Induction of STAT1 phosphorylation at serine 727 and expression of proinflammatory cytokines by porcine reproductive and respiratory syndrome virus
Porcine reproductive and respiratory syndrome virus (PRRSV) is a viral pathogen that causes acute respiratory illnesses in young pigs. Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to cont...
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| description | Porcine reproductive and respiratory syndrome virus (PRRSV) is a viral pathogen that causes acute respiratory illnesses in young pigs. Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to contribute to PRRSV pathogenesis. In this study, PRRSV VR-2385, a Type 2 strain with moderate virulence, was found to induce phosphorylation of signal transducer and activator of transcription 1 (STAT1) at serine 727 (pSTAT1-S727) in MARC-145 cells. No phosphorylated STAT1 at tyrosine 701 was detected, which indicates that the pSTAT1-S727 elevation was interferon-independent. The PRRSV-induced pSTAT1-S727, however, was dose-dependent and its levels increased with infection time. IngelVac PRRS MLV strain had a minimal effect on pSTAT1-S727. Compared to MLV-infected cells, VR-2385 infection caused significantly higher level of expression of proinflammatory cytokines, including interleukin 1 beta (IL-1beta) and IL-8. The VR-2385-induced pSTAT1-S727 and cytokine expression were reduced after SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), or methylthioadenosine (MTA), a methyl transferase inhibitor, was added to the cells. The SB203580 and MTA-mediated inhibition suggested that the virus-induced pSTAT1-S727 was dependent on p38 MAPK pathway. In primary porcine alveolar macrophages (PAMs), VR-2385 also induced pSTAT1-S727 and expression of proinflammatory cytokines and chemokines, including IL-1beta, IL-8, chemokine ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 10 (CXCL10). Similarly, SB203580 treatment of PAM cells blocked the elevation of pSTAT1-S727 and cytokine expression. Overexpression of individual viral proteins showed that non-structural protein 12 (nsp12) was able to induce elevation of pSTAT1-S727 and the expression of IL-1β and IL-8. These results indicated that PRRSV VR-2385 induces pSTAT1-S727 and the expression of proinflammatory cytokines, which contributes to the insight of PRRSV pathogenesis. |
| doi_str_mv | 10.1371/journal.pone.0061967 |
| format | Article |
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Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to contribute to PRRSV pathogenesis. In this study, PRRSV VR-2385, a Type 2 strain with moderate virulence, was found to induce phosphorylation of signal transducer and activator of transcription 1 (STAT1) at serine 727 (pSTAT1-S727) in MARC-145 cells. No phosphorylated STAT1 at tyrosine 701 was detected, which indicates that the pSTAT1-S727 elevation was interferon-independent. The PRRSV-induced pSTAT1-S727, however, was dose-dependent and its levels increased with infection time. IngelVac PRRS MLV strain had a minimal effect on pSTAT1-S727. Compared to MLV-infected cells, VR-2385 infection caused significantly higher level of expression of proinflammatory cytokines, including interleukin 1 beta (IL-1beta) and IL-8. The VR-2385-induced pSTAT1-S727 and cytokine expression were reduced after SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), or methylthioadenosine (MTA), a methyl transferase inhibitor, was added to the cells. The SB203580 and MTA-mediated inhibition suggested that the virus-induced pSTAT1-S727 was dependent on p38 MAPK pathway. In primary porcine alveolar macrophages (PAMs), VR-2385 also induced pSTAT1-S727 and expression of proinflammatory cytokines and chemokines, including IL-1beta, IL-8, chemokine ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 10 (CXCL10). Similarly, SB203580 treatment of PAM cells blocked the elevation of pSTAT1-S727 and cytokine expression. Overexpression of individual viral proteins showed that non-structural protein 12 (nsp12) was able to induce elevation of pSTAT1-S727 and the expression of IL-1β and IL-8. These results indicated that PRRSV VR-2385 induces pSTAT1-S727 and the expression of proinflammatory cytokines, which contributes to the insight of PRRSV pathogenesis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0061967</identifier><identifier>PMID: 