ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION
The current study examined the role of endothelin-1 (ET-1) in mediating acute lung inflammation induced by short-term cigarette smoke exposure. Hamsters received intraperitoneal injections of ET-1, followed by a 2-hour period of smoke exposure, for 3 consecutive days. The lungs were then evaluated f...
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| Veröffentlicht in: | Experimental lung research 2008-01, Vol.34 (10), p.707-716 |
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| creator | Bhavsar, Tapan M. Liu, Xingjian Cerreta, Joseph M. Liu, Ming Cantor, Jerome O. |
| description | The current study examined the role of endothelin-1 (ET-1) in mediating acute lung inflammation induced by short-term cigarette smoke exposure. Hamsters received intraperitoneal injections of ET-1, followed by a 2-hour period of smoke exposure, for 3 consecutive days. The lungs were then evaluated for inflammatory changes, using the following parameters: (1) lung histopathology, (2) neutrophil content of bronchoalveolar lavage fluid (BALF), (3) percent tumor necrosis factor receptor 1 (TNFR1)-labeled BALF macrophages, and (4) alveolar septal cell apoptosis. Results indicate that ET-1 significantly amplified the effect of smoke on each of these inflammatory markers and that these responses could be blocked by pretreatment with a novel endothelin receptor A antagonist, HJP272. In particular, exogenous ET-1 induced a marked increase in BALF neutrophils, consistent with a role for this mediator as an inflammatory cell "gatekeeper." |
| doi_str_mv | 10.1080/01902140802389701 |
| format | Article |
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Hamsters received intraperitoneal injections of ET-1, followed by a 2-hour period of smoke exposure, for 3 consecutive days. The lungs were then evaluated for inflammatory changes, using the following parameters: (1) lung histopathology, (2) neutrophil content of bronchoalveolar lavage fluid (BALF), (3) percent tumor necrosis factor receptor 1 (TNFR1)-labeled BALF macrophages, and (4) alveolar septal cell apoptosis. Results indicate that ET-1 significantly amplified the effect of smoke on each of these inflammatory markers and that these responses could be blocked by pretreatment with a novel endothelin receptor A antagonist, HJP272. In particular, exogenous ET-1 induced a marked increase in BALF neutrophils, consistent with a role for this mediator as an inflammatory cell "gatekeeper."</description><identifier>ISSN: 0190-2148</identifier><identifier>EISSN: 1521-0499</identifier><identifier>DOI: 10.1080/01902140802389701</identifier><identifier>PMID: 19085567</identifier><language>eng</language><publisher>England: Informa UK Ltd</publisher><subject>Acute Disease ; Animals ; Apoptosis ; cigarette ; Cricetinae ; endothelin ; Endothelin-1 - pharmacology ; Hydroxyquinolines - pharmacology ; inflammation ; lung ; Lung - pathology ; Mesocricetus ; Pneumonia - etiology ; Receptors, Tumor Necrosis Factor, Type I - analysis ; smoke ; Tobacco Smoke Pollution - adverse effects</subject><ispartof>Experimental lung research, 2008-01, Vol.34 (10), p.707-716</ispartof><rights>2008 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-7f02a3efd225cd91d33cc2e615bd5b7ff3565e8b2ad7b5c480905d6e0ef485473</citedby><cites>FETCH-LOGICAL-c404t-7f02a3efd225cd91d33cc2e615bd5b7ff3565e8b2ad7b5c480905d6e0ef485473</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.1080/01902140802389701$$EPDF$$P50$$Ginformaworld$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.1080/01902140802389701$$EHTML$$P50$$Ginformaworld$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,59646,60435,61220,61401</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19085567$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bhavsar, Tapan M.</creatorcontrib><creatorcontrib>Liu, Xingjian</creatorcontrib><creatorcontrib>Cerreta, Joseph M.</creatorcontrib><creatorcontrib>Liu, Ming</creatorcontrib><creatorcontrib>Cantor, Jerome O.</creatorcontrib><title>ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION</title><title>Experimental lung research</title><addtitle>Exp Lung Res</addtitle><description>The current study examined the role of endothelin-1 (ET-1) in mediating acute lung inflammation induced by short-term cigarette smoke exposure. Hamsters received intraperitoneal injections of ET-1, followed by a 2-hour period of smoke exposure, for 3 consecutive days. The lungs were then evaluated for inflammatory changes, using the following parameters: (1) lung histopathology, (2) neutrophil content of bronchoalveolar lavage fluid (BALF), (3) percent tumor necrosis factor receptor 1 (TNFR1)-labeled BALF macrophages, and (4) alveolar septal cell apoptosis. Results indicate that ET-1 significantly amplified the effect of smoke on each of these inflammatory markers and that these responses could be blocked by pretreatment with a novel endothelin receptor A antagonist, HJP272. In particular, exogenous ET-1 induced a marked increase in BALF neutrophils, consistent with a role for this mediator as an inflammatory cell "gatekeeper."