Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E
Abstract Porcine reproductive and respiratory syndrome virus (PRRSV) infection results in extensive tissue inflammation and damage, which are believed to be responsible for increased susceptibility to secondary infection and even for death. However, its pathogenic mechanisms are not fully understood...
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Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2013-08, Vol.442 (2), p.156-162 |
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description | Abstract Porcine reproductive and respiratory syndrome virus (PRRSV) infection results in extensive tissue inflammation and damage, which are believed to be responsible for increased susceptibility to secondary infection and even for death. However, its pathogenic mechanisms are not fully understood. To explore the mechanism underlying the PRRSV-induced tissue inflammation and damage, we investigated whether PRRSV activates porcine alveolar macrophage (PAM) inflammasomes which mediate por-IL-1β maturation/release and subsequently induce tissue inflammation and injury. Our results showed that PRRSV and its small envelope protein E significantly increased IL-1β release from LPS-primed PAMs; however, only PRRSV not protein E significantly increased IL-1β release from no-LPS-primed PAMs, which indicates PRRSV can activate inflammasomes of PAMs by its encoded protein E. These results provide a molecular basis for the pathogenic mechanism of PRRSV on inducing extensive tissue inflammation and damage, and suggest that the inflammasome may provide a potential therapeutic target for PRRS prevention and treatment. |
doi_str_mv | 10.1016/j.virol.2013.04.007 |
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However, its pathogenic mechanisms are not fully understood. To explore the mechanism underlying the PRRSV-induced tissue inflammation and damage, we investigated whether PRRSV activates porcine alveolar macrophage (PAM) inflammasomes which mediate por-IL-1β maturation/release and subsequently induce tissue inflammation and injury. Our results showed that PRRSV and its small envelope protein E significantly increased IL-1β release from LPS-primed PAMs; however, only PRRSV not protein E significantly increased IL-1β release from no-LPS-primed PAMs, which indicates PRRSV can activate inflammasomes of PAMs by its encoded protein E. These results provide a molecular basis for the pathogenic mechanism of PRRSV on inducing extensive tissue inflammation and damage, and suggest that the inflammasome may provide a potential therapeutic target for PRRS prevention and treatment.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/j.virol.2013.04.007</identifier><identifier>PMID: 23664331</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Cells, Cultured ; Envelope protein E ; Host-Pathogen Interactions ; Infectious Disease ; Inflammasomes ; Inflammasomes - immunology ; Interleukin-1beta - immunology ; Interleukin-1β ; Macrophages ; Macrophages, Alveolar - immunology ; Macrophages, Alveolar - virology ; Porcine reproductive and respiratory syndrome virus ; Porcine respiratory and reproductive syndrome virus ; Porcine respiratory and reproductive syndrome virus - immunology ; Swine ; Viral Envelope Proteins - immunology</subject><ispartof>Virology (New York, N.Y.), 2013-08, Vol.442 (2), p.156-162</ispartof><rights>Elsevier Inc.</rights><rights>2013 Elsevier Inc.</rights><rights>Copyright © 2013 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c492t-aaa0e38f6b00743671ea0c8662b1a12646efacbd8e3596cdfe3d4efd8536ce303</citedby><cites>FETCH-LOGICAL-c492t-aaa0e38f6b00743671ea0c8662b1a12646efacbd8e3596cdfe3d4efd8536ce303</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0042682213002018$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23664331$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Kao</creatorcontrib><creatorcontrib>Hou, Qiang</creatorcontrib><creatorcontrib>Zhong, Zhenyu</creatorcontrib><creatorcontrib>Li, Xiujin</creatorcontrib><creatorcontrib>Chen, Huihui</creatorcontrib><creatorcontrib>Li, Wenyan</creatorcontrib><creatorcontrib>Wen, Jiexia</creatorcontrib><creatorcontrib>Wang, Liyue</creatorcontrib><creatorcontrib>Liu, Weiquan</creatorcontrib><creatorcontrib>Zhong, Fei</creatorcontrib><title>Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>Abstract Porcine reproductive and respiratory syndrome virus (PRRSV) infection results in extensive tissue inflammation and damage, which are believed to be responsible for increased susceptibility to secondary infection and even for death. However, its pathogenic mechanisms are not fully understood. To explore the mechanism underlying the PRRSV-induced tissue inflammation and damage, we investigated whether PRRSV activates porcine alveolar macrophage (PAM) inflammasomes which mediate por-IL-1β maturation/release and subsequently induce tissue inflammation and injury. Our results showed that PRRSV and its small envelope protein E significantly increased IL-1β release from LPS-primed PAMs; however, only PRRSV not protein E significantly increased IL-1β release from no-LPS-primed PAMs, which indicates PRRSV can activate inflammasomes of PAMs by its encoded protein E. These results provide a molecular basis for the pathogenic mechanism of PRRSV on inducing extensive tissue inflammation and damage, and suggest that the inflammasome may provide a potential therapeutic target for PRRS prevention and treatment.