23637938</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alveoli ; Animals ; Biological response modifiers ; Biology ; Cell Line ; Chemokines ; CXCL10 protein ; Cytokines ; Cytokines - genetics ; Economic impact ; Enzyme Inhibitors - pharmacology ; Gene Expression Regulation - drug effects ; Genomes ; Health aspects ; Hogs ; Humans ; Illnesses ; Infections ; Inflammation ; Inflammation Mediators - metabolism ; Inhibitors ; Interferon ; Interleukin 1 ; Interleukin 8 ; Kinases ; Laboratories ; Life sciences ; Livestock ; Macrophages ; Macrophages, Alveolar - metabolism ; Macrophages, Alveolar - virology ; MAP kinase ; Methyltransferases - antagonists & inhibitors ; Monocyte chemoattractant protein 1 ; p38 Mitogen-Activated Protein Kinases ; Pathogenesis ; Pathogens ; Phosphorylation ; Physiological aspects ; Porcine reproductive and respiratory syndrome ; Porcine Reproductive and Respiratory Syndrome - genetics ; Porcine Reproductive and Respiratory Syndrome - metabolism ; Porcine respiratory and reproductive syndrome virus - physiology ; Protein kinase ; Proteins ; Respiratory diseases ; Risk factors ; Rodents ; Serine ; Serine - metabolism ; Signal Transduction ; Stat1 protein ; STAT1 Transcription Factor - metabolism ; Swine ; Transcription ; Tumor necrosis factor-TNF ; Tyrosine ; Veterinary colleges ; Veterinary medicine ; Veterinary Science ; Viral Proteins - metabolism ; Virology ; Virulence ; Virulence (Microbiology) ; Viruses</subject><ispartof>PloS one, 2013-04, Vol.8 (4), p.e61967</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Yu et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Yu et al 2013 Yu et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c6077-bed4db4cbb27d29de0c6a190071f08f0e168cafa2b0b6ea76e51e3cd0e61a6663</citedby><cites>FETCH-LOGICAL-c6077-bed4db4cbb27d29de0c6a190071f08f0e168cafa2b0b6ea76e51e3cd0e61a6663</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/PMC3634824/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3634824/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23637938$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yu, Ying</creatorcontrib><creatorcontrib>Wang, Rong</creatorcontrib><creatorcontrib>Nan, Yuchen</creatorcontrib><creatorcontrib>Zhang, Linsheng</creatorcontrib><creatorcontrib>Zhang, Yanjin</creatorcontrib><title>Induction of STAT1 phosphorylation at serine 727 and expression of proinflammatory cytokines by porcine reproductive and respiratory syndrome virus</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Porcine reproductive and respiratory syndrome virus (PRRSV) is a viral pathogen that causes acute respiratory illnesses in young pigs. Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to contribute to PRRSV pathogenesis. In this study, PRRSV VR-2385, a Type 2 strain with moderate virulence, was found to induce phosphorylation of signal transducer and activator of transcription 1 (STAT1) at serine 727 (pSTAT1-S727) in MARC-145 cells. No phosphorylated STAT1 at tyrosine 701 was detected, which indicates that the pSTAT1-S727 elevation was interferon-independent. The PRRSV-induced pSTAT1-S727, however, was dose-dependent and its levels increased with infection time. IngelVac PRRS MLV strain had a minimal effect on pSTAT1-S727. Compared to MLV-infected cells, VR-2385 infection caused significantly higher level of expression of proinflammatory cytokines, including interleukin 1 beta (IL-1beta) and IL-8. The VR-2385-induced pSTAT1-S727 and cytokine expression were reduced after SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), or methylthioadenosine (MTA), a methyl transferase inhibitor, was added to the cells. The SB203580 and MTA-mediated inhibition suggested that the virus-induced pSTAT1-S727 was dependent on p38 MAPK pathway. In primary porcine alveolar macrophages (PAMs), VR-2385 also induced pSTAT1-S727 and expression of proinflammatory cytokines and chemokines, including IL-1beta, IL-8, chemokine ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 10 (CXCL10). Similarly, SB203580 treatment of PAM cells blocked the elevation of pSTAT1-S727 and cytokine expression. Overexpression of individual viral proteins showed that non-structural protein 12 (nsp12) was able to induce elevation of pSTAT1-S727 and the expression of IL-1β and IL-8. These results indicated that PRRSV VR-2385 induces pSTAT1-S727 and the expression of proinflammatory cytokines, which contributes to the insight of PRRSV pathogenesis.