Human parvovirus B19 nonstructural protein NS1 activates NLRP3 inflammasome signaling in adult‑onset Still's disease
Dysregulation of inflammasomes serves a pathogenic role in autoinflammatory diseases (AIDs) and adult-onset Still's disease (AOSD) has been categorized as an AID. The present study investigated the expression of NLR family pyrin domain containing proteins (NLRPs) inflammasome in patients with A...
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| Veröffentlicht in: | Molecular medicine reports 2018-02, Vol.17 (2), p.3364-3371 |
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| creator | Chen, Der-Yuan Chen, Yi-Ming Chen, Hsin-Hua Hsieh, Chia-Wei Gung, Ning-Rong Hung, Wei-Ting Tzang, Bor-Show Hsu, Tsai-Ching |
| description | Dysregulation of inflammasomes serves a pathogenic role in autoinflammatory diseases (AIDs) and adult-onset Still's disease (AOSD) has been categorized as an AID. The present study investigated the expression of NLR family pyrin domain containing proteins (NLRPs) inflammasome in patients with AOSD, the effect of inflammasome inhibitors on NLRP3 signaling and whether human parvovirus B19‑associated antigens can activate NLRP3 in patients with AOSD. mRNA expression levels of NLRPs in peripheral blood mononuclear cells (PBMCs) from 34 patients with AOSD and 14 healthy individuals were determined using reverse transcription‑quantitative polymerase chain reaction. Protein expression of NLRP3 was evaluated by western blotting. Supernatant cytokine levels were measured by ELISA. Among the NLRPs investigated in the present study, NLRP3 transcripts were markedly elevated and expression of NLRP2, NLRP7 and NLRP12 was decreased in patients with AOSD compared with the controls. Treatment with NLRP3 inhibitors significantly reduced downstream NLRP3 signaling in PBMCs form patients with AOSD. B19‑nonstructural protein (NS)1 stimulation of PBMCs from patients with AOSD induced significant upregulation of transcript levels of NLRP3, caspase‑1 and interleukin (IL)‑1β compared with PBMCs from healthy controls. B19‑NS1 stimulation of PBMCs from patients with AOSD induced significant increase in supernatant levels of IL‑1β and protein expression of NLRP3, caspase‑1, IL‑1β, and IL‑18 compared with healthy controls. Elevated expression of NLRP3 and its downstream inflammasome signaling components in patients with AOSD indicated a potential pathogenic role of B19‑NS1. Thus, B19‑NS1 may induce expression of IL‑1β and IL‑18 through activation of caspase‑1‑associated NLRP3‑inflammasome in AOSD. |
| doi_str_mv | 10.3892/mmr.2017.8275 |
| format | Article |
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The present study investigated the expression of NLR family pyrin domain containing proteins (NLRPs) inflammasome in patients with AOSD, the effect of inflammasome inhibitors on NLRP3 signaling and whether human parvovirus B19‑associated antigens can activate NLRP3 in patients with AOSD. mRNA expression levels of NLRPs in peripheral blood mononuclear cells (PBMCs) from 34 patients with AOSD and 14 healthy individuals were determined using reverse transcription‑quantitative polymerase chain reaction. Protein expression of NLRP3 was evaluated by western blotting. Supernatant cytokine levels were measured by ELISA. Among the NLRPs investigated in the present study, NLRP3 transcripts were markedly elevated and expression of NLRP2, NLRP7 and NLRP12 was decreased in patients with AOSD compared with the controls. Treatment with NLRP3 inhibitors significantly reduced downstream NLRP3 signaling in PBMCs form patients with AOSD. B19‑nonstructural protein (NS)1 stimulation of PBMCs from patients with AOSD induced significant upregulation of transcript levels of NLRP3, caspase‑1 and interleukin (IL)‑1β compared with PBMCs from healthy controls. B19‑NS1 stimulation of PBMCs from patients with AOSD induced significant increase in supernatant levels of IL‑1β and protein expression of NLRP3, caspase‑1, IL‑1β, and IL‑18 compared with healthy controls. Elevated expression of NLRP3 and its downstream inflammasome signaling components in patients with AOSD indicated a potential pathogenic role of B19‑NS1. Thus, B19‑NS1 may induce expression of IL‑1β and IL‑18 through activation of caspase‑1‑associated NLRP3‑inflammasome in AOSD.