuclease 7 ; Ribonucleases - metabolism ; Risk factors ; Rodents ; Signal transduction ; Signal Transduction - physiology ; Smoke ; Smoking ; Smoking - adverse effects ; Wound care ; Wound healing ; Wound Healing - drug effects ; Wounding</subject><ispartof>PloS one, 2016-11, Vol.11 (11), p.e0166255-e0166255</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Amatngalim et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Amatngalim et al 2016 Amatngalim et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c725t-9c62c2fcfb2c0ee74391764b639bbb7d98ab0735cbf24fefc31d8467e239b6dc3</citedby><cites>FETCH-LOGICAL-c725t-9c62c2fcfb2c0ee74391764b639bbb7d98ab0735cbf24fefc31d8467e239b6dc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/1837599550/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1837599550?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27829065$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Chen, Peter</contributor><creatorcontrib>Amatngalim, Gimano D</creatorcontrib><creatorcontrib>Broekman, Winifred</creatorcontrib><creatorcontrib>Daniel, Nadia M</creatorcontrib><creatorcontrib>van der Vlugt, Luciën E P M</creatorcontrib><creatorcontrib>van Schadewijk, Annemarie</creatorcontrib><creatorcontrib>Taube, Christian</creatorcontrib><creatorcontrib>Hiemstra, Pieter S</creatorcontrib><title>Cigarette Smoke Modulates Repair and Innate Immunity following Injury to Airway Epithelial Cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Cigarette smoking is the main risk factor associated with chronic obstructive pulmonary disease (COPD), and contributes to COPD development and progression by causing epithelial injury and inflammation. Whereas it is known that cigarette smoke (CS) may affect the innate immune function of airway epithelial cells and epithelial repair, this has so far not been explored in an integrated design using mucociliary differentiated airway epithelial cells. In this study, we examined the effect of whole CS exposure on wound repair and the innate immune activity of mucociliary differentiated primary bronchial epithelial cells, upon injury induced by disruption of epithelial barrier integrity or by mechanical wounding. Upon mechanical injury CS caused a delayed recovery in the epithelial barrier integrity and wound closure. Furthermore CS enhanced innate immune responses, as demonstrated by increased expression of the antimicrobial protein RNase 7. These differential effects on epithelial repair and innate immunity were both mediated by CS-induced oxidative stress. Overall, our findings demonstrate modulation of wound repair and innate immune responses of injured airway epithelial cells that may contribute to COPD development and progression.</description><subject>Biology and Life Sciences</subject><subject>Blotting, Western</subject><subject>Bronchi - cytology</subject><subject>Bronchi - drug effects</subject><subject>Cell adhesion & migration</subject><subject>Cells, Cultured</subject><subject>Chronic obstructive lung disease</subject><subject>Chronic obstructive pulmonary disease</subject><subject>Cigarette smoke</subject><subject>Cigarette smoking</subject><subject>Epidermal growth factor</subject><subject>Epithelial cells</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunity</subject><subject>Immunity, Innate - drug effects</subject><subject>Inflammation</subject><subject>Injuries</subject><subject>Innate immunity</subject><subject>Integrity</subject><subject>Lung cancer</subject><subject>Lung diseases</subject><subject>MAP Kinase Signaling System - 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Whereas it is known that cigarette smoke (CS) may affect the innate immune function of airway epithelial cells and epithelial repair, this has so far not been explored in an integrated design using mucociliary differentiated airway epithelial cells. In this study, we examined the effect of whole CS exposure on wound repair and the innate immune activity of mucociliary differentiated primary bronchial epithelial cells, upon injury induced by disruption of epithelial barrier integrity or by mechanical wounding. Upon mechanical injury CS caused a delayed recovery in the epithelial barrier integrity and wound closure. Furthermore CS enhanced innate immune responses, as demonstrated by increased expression of the antimicrobial protein RNase 7. These differential effects on epithelial repair and innate immunity were both mediated by CS-induced oxidative stress. Overall, our findings demonstrate modulation of wound repair and innate immune responses of injured airway epithelial cells that may contribute to COPD development and progression.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27829065</pmid><doi>10.1371/journal.pone.0166255</doi><tpages>e0166255</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-11, Vol.11 (11), p.e0166255-e0166255 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1837599550 |
| source | PMC (PubMed Central); Publicly Available Content (ProQuest) |
| subjects | Biology and Life Sciences Blotting, Western Bronchi - cytology Bronchi - drug effects Cell adhesion & migration Cells, Cultured Chronic obstructive lung disease Chronic obstructive pulmonary disease Cigarette smoke Cigarette smoking Epidermal growth factor Epithelial cells Humans Immune response Immunity Immunity, Innate - drug effects Inflammation Injuries Innate immunity Integrity Lung cancer Lung diseases MAP Kinase Signaling System - physiology Medicine and Health Sciences Microscopy, Fluorescence Mucous membrane Obstructive lung disease Oxidative stress Oxidative Stress - drug effects Pathogens Real-Time Polymerase Chain Reaction Receptor, Epidermal Growth Factor - physiology Repair Respiratory Mucosa - drug effects Respiratory Mucosa - immunology Respiratory tract Ribonuclease Ribonuclease 7 Ribonucleases - metabolism Risk factors Rodents Signal transduction Signal Transduction - physiology Smoke Smoking Smoking - adverse effects Wound care Wound healing Wound Healing - drug effects Wounding |
| title | Cigarette Smoke Modulates Repair and Innate Immunity following Injury to Airway Epithelial Cells |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-19T03%3A55%3A51IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cigarette%20Smoke%20Modulates%20Repair%20and%20Innate%20Immunity%20following%20Injury%20to%20Airway%20Epithelial%20Cells&rft.jtitle=PloS%20one&rft.au=Amatngalim,%20Gimano%20D&rft.date=2016-11-09&rft.volume=11&rft.issue=11&rft.spage=e0166255&rft.epage=e0166255&rft.pages=e0166255-e0166255&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0166255&rft_dat=%3Cgale_plos_%3EA471841353%3C/gale_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c725t-9c62c2fcfb2c0ee74391764b639bbb7d98ab0735cbf24fefc31d8467e239b6dc3%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=1837599550&rft_id=info:pmid/27829065&rft_galeid=A471841353&rfr_iscdi=true |