Pyroptosis induced by enterovirus 71 and coxsackievirus B3 infection affects viral replication and host response
Enterovirus 71 (EV71) is the primary causative pathogen of hand, foot, and mouth disease (HFMD), affecting children with severe neurological complications. Pyroptosis is a programmed cell death characterized by cell lysis and inflammatory response. Although proinflammatory response has been implicat...
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| Veröffentlicht in: | Scientific reports 2018-02, Vol.8 (1), p.2887-12, Article 2887 |
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| creator | Wang, Yan Qin, Ying Wang, Tianying Chen, Yang Lang, Xiujuan Zheng, Jia Gao, Shuoyang Chen, Sijia Zhong, Xiaoyan Mu, Yusong Wu, Xiaoyu Zhang, Fengming Zhao, Wenran Zhong, Zhaohua |
| description | Enterovirus 71 (EV71) is the primary causative pathogen of hand, foot, and mouth disease (HFMD), affecting children with severe neurological complications. Pyroptosis is a programmed cell death characterized by cell lysis and inflammatory response. Although proinflammatory response has been implicated to play important roles in EV71-caused diseases, the involvement of pyroptosis in the pathogenesis of EV71 is poorly defined. We show that EV71 infection induced caspase-1 activation. Responding to the activation of caspase-1, the expression and secretion of both IL-1β and IL-18 were increased in EV71-infected cells. The treatment of caspase-1 inhibitor markedly improved the systemic response of the EV71-infected mice. Importantly, caspase-1 inhibitor suppressed EV71 replication in mouse brains. Similarly, pyroptosis was activated by the infection of coxsackievirus B3 (CVB3), an important member of the
Enterovirus
genus. Caspase-1 activation and the increased expression of IL-18 and NLRP3 were demonstrated in HeLa cells infected with CVB3. Caspase-1 inhibitor also alleviated the overall conditions of virus-infected mice with markedly decreased replication of CVB3 and reduced expression of caspase-1. These results indicate that pyroptosis is involved in the pathogenesis of both EV71 and CVB3 infections, and the treatment of caspase-1 inhibitor is beneficial to the host response during enterovirus infection. |
| doi_str_mv | 10.1038/s41598-018-20958-1 |
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Enterovirus
genus. Caspase-1 activation and the increased expression of IL-18 and NLRP3 were demonstrated in HeLa cells infected with CVB3. Caspase-1 inhibitor also alleviated the overall conditions of virus-infected mice with markedly decreased replication of CVB3 and reduced expression of caspase-1. These results indicate that pyroptosis is involved in the pathogenesis of both EV71 and CVB3 infections, and the treatment of caspase-1 inhibitor is beneficial to the host response during enterovirus infection.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-018-20958-1</identifier><identifier>PMID: 29440739</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/106 ; 13/109 ; 14 ; 14/34 ; 14/63 ; 38 ; 38/109 ; 38/77 ; 38/90 ; 631/326/596/2553 ; 631/326/596/2555 ; 692/420/254 ; Apoptosis ; Caspase ; Caspase-1 ; Cell death ; Children ; Coxsackieviruses ; Enterovirus ; Hand-foot-and-mouth disease ; Humanities and Social Sciences ; Infections ; Inflammation ; Interleukin 18 ; Lysis ; multidisciplinary ; Neurological complications ; Pathogenesis ; Pyroptosis ; Replication ; Science ; Science (multidisciplinary)</subject><ispartof>Scientific reports, 2018-02, Vol.8 (1), p.2887-12, Article 2887</ispartof><rights>The Author(s) 2018</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/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><citedby>FETCH-LOGICAL-c474t-d6d2d3a2a6d1a87fc5ad0927828386543a65cf0723d57b6f3feffbf99e85ce5c3</citedby><cites>FETCH-LOGICAL-c474t-d6d2d3a2a6d1a87fc5ad0927828386543a65cf0723d57b6f3feffbf99e85ce5c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811489/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5811489/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29440739$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Yan</creatorcontrib><creatorcontrib>Qin, Ying</creatorcontrib><creatorcontrib>Wang, Tianying</creatorcontrib><creatorcontrib>Chen, Yang</creatorcontrib><creatorcontrib>Lang, Xiujuan</creatorcontrib><creatorcontrib>Zheng, Jia</creatorcontrib><creatorcontrib>Gao, Shuoyang</creatorcontrib><creatorcontrib>Chen, Sijia</creatorcontrib><creatorcontrib>Zhong, Xiaoyan</creatorcontrib><creatorcontrib>Mu, Yusong</creatorcontrib><creatorcontrib>Wu, Xiaoyu</creatorcontrib><creatorcontrib>Zhang, Fengming</creatorcontrib><creatorcontrib>Zhao, Wenran</creatorcontrib><creatorcontrib>Zhong, Zhaohua</creatorcontrib><title>Pyroptosis induced by enterovirus 71 and coxsackievirus B3 infection affects viral replication and host response</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Enterovirus 71 (EV71) is the primary causative pathogen of hand, foot, and mouth disease (HFMD), affecting children with severe neurological complications. Pyroptosis is a programmed cell death characterized by cell lysis and inflammatory response. Although proinflammatory response has been implicated to play important roles in EV71-caused diseases, the involvement of pyroptosis in the pathogenesis of EV71 is poorly defined. We show that EV71 infection induced caspase-1 activation. Responding to the activation of caspase-1, the expression and secretion of both IL-1β and IL-18 were increased in EV71-infected cells. The treatment of caspase-1 inhibitor markedly improved the systemic response of the EV71-infected mice. Importantly, caspase-1 inhibitor suppressed EV71 replication in mouse brains. Similarly, pyroptosis was activated by the infection of coxsackievirus B3 (CVB3), an important member of the