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.8275</identifier><identifier>PMID: 29257322</identifier><language>eng</language><publisher>Greece: Spandidos Publications UK Ltd</publisher><subject>Adult ; Antigens ; Arthritis ; Caspase ; Caspase-1 ; Cytokines ; Deoxyribonucleic acid ; Disease ; DNA ; Enzyme-linked immunosorbent assay ; Female ; Fever ; Gene expression ; Gene Expression Regulation ; Humans ; Inflammasomes ; Inflammasomes - genetics ; Inflammasomes - immunology ; Inflammation ; Interleukin 18 ; Juvenile rheumatoid arthritis ; Leukocytes (mononuclear) ; Male ; NLR Family, Pyrin Domain-Containing 3 Protein - genetics ; NLR Family, Pyrin Domain-Containing 3 Protein - immunology ; Parvoviridae Infections - complications ; Parvoviridae Infections - genetics ; Parvoviridae Infections - immunology ; Parvoviridae Infections - virology ; Parvovirus B19, Human - immunology ; Parvoviruses ; Pathogenesis ; Peripheral blood mononuclear cells ; Polymerase chain reaction ; Proteins ; Pyrin protein ; Reverse transcription ; Rheumatic diseases ; RNA, Messenger - genetics ; Rodents ; Signal Transduction ; Still's Disease, Adult-Onset - complications ; Still's Disease, Adult-Onset - genetics ; Still's Disease, Adult-Onset - immunology ; Still's Disease, Adult-Onset - virology ; Studies ; Viral infections ; Western blotting</subject><ispartof>Molecular medicine reports, 2018-02, Vol.17 (2), p.3364-3371</ispartof><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c426t-5dd1b42602ae4209fae4e091ee68179589d700f5db0497bbf1b0a8faa374eaf3</citedby><cites>FETCH-LOGICAL-c426t-5dd1b42602ae4209fae4e091ee68179589d700f5db0497bbf1b0a8faa374eaf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29257322$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Der-Yuan</creatorcontrib><creatorcontrib>Chen, Yi-Ming</creatorcontrib><creatorcontrib>Chen, Hsin-Hua</creatorcontrib><creatorcontrib>Hsieh, Chia-Wei</creatorcontrib><creatorcontrib>Gung, Ning-Rong</creatorcontrib><creatorcontrib>Hung, Wei-Ting</creatorcontrib><creatorcontrib>Tzang, Bor-Show</creatorcontrib><creatorcontrib>Hsu, Tsai-Ching</creatorcontrib><title>Human parvovirus B19 nonstructural protein NS1 activates NLRP3 inflammasome signaling in adult‑onset Still's disease</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Dysregulation of inflammasomes serves a pathogenic role in autoinflammatory diseases (AIDs) and adult-onset Still's disease (AOSD) has been categorized as an AID. The present study investigated the expression of NLR family pyrin domain containing proteins (NLRPs) inflammasome in patients with AOSD, the effect of inflammasome inhibitors on NLRP3 signaling and whether human parvovirus B19‑associated antigens can activate NLRP3 in patients with AOSD. mRNA expression levels of NLRPs in peripheral blood mononuclear cells (PBMCs) from 34 patients with AOSD and 14 healthy individuals were determined using reverse transcription‑quantitative polymerase chain reaction. Protein expression of NLRP3 was evaluated by western blotting. Supernatant cytokine levels were measured by ELISA. Among the NLRPs investigated in the present study, NLRP3 transcripts were markedly elevated and expression of NLRP2, NLRP7 and NLRP12 was decreased in patients with AOSD compared with the controls. Treatment with NLRP3 inhibitors significantly reduced downstream NLRP3 signaling in PBMCs form patients with AOSD. B19‑nonstructural protein (NS)1 stimulation of PBMCs from patients with AOSD induced significant upregulation of transcript levels of NLRP3, caspase‑1 and interleukin (IL)‑1β compared with PBMCs from healthy controls. B19‑NS1 stimulation of PBMCs from patients with AOSD induced significant increase in supernatant levels of IL‑1β and protein expression of NLRP3, caspase‑1, IL‑1β, and IL‑18 compared with healthy controls. Elevated expression of NLRP3 and its downstream inflammasome signaling components in patients with AOSD indicated a potential pathogenic role of B19‑NS1. Thus, B19‑NS1 may induce expression of IL‑1β and IL‑18 through activation of caspase‑1‑associated NLRP3‑inflammasome in AOSD.