Newcastle disease virus infection induces activation of the NLRP3 inflammasome
Abstract Inflammatory responses are important aspects of the innate immune system during virus infection. We found that Newcastle disease virus can induce inflammasome activation in the human macrophage-like cell line THP-1. Viral replication was required for inflammasome activation, and small hairp...
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Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2016-09, Vol.496, p.90-96 |
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creator | Wang, Binbin Zhu, Jie Li, Dandan Wang, Yang Zhan, Yuan Tan, Lei Qiu, Xusheng Sun, Yingjie Song, Cuiping Meng, Chunchun Ying, Liao Xiang, Mao Meng, Guangxun Ding, Chan |
description | Abstract Inflammatory responses are important aspects of the innate immune system during virus infection. We found that Newcastle disease virus can induce inflammasome activation in the human macrophage-like cell line THP-1. Viral replication was required for inflammasome activation, and small hairpin RNA knockdown experiments indicated that IL-1β secretion was mediated by the NLRP3 inflammasome. We also verified the results in LPS-primed bone marrow-derived macrophages (BMDMs) from NLRP3-deficient and wild type mice. NDV is considered to be a promising oncolytic virus. Stimulating the immune system has been proposed as a key mechanism of oncolytic specificity, and the inflammasome appears to be an important mechanism by which NDV is controlled. Knockdown of inflammasome components or chemical inhibition of caspase-1 activity shows that cell survival was augmented and benefited NDV replication. This study shows that NLRP3 inflammasome activation is an innate cellular response to NDV infection and offers insights into the oncolytic specificity of NDV. |
doi_str_mv | 10.1016/j.virol.2016.05.023 |
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We found that Newcastle disease virus can induce inflammasome activation in the human macrophage-like cell line THP-1. Viral replication was required for inflammasome activation, and small hairpin RNA knockdown experiments indicated that IL-1β secretion was mediated by the NLRP3 inflammasome. We also verified the results in LPS-primed bone marrow-derived macrophages (BMDMs) from NLRP3-deficient and wild type mice. NDV is considered to be a promising oncolytic virus. Stimulating the immune system has been proposed as a key mechanism of oncolytic specificity, and the inflammasome appears to be an important mechanism by which NDV is controlled. Knockdown of inflammasome components or chemical inhibition of caspase-1 activity shows that cell survival was augmented and benefited NDV replication. This study shows that NLRP3 inflammasome activation is an innate cellular response to NDV infection and offers insights into the oncolytic specificity of NDV.</description><identifier>ISSN: 0042-6822</identifier><identifier>EISSN: 1096-0341</identifier><identifier>DOI: 10.1016/j.virol.2016.05.023</identifier><identifier>PMID: 27269659</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Caspase 1 - metabolism ; Caspase Inhibitors - pharmacology ; Caspase-1 ; Cell Line ; Disease Models, Animal ; Female ; Humans ; Infectious Disease ; Inflammasome ; Inflammasomes - metabolism ; Interleukin-1beta - biosynthesis ; Macrophage Activation - immunology ; Macrophages - immunology ; Macrophages - metabolism ; Macrophages - virology ; Mice ; Mice, Knockout ; NDV ; Newcastle Disease - genetics ; Newcastle Disease - metabolism ; Newcastle Disease - virology ; Newcastle disease virus - physiology ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; NLRP3 ; THP‐1 cells ; Virus Replication</subject><ispartof>Virology (New York, N.Y.), 2016-09, Vol.496, p.90-96</ispartof><rights>Elsevier Inc.