</description><subject>Animals</subject><subject>Cells, Cultured</subject><subject>Envelope protein E</subject><subject>Host-Pathogen Interactions</subject><subject>Infectious Disease</subject><subject>Inflammasomes</subject><subject>Inflammasomes - immunology</subject><subject>Interleukin-1beta - immunology</subject><subject>Interleukin-1β</subject><subject>Macrophages</subject><subject>Macrophages, Alveolar - immunology</subject><subject>Macrophages, Alveolar - virology</subject><subject>Porcine reproductive and respiratory syndrome virus</subject><subject>Porcine respiratory and reproductive syndrome virus</subject><subject>Porcine respiratory and reproductive syndrome virus - immunology</subject><subject>Swine</subject><subject>Viral Envelope Proteins - immunology</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNks-KFDEQxoMo7rj6BILk6KXb_OlJ9xwUZNl1FxYU1HOoSao1Yzppk-6GeQcf2rQzevCip5DUV9-Pqi-EPOes5oyrV4d6cSn6WjAua9bUjLUPyIaznaqYbPhDsmGsEZXqhLggT3I-sHJvW_aYXAipVCMl35AfH2IyLiBNOKZoZzO5BSkEWx7y6BJMMR1pPgab4oC0EOdMYVXBhJm60HsYBsilmGns6Xi2A79g9JDoACbF8St8KfXFAXVTpnkA7ymGBX0ckRbwhC7Q66fkUQ8-47PzeUk-31x_urqt7t-_u7t6e1-ZZiemCgAYyq5X-zJyI1XLEZjplBJ7DlyoRmEPZm87lNudMrZHaRvsbbeVyqBk8pK8PPkW8vcZ86QHlw16DwHjnDXfFuPi3P6HVKqdKJiOF6k8ScvAOSfs9ZjcAOmoOdNrYvqgfyWm18Q0a3ShlK4XZ8C8H9D-6fkdURG8PgmwbGRxmHQ2DoNB6xKaSdvo_gF481e_8S44A_4bHjEf4pxCWbbmOgvN9Mf106x_hkvGik8nfwKbCcEv</recordid><startdate>20130801</startdate><enddate>20130801</enddate><creator>Zhang, Kao</creator><creator>Hou, Qiang</creator><creator>Zhong, Zhenyu</creator><creator>Li, Xiujin</creator><creator>Chen, Huihui</creator><creator>Li, Wenyan</creator><creator>Wen, Jiexia</creator><creator>Wang, Liyue</creator><creator>Liu, Weiquan</creator><creator>Zhong, Fei</creator><general>Elsevier Inc</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7T5</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20130801</creationdate><title>Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E</title><author>Zhang, Kao ; Hou, Qiang ; Zhong, Zhenyu ; Li, Xiujin ; Chen, Huihui ; Li, Wenyan ; Wen, Jiexia ; Wang, Liyue ; Liu, Weiquan ; Zhong, Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c492t-aaa0e38f6b00743671ea0c8662b1a12646efacbd8e3596cdfe3d4efd8536ce303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Cells, Cultured</topic><topic>Envelope protein E</topic><topic>Host-Pathogen Interactions</topic><topic>Infectious Disease</topic><topic>Inflammasomes</topic><topic>Inflammasomes - immunology</topic><topic>Interleukin-1beta - immunology</topic><topic>Interleukin-1β</topic><topic>Macrophages</topic><topic>Macrophages, Alveolar - immunology</topic><topic>Macrophages, Alveolar - virology</topic><topic>Porcine reproductive and respiratory syndrome virus</topic><topic>Porcine respiratory and reproductive syndrome virus</topic><topic>Porcine respiratory and reproductive syndrome virus - immunology</topic><topic>Swine</topic><topic>Viral Envelope Proteins - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Kao</creatorcontrib><creatorcontrib>Hou, Qiang</creatorcontrib><creatorcontrib>Zhong, Zhenyu</creatorcontrib><creatorcontrib>Li, Xiujin</creatorcontrib><creatorcontrib>Chen, Huihui</creatorcontrib><creatorcontrib>Li, Wenyan</creatorcontrib><creatorcontrib>Wen, Jiexia</creatorcontrib><creatorcontrib>Wang, Liyue</creatorcontrib><creatorcontrib>Liu, Weiquan</creatorcontrib><creatorcontrib>Zhong, Fei</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Kao</au><au>Hou, Qiang</au><au>Zhong, Zhenyu</au><au>Li, Xiujin</au><au>Chen, Huihui</au><au>Li, Wenyan</au><au>Wen, Jiexia</au><au>Wang, Liyue</au><au>Liu, Weiquan</au><au>Zhong, Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>2013-08-01</date><risdate>2013</risdate><volume>442</volume><issue>2</issue><spage>156</spage><epage>162</epage><pages>156-162</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>Abstract Porcine reproductive and respiratory syndrome virus (PRRSV) infection results in extensive tissue inflammation and damage, which are believed to be responsible for increased susceptibility to secondary infection and even for death. However, its pathogenic mechanisms are not fully understood. To explore the mechanism underlying the PRRSV-induced tissue inflammation and damage, we investigated whether PRRSV activates porcine alveolar macrophage (PAM) inflammasomes which mediate por-IL-1β maturation/release and subsequently induce tissue inflammation and injury. Our results showed that PRRSV and its small envelope protein E significantly increased IL-1β release from LPS-primed PAMs; however, only PRRSV not protein E significantly increased IL-1β release from no-LPS-primed PAMs, which indicates PRRSV can activate inflammasomes of PAMs by its encoded protein E. These results provide a molecular basis for the pathogenic mechanism of PRRSV on inducing extensive tissue inflammation and damage, and suggest that the inflammasome may provide a potential therapeutic target for PRRS prevention and treatment.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>23664331</pmid><doi>10.1016/j.virol.2013.04.007</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Cells, Cultured Envelope protein E Host-Pathogen Interactions Infectious Disease Inflammasomes Inflammasomes - immunology Interleukin-1beta - immunology Interleukin-1β Macrophages Macrophages, Alveolar - immunology Macrophages, Alveolar - virology Porcine reproductive and respiratory syndrome virus Porcine respiratory and reproductive syndrome virus Porcine respiratory and reproductive syndrome virus - immunology Swine Viral Envelope Proteins - immunology |
title | Porcine reproductive and respiratory syndrome virus activates inflammasomes of porcine alveolar macrophages via its small envelope protein E |
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