</description><subject>Adult</subject><subject>Antigens</subject><subject>Arthritis</subject><subject>Caspase</subject><subject>Caspase-1</subject><subject>Cytokines</subject><subject>Deoxyribonucleic acid</subject><subject>Disease</subject><subject>DNA</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Female</subject><subject>Fever</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Humans</subject><subject>Inflammasomes</subject><subject>Inflammasomes - genetics</subject><subject>Inflammasomes - immunology</subject><subject>Inflammation</subject><subject>Interleukin 18</subject><subject>Juvenile rheumatoid arthritis</subject><subject>Leukocytes (mononuclear)</subject><subject>Male</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - immunology</subject><subject>Parvoviridae Infections - complications</subject><subject>Parvoviridae Infections - genetics</subject><subject>Parvoviridae Infections - immunology</subject><subject>Parvoviridae Infections - virology</subject><subject>Parvovirus B19, Human - immunology</subject><subject>Parvoviruses</subject><subject>Pathogenesis</subject><subject>Peripheral blood mononuclear cells</subject><subject>Polymerase chain reaction</subject><subject>Proteins</subject><subject>Pyrin protein</subject><subject>Reverse transcription</subject><subject>Rheumatic diseases</subject><subject>RNA, Messenger - genetics</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Still's Disease, Adult-Onset - complications</subject><subject>Still's Disease, Adult-Onset - genetics</subject><subject>Still's Disease, Adult-Onset - immunology</subject><subject>Still's Disease, Adult-Onset - virology</subject><subject>Studies</subject><subject>Viral infections</subject><subject>Western blotting</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpdkctq20AUhofQUOfSZbZloItmI2cukkezbELSFEwaYu_FkXQUxsxI7lwM3fUV8op5ko6J20VW5-fw8cPPR8gFZ3NZa3HlnJ8LxtW8Fqo6IidcaV5IxsoPhyy0VjNyGsKGsUUlKv2RzIQWlZJCnJDdfXIw0i343bQzPgV6zTUdpzFEn7qYPFi69VNEM9KHFafQRbODiIE-LJ8eJTXjYME5CJNDGszzCNaMz_lNoU82vv55yVUY6Soaa78G2puAEPCcHA9gA3463DOyvrtd39wXy5_ff9x8WxZdKRaxqPqetzkxAVgKpod8kGmOuKjzuKrWvWJsqPqWlVq17cBbBvUAIFWJMMgzcvlWmyf8Shhi40zo0FoYcUqh4VrViteikhn98g7dTMnnOXtKs1LJUpeZKt6ozk8heByarTcO_O-Gs2bvo8k-mr2PZu8j858Pral12P-n_wmQfwEX5Igk</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Chen, Der-Yuan</creator><creator>Chen, Yi-Ming</creator><creator>Chen, Hsin-Hua</creator><creator>Hsieh, Chia-Wei</creator><creator>Gung, Ning-Rong</creator><creator>Hung, Wei-Ting</creator><creator>Tzang, Bor-Show</creator><creator>Hsu, Tsai-Ching</creator><general>Spandidos Publications UK Ltd</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><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQGLB</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope></search><sort><creationdate>20180201</creationdate><title>Human parvovirus B19 nonstructural protein NS1 activates NLRP3 inflammasome signaling in adult‑onset Still's disease</title><author>Chen, Der-Yuan ; Chen, Yi-Ming ; Chen, Hsin-Hua ; Hsieh, Chia-Wei ; Gung, Ning-Rong ; Hung, Wei-Ting ; Tzang, Bor-Show ; Hsu, Tsai-Ching</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c426t-5dd1b42602ae4209fae4e091ee68179589d700f5db0497bbf1b0a8faa374eaf3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adult</topic><topic>Antigens</topic><topic>Arthritis</topic><topic>Caspase</topic><topic>Caspase-1</topic><topic>Cytokines</topic><topic>Deoxyribonucleic acid</topic><topic>Disease</topic><topic>DNA</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Female</topic><topic>Fever</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Humans</topic><topic>Inflammasomes</topic><topic>Inflammasomes - genetics</topic><topic>Inflammasomes - immunology</topic><topic>Inflammation</topic><topic>Interleukin 18</topic><topic>Juvenile rheumatoid arthritis</topic><topic>Leukocytes (mononuclear)</topic><topic>Male</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - genetics</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - immunology</topic><topic>Parvoviridae Infections - complications</topic><topic>Parvoviridae Infections - genetics</topic><topic>Parvoviridae Infections - immunology</topic><topic>Parvoviridae Infections - virology</topic><topic>Parvovirus B19, Human - immunology</topic><topic>Parvoviruses</topic><topic>Pathogenesis</topic><topic>Peripheral blood mononuclear cells</topic><topic>Polymerase chain reaction</topic><topic>Proteins</topic><topic>Pyrin protein</topic><topic>Reverse transcription</topic><topic>Rheumatic diseases</topic><topic>RNA, Messenger - genetics</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Still's Disease, Adult-Onset - complications</topic><topic>Still's Disease, Adult-Onset - genetics</topic><topic>Still's Disease, Adult-Onset - immunology</topic><topic>Still's Disease, Adult-Onset - virology</topic><topic>Studies</topic><topic>Viral infections</topic><topic>Western