</rights><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c414t-67194245f2fd5fba22311a22ba53d794d31f17ffccf7676f09b4def5b5030c2f3</citedby><cites>FETCH-LOGICAL-c414t-67194245f2fd5fba22311a22ba53d794d31f17ffccf7676f09b4def5b5030c2f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0042682216301325$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65534</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27269659$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Binbin</creatorcontrib><creatorcontrib>Zhu, Jie</creatorcontrib><creatorcontrib>Li, Dandan</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Zhan, Yuan</creatorcontrib><creatorcontrib>Tan, Lei</creatorcontrib><creatorcontrib>Qiu, Xusheng</creatorcontrib><creatorcontrib>Sun, Yingjie</creatorcontrib><creatorcontrib>Song, Cuiping</creatorcontrib><creatorcontrib>Meng, Chunchun</creatorcontrib><creatorcontrib>Ying, Liao</creatorcontrib><creatorcontrib>Xiang, Mao</creatorcontrib><creatorcontrib>Meng, Guangxun</creatorcontrib><creatorcontrib>Ding, Chan</creatorcontrib><title>Newcastle disease virus infection induces activation of the NLRP3 inflammasome</title><title>Virology (New York, N.Y.)</title><addtitle>Virology</addtitle><description>Abstract Inflammatory responses are important aspects of the innate immune system during virus infection. We found that Newcastle disease virus can induce inflammasome activation in the human macrophage-like cell line THP-1. Viral replication was required for inflammasome activation, and small hairpin RNA knockdown experiments indicated that IL-1β secretion was mediated by the NLRP3 inflammasome. We also verified the results in LPS-primed bone marrow-derived macrophages (BMDMs) from NLRP3-deficient and wild type mice. NDV is considered to be a promising oncolytic virus. Stimulating the immune system has been proposed as a key mechanism of oncolytic specificity, and the inflammasome appears to be an important mechanism by which NDV is controlled. Knockdown of inflammasome components or chemical inhibition of caspase-1 activity shows that cell survival was augmented and benefited NDV replication. This study shows that NLRP3 inflammasome activation is an innate cellular response to NDV infection and offers insights into the oncolytic specificity of NDV.</description><subject>Animals</subject><subject>Caspase 1 - metabolism</subject><subject>Caspase Inhibitors - pharmacology</subject><subject>Caspase-1</subject><subject>Cell Line</subject><subject>Disease Models, Animal</subject><subject>Female</subject><subject>Humans</subject><subject>Infectious Disease</subject><subject>Inflammasome</subject><subject>Inflammasomes - metabolism</subject><subject>Interleukin-1beta - biosynthesis</subject><subject>Macrophage Activation - immunology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - virology</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>NDV</subject><subject>Newcastle Disease - genetics</subject><subject>Newcastle Disease - metabolism</subject><subject>Newcastle Disease - virology</subject><subject>Newcastle disease virus - physiology</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>NLRP3</subject><subject>THP‐1 cells</subject><subject>Virus Replication</subject><issn>0042-6822</issn><issn>1096-0341</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EokvhFyChHLkkjL83B5BQxZe0WqoCZ8txxsJLEhc7WdR_j9MtPfTCxfZrve-M5hlCXlJoKFD15tAcQ4pDw4poQDbA-COyodCqGrigj8kGQLBabRk7I89yPkDRWsNTcsY0U62S7Ybs9_jH2TwPWPUho81YlapLrsLk0c0hTuXVLw5zZYs82tuv6Kv5J1b73dUlX52DHUeb44jPyRNvh4wv7u5z8uPjh-8Xn-vd109fLt7vaieomGulaSuYkJ75XvrOMsYpLWdnJe91K3pOPdXeO-e10spD24kevewkcHDM83Py-lT3OsXfC-bZjCE7HAY7YVyyoVvYci30VhcrP1ldijkn9OY6hdGmG0PBrCDNwdyCNCtIA9IUkCX16q7B0o3Y32f-kSuGtycDljGPAZPJLuDksA-pgDN9DP9p8O5B3g1hCs4Ov_AG8yEuaSoEDTWZGTDf1l2uq6SKA-VM8r87d5pJ</recordid><startdate>20160901</startdate><enddate>20160901</enddate><creator>Wang, Binbin</creator><creator>Zhu, Jie</creator><creator>Li, Dandan</creator><creator>Wang, Yang</creator><creator>Zhan, Yuan</creator><creator>Tan, Lei</creator><creator>Qiu, Xusheng</creator><creator>Sun, Yingjie</creator><creator>Song, Cuiping</creator><creator>Meng, Chunchun</creator><creator>Ying, Liao</creator><creator>Xiang, Mao</creator><creator>Meng, Guangxun</creator><creator>Ding, Chan</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></search><sort><creationdate>20160901</creationdate><title>Newcastle disease virus infection induces activation of the NLRP3 inflammasome</title><author>Wang, Binbin ; Zhu, Jie ; Li, Dandan ; Wang, Yang ; Zhan, Yuan ; Tan, Lei ; Qiu, Xusheng ; Sun, Yingjie ; Song, Cuiping ; Meng, Chunchun ; Ying, Liao ; Xiang, Mao ; Meng, Guangxun ; Ding, Chan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c414t-67194245f2fd5fba22311a22ba53d794d31f17ffccf7676f09b4def5b5030c2f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Caspase 1 - metabolism</topic><topic>Caspase Inhibitors - pharmacology</topic><topic>Caspase-1</topic><topic>Cell Line</topic><topic>Disease Models, Animal</topic><topic>Female</topic><topic>Humans</topic><topic>Infectious Disease</topic><topic>Inflammasome</topic><topic>Inflammasomes - metabolism</topic><topic>Interleukin-1beta - biosynthesis</topic><topic>Macrophage Activation - immunology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - virology</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>NDV</topic><topic>Newcastle Disease - genetics</topic><topic>Newcastle Disease - metabolism</topic><topic>Newcastle Disease - virology</topic><topic>Newcastle disease virus - physiology</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>NLRP3</topic><topic>THP‐1 cells</topic><topic>Virus Replication</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Binbin</creatorcontrib><creatorcontrib>Zhu, Jie</creatorcontrib><creatorcontrib>Li, Dandan</creatorcontrib><creatorcontrib>Wang, Yang</creatorcontrib><creatorcontrib>Zhan, Yuan</creatorcontrib><creatorcontrib>Tan, Lei</creatorcontrib><creatorcontrib>Qiu, Xusheng</creatorcontrib><creatorcontrib>Sun, Yingjie</creatorcontrib><creatorcontrib>Song, Cuiping</creatorcontrib><creatorcontrib>Meng, Chunchun</creatorcontrib><creatorcontrib>Ying, Liao</creatorcontrib><creatorcontrib>Xiang, Mao</creatorcontrib><creatorcontrib>Meng, Guangxun</creatorcontrib><creatorcontrib>Ding, Chan</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><jtitle>Virology (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Binbin</au><au>Zhu, Jie</au><au>Li, Dandan</au><au>Wang, Yang</au><au>Zhan, Yuan</au><au>Tan, Lei</au><au>Qiu, Xusheng</au><au>Sun, Yingjie</au><au>Song, Cuiping</au><au>Meng, Chunchun</au><au>Ying, Liao</au><au>Xiang, Mao</au><au>Meng, Guangxun</au><au>Ding, Chan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Newcastle disease virus infection induces activation of the NLRP3 inflammasome</atitle><jtitle>Virology (New York, N.Y.)</jtitle><addtitle>Virology</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>496</volume><spage>90</spage><epage>96</epage><pages>90-96</pages><issn>0042-6822</issn><eissn>1096-0341</eissn><abstract>Abstract Inflammatory responses are important aspects of the innate immune system during virus infection. We found that Newcastle disease virus can induce inflammasome activation in the human macrophage-like cell line THP-1. Viral replication was required for inflammasome activation, and small hairpin RNA knockdown experiments indicated that IL-1β secretion was mediated by the NLRP3 inflammasome. We also verified the results in LPS-primed bone marrow-derived macrophages (BMDMs) from NLRP3-deficient and wild type mice. NDV is considered to be a promising oncolytic virus. Stimulating the immune system has been proposed as a key mechanism of oncolytic specificity, and the inflammasome appears to be an important mechanism by which NDV is controlled. Knockdown of inflammasome components or chemical inhibition of caspase-1 activity shows that cell survival was augmented and benefited NDV replication. 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subjects | Animals Caspase 1 - metabolism Caspase Inhibitors - pharmacology Caspase-1 Cell Line Disease Models, Animal Female Humans Infectious Disease Inflammasome Inflammasomes - metabolism Interleukin-1beta - biosynthesis Macrophage Activation - immunology Macrophages - immunology Macrophages - metabolism Macrophages - virology Mice Mice, Knockout NDV Newcastle Disease - genetics Newcastle Disease - metabolism Newcastle Disease - virology Newcastle disease virus - physiology NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - metabolism NLRP3 THP‐1 cells Virus Replication |
title | Newcastle disease virus infection induces activation of the NLRP3 inflammasome |
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