</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>cigarette</subject><subject>Cricetinae</subject><subject>endothelin</subject><subject>Endothelin-1 - pharmacology</subject><subject>Hydroxyquinolines - pharmacology</subject><subject>inflammation</subject><subject>lung</subject><subject>Lung - pathology</subject><subject>Mesocricetus</subject><subject>Pneumonia - etiology</subject><subject>Receptors, Tumor Necrosis Factor, Type I - analysis</subject><subject>smoke</subject><subject>Tobacco Smoke Pollution - adverse effects</subject><issn>0190-2148</issn><issn>1521-0499</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kGFLwzAQhoMobk5_gF-kf6B6SZs2RRFKl81i1wprP5e0SdhGt450Q_bv7dhARNinO-7e5-XuRegRwzMGBi-AAyDY7VvisMAHfIWGmBJsgxsE12h43Nu9gA3QXdetAIBQ5t2iQT9nlHr-EL3zdJzlHzyJUxtbX1nO0zwOcz635rPsk9txOi4iPrbCqMi5lRTp1IrTSRLOZmEeZ-k9utGi6dTDuY5QMeF59GEn2TSOwsSuXXB3tq-BCEdpSQitZYCl49Q1UR6mlaSVr7VDPapYRYT0K1q7DAKg0lOgtMuo6zsjhE--tWm7zihdbs1yLcyhxFAesyj_ZdEzTydmu6_WSv4S5-d7wdtJsNzo1qzFd2saWe7EoWmNNmJTL7vSueT_-gdfKNHsFrUwqly1e7Pp87hw3Q8pSnhW</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Bhavsar, Tapan M.</creator><creator>Liu, Xingjian</creator><creator>Cerreta, Joseph M.</creator><creator>Liu, Ming</creator><creator>Cantor, Jerome O.</creator><general>Informa UK Ltd</general><general>Taylor & Francis</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20080101</creationdate><title>ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION</title><author>Bhavsar, Tapan M. ; Liu, Xingjian ; Cerreta, Joseph M. ; Liu, Ming ; Cantor, Jerome O.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-7f02a3efd225cd91d33cc2e615bd5b7ff3565e8b2ad7b5c480905d6e0ef485473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>cigarette</topic><topic>Cricetinae</topic><topic>endothelin</topic><topic>Endothelin-1 - pharmacology</topic><topic>Hydroxyquinolines - pharmacology</topic><topic>inflammation</topic><topic>lung</topic><topic>Lung - pathology</topic><topic>Mesocricetus</topic><topic>Pneumonia - etiology</topic><topic>Receptors, Tumor Necrosis Factor, Type I - analysis</topic><topic>smoke</topic><topic>Tobacco Smoke Pollution - adverse effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bhavsar, Tapan M.</creatorcontrib><creatorcontrib>Liu, Xingjian</creatorcontrib><creatorcontrib>Cerreta, Joseph M.</creatorcontrib><creatorcontrib>Liu, Ming</creatorcontrib><creatorcontrib>Cantor, Jerome O.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Experimental lung research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bhavsar, Tapan M.</au><au>Liu, Xingjian</au><au>Cerreta, Joseph M.</au><au>Liu, Ming</au><au>Cantor, Jerome O.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION</atitle><jtitle>Experimental lung research</jtitle><addtitle>Exp Lung Res</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>34</volume><issue>10</issue><spage>707</spage><epage>716</epage><pages>707-716</pages><issn>0190-2148</issn><eissn>1521-0499</eissn><abstract>The current study examined the role of endothelin-1 (ET-1) in mediating acute lung inflammation induced by short-term cigarette smoke exposure. Hamsters received intraperitoneal injections of ET-1, followed by a 2-hour period of smoke exposure, for 3 consecutive days. The lungs were then evaluated for inflammatory changes, using the following parameters: (1) lung histopathology, (2) neutrophil content of bronchoalveolar lavage fluid (BALF), (3) percent tumor necrosis factor receptor 1 (TNFR1)-labeled BALF macrophages, and (4) alveolar septal cell apoptosis. Results indicate that ET-1 significantly amplified the effect of smoke on each of these inflammatory markers and that these responses could be blocked by pretreatment with a novel endothelin receptor A antagonist, HJP272. In particular, exogenous ET-1 induced a marked increase in BALF neutrophils, consistent with a role for this mediator as an inflammatory cell "gatekeeper."</abstract><cop>England</cop><pub>Informa UK Ltd</pub><pmid>19085567</pmid><doi>10.1080/01902140802389701</doi><tpages>10</tpages></addata></record> |
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| ispartof | Experimental lung research, 2008-01, Vol.34 (10), p.707-716 |
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| source | MEDLINE; Taylor & Francis Journals Complete |
| subjects | Acute Disease Animals Apoptosis cigarette Cricetinae endothelin Endothelin-1 - pharmacology Hydroxyquinolines - pharmacology inflammation lung Lung - pathology Mesocricetus Pneumonia - etiology Receptors, Tumor Necrosis Factor, Type I - analysis smoke Tobacco Smoke Pollution - adverse effects |
| title | ENDOTHELIN-1 POTENTIATES SMOKE-INDUCED ACUTE LUNG INFLAMMATION |
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