blotting</topic><toplevel>online_resources</toplevel><creatorcontrib>Chen, Der-Yuan</creatorcontrib><creatorcontrib>Chen, Yi-Ming</creatorcontrib><creatorcontrib>Chen, Hsin-Hua</creatorcontrib><creatorcontrib>Hsieh, Chia-Wei</creatorcontrib><creatorcontrib>Gung, Ning-Rong</creatorcontrib><creatorcontrib>Hung, Wei-Ting</creatorcontrib><creatorcontrib>Tzang, Bor-Show</creatorcontrib><creatorcontrib>Hsu, Tsai-Ching</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health & Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health & Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Applied & Life Sciences</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Der-Yuan</au><au>Chen, Yi-Ming</au><au>Chen, Hsin-Hua</au><au>Hsieh, Chia-Wei</au><au>Gung, Ning-Rong</au><au>Hung, Wei-Ting</au><au>Tzang, Bor-Show</au><au>Hsu, Tsai-Ching</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Human parvovirus B19 nonstructural protein NS1 activates NLRP3 inflammasome signaling in adult‑onset Still's disease</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>17</volume><issue>2</issue><spage>3364</spage><epage>3371</epage><pages>3364-3371</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Dysregulation of inflammasomes serves a pathogenic role in autoinflammatory diseases (AIDs) and adult-onset Still's disease (AOSD) has been categorized as an AID. The present study investigated the expression of NLR family pyrin domain containing proteins (NLRPs) inflammasome in patients with AOSD, the effect of inflammasome inhibitors on NLRP3 signaling and whether human parvovirus B19‑associated antigens can activate NLRP3 in patients with AOSD. mRNA expression levels of NLRPs in peripheral blood mononuclear cells (PBMCs) from 34 patients with AOSD and 14 healthy individuals were determined using reverse transcription‑quantitative polymerase chain reaction. Protein expression of NLRP3 was evaluated by western blotting. Supernatant cytokine levels were measured by ELISA. Among the NLRPs investigated in the present study, NLRP3 transcripts were markedly elevated and expression of NLRP2, NLRP7 and NLRP12 was decreased in patients with AOSD compared with the controls. Treatment with NLRP3 inhibitors significantly reduced downstream NLRP3 signaling in PBMCs form patients with AOSD. B19‑nonstructural protein (NS)1 stimulation of PBMCs from patients with AOSD induced significant upregulation of transcript levels of NLRP3, caspase‑1 and interleukin (IL)‑1β compared with PBMCs from healthy controls. B19‑NS1 stimulation of PBMCs from patients with AOSD induced significant increase in supernatant levels of IL‑1β and protein expression of NLRP3, caspase‑1, IL‑1β, and IL‑18 compared with healthy controls. Elevated expression of NLRP3 and its downstream inflammasome signaling components in patients with AOSD indicated a potential pathogenic role of B19‑NS1. Thus, B19‑NS1 may induce expression of IL‑1β and IL‑18 through activation of caspase‑1‑associated NLRP3‑inflammasome in AOSD.</abstract><cop>Greece</cop><pub>Spandidos Publications UK Ltd</pub><pmid>29257322</pmid><doi>10.3892/mmr.2017.8275</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| source | Spandidos Publications Journals; MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adult Antigens Arthritis Caspase Caspase-1 Cytokines Deoxyribonucleic acid Disease DNA Enzyme-linked immunosorbent assay Female Fever Gene expression Gene Expression Regulation Humans Inflammasomes Inflammasomes - genetics Inflammasomes - immunology Inflammation Interleukin 18 Juvenile rheumatoid arthritis Leukocytes (mononuclear) Male NLR Family, Pyrin Domain-Containing 3 Protein - genetics NLR Family, Pyrin Domain-Containing 3 Protein - immunology Parvoviridae Infections - complications Parvoviridae Infections - genetics Parvoviridae Infections - immunology Parvoviridae Infections - virology Parvovirus B19, Human - immunology Parvoviruses Pathogenesis Peripheral blood mononuclear cells Polymerase chain reaction Proteins Pyrin protein Reverse transcription Rheumatic diseases RNA, Messenger - genetics Rodents Signal Transduction Still's Disease, Adult-Onset - complications Still's Disease, Adult-Onset - genetics Still's Disease, Adult-Onset - immunology Still's Disease, Adult-Onset - virology Studies Viral infections Western blotting |
| title | Human parvovirus B19 nonstructural protein NS1 activates NLRP3 inflammasome signaling in adult‑onset Still's disease |
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