Enterovirus
genus. Caspase-1 activation and the increased expression of IL-18 and NLRP3 were demonstrated in HeLa cells infected with CVB3. Caspase-1 inhibitor also alleviated the overall conditions of virus-infected mice with markedly decreased replication of CVB3 and reduced expression of caspase-1. These results indicate that pyroptosis is involved in the pathogenesis of both EV71 and CVB3 infections, and the treatment of caspase-1 inhibitor is beneficial to the host response during enterovirus infection.</description><subject>13</subject><subject>13/106</subject><subject>13/109</subject><subject>14</subject><subject>14/34</subject><subject>14/63</subject><subject>38</subject><subject>38/109</subject><subject>38/77</subject><subject>38/90</subject><subject>631/326/596/2553</subject><subject>631/326/596/2555</subject><subject>692/420/254</subject><subject>Apoptosis</subject><subject>Caspase</subject><subject>Caspase-1</subject><subject>Cell death</subject><subject>Children</subject><subject>Coxsackieviruses</subject><subject>Enterovirus</subject><subject>Hand-foot-and-mouth disease</subject><subject>Humanities and Social Sciences</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Interleukin 18</subject><subject>Lysis</subject><subject>multidisciplinary</subject><subject>Neurological complications</subject><subject>Pathogenesis</subject><subject>Pyroptosis</subject><subject>Replication</subject><subject>Science</subject><subject>Science 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NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Yan</au><au>Qin, Ying</au><au>Wang, Tianying</au><au>Chen, Yang</au><au>Lang, Xiujuan</au><au>Zheng, Jia</au><au>Gao, Shuoyang</au><au>Chen, Sijia</au><au>Zhong, Xiaoyan</au><au>Mu, Yusong</au><au>Wu, Xiaoyu</au><au>Zhang, Fengming</au><au>Zhao, Wenran</au><au>Zhong, Zhaohua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pyroptosis induced by enterovirus 71 and coxsackievirus B3 infection affects viral replication and host response</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2018-02-13</date><risdate>2018</risdate><volume>8</volume><issue>1</issue><spage>2887</spage><epage>12</epage><pages>2887-12</pages><artnum>2887</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Enterovirus 71 (EV71) is the primary causative pathogen of hand, foot, and mouth disease (HFMD), affecting children with severe neurological complications. Pyroptosis is a programmed cell death characterized by cell lysis and inflammatory response. Although proinflammatory response has been implicated to play important roles in EV71-caused diseases, the involvement of pyroptosis in the pathogenesis of EV71 is poorly defined. We show that EV71 infection induced caspase-1 activation. Responding to the activation of caspase-1, the expression and secretion of both IL-1β and IL-18 were increased in EV71-infected cells. The treatment of caspase-1 inhibitor markedly improved the systemic response of the EV71-infected mice. Importantly, caspase-1 inhibitor suppressed EV71 replication in mouse brains. Similarly, pyroptosis was activated by the infection of coxsackievirus B3 (CVB3), an important member of the
Enterovirus
genus. Caspase-1 activation and the increased expression of IL-18 and NLRP3 were demonstrated in HeLa cells infected with CVB3. Caspase-1 inhibitor also alleviated the overall conditions of virus-infected mice with markedly decreased replication of CVB3 and reduced expression of caspase-1. These results indicate that pyroptosis is involved in the pathogenesis of both EV71 and CVB3 infections, and the treatment of caspase-1 inhibitor is beneficial to the host response during enterovirus infection.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>29440739</pmid><doi>10.1038/s41598-018-20958-1</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 13 13/106 13/109 14 14/34 14/63 38 38/109 38/77 38/90 631/326/596/2553 631/326/596/2555 692/420/254 Apoptosis Caspase Caspase-1 Cell death Children Coxsackieviruses Enterovirus Hand-foot-and-mouth disease Humanities and Social Sciences Infections Inflammation Interleukin 18 Lysis multidisciplinary Neurological complications Pathogenesis Pyroptosis Replication Science Science (multidisciplinary) |
| title | Pyroptosis induced by enterovirus 71 and coxsackievirus B3 infection affects viral replication and host response |
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