</description><subject>Alveoli</subject><subject>Animals</subject><subject>Biological response modifiers</subject><subject>Biology</subject><subject>Cell Line</subject><subject>Chemokines</subject><subject>CXCL10 protein</subject><subject>Cytokines</subject><subject>Cytokines - genetics</subject><subject>Economic impact</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Genomes</subject><subject>Health aspects</subject><subject>Hogs</subject><subject>Humans</subject><subject>Illnesses</subject><subject>Infections</subject><subject>Inflammation</subject><subject>Inflammation Mediators - metabolism</subject><subject>Inhibitors</subject><subject>Interferon</subject><subject>Interleukin 1</subject><subject>Interleukin 8</subject><subject>Kinases</subject><subject>Laboratories</subject><subject>Life sciences</subject><subject>Livestock</subject><subject>Macrophages</subject><subject>Macrophages, Alveolar - metabolism</subject><subject>Macrophages, Alveolar - virology</subject><subject>MAP kinase</subject><subject>Methyltransferases - antagonists & inhibitors</subject><subject>Monocyte chemoattractant protein 1</subject><subject>p38 Mitogen-Activated Protein Kinases</subject><subject>Pathogenesis</subject><subject>Pathogens</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Porcine reproductive and respiratory syndrome</subject><subject>Porcine Reproductive and Respiratory Syndrome - genetics</subject><subject>Porcine Reproductive and Respiratory Syndrome - metabolism</subject><subject>Porcine respiratory and reproductive syndrome virus - physiology</subject><subject>Protein kinase</subject><subject>Proteins</subject><subject>Respiratory diseases</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Serine</subject><subject>Serine - metabolism</subject><subject>Signal Transduction</subject><subject>Stat1 protein</subject><subject>STAT1 Transcription Factor - metabolism</subject><subject>Swine</subject><subject>Transcription</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tyrosine</subject><subject>Veterinary colleges</subject><subject>Veterinary medicine</subject><subject>Veterinary Science</subject><subject>Viral Proteins - metabolism</subject><subject>Virology</subject><subject>Virulence</subject><subject>Virulence (Microbiology)</subject><subject>Viruses</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11r2zAUhs3YWLtu_2BsgsFgF8n0YUv2zSCUfQQKhTXbrZCl40SdbbmSHZrfsT88JXFLDBsMISSk533P4UgnSV4TPCdMkI-3bvCtqueda2GOMScFF0-Sc1IwOuMUs6cn-7PkRQi3GGcs5_x5ckYZZ6Jg-Xnye9maQffWtchV6Ga1WBHUbVyI0-9qdbhQPQrgbQtIUIFUaxDcdx5CGFWdd7atatU0qo8qpHe9-xXxgMod6pzXe6mHiB1CbeHgEQ0664-KsGuNdw2grfVDeJk8q1Qd4NW4XiQ_vnxeXX6bXV1_XV4urmaaYyFmJZjUlKkuSyoMLQxgzRUpMBakwnmFgfBcq0rREpcclOCQEWDaYOBEcc7ZRfL26NvVLsixnkESlnKSpVmeRWJ5JIxTt7LztlF-J52y8nDg_Foq31tdg8y0LnMlCBci5sSLIhcFL2NGeWaAZix6fRqjDWUDRkPbe1VPTKc3rd3ItdvK-FZpTtNo8G408O5ugND_I-WRWquYVXwXF810Y4OWi1TkmDJG99T8L1QcBhqr44-qbDyfCD5MBJHp4b5fqyEEubz5_v_s9c8p-_6E3YCq-01w9bD_eGEKpkdQexeCh-qxcgTLfUM8VEPuG0KODRFlb06r_ih66AD2B80MCeo</recordid><startdate>20130424</startdate><enddate>20130424</enddate><creator>Yu, Ying</creator><creator>Wang, Rong</creator><creator>Nan, Yuchen</creator><creator>Zhang, Linsheng</creator><creator>Zhang, Yanjin</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130424</creationdate><title>Induction of STAT1 phosphorylation at serine 727 and expression of proinflammatory cytokines by porcine reproductive and respiratory syndrome virus</title><author>Yu, Ying ; Wang, Rong ; Nan, Yuchen ; Zhang, Linsheng ; Zhang, Yanjin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c6077-bed4db4cbb27d29de0c6a190071f08f0e168cafa2b0b6ea76e51e3cd0e61a6663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Alveoli</topic><topic>Animals</topic><topic>Biological response modifiers</topic><topic>Biology</topic><topic>Cell Line</topic><topic>Chemokines</topic><topic>CXCL10 protein</topic><topic>Cytokines</topic><topic>Cytokines - genetics</topic><topic>Economic impact</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Genomes</topic><topic>Health aspects</topic><topic>Hogs</topic><topic>Humans</topic><topic>Illnesses</topic><topic>Infections</topic><topic>Inflammation</topic><topic>Inflammation Mediators - metabolism</topic><topic>Inhibitors</topic><topic>Interferon</topic><topic>Interleukin 1</topic><topic>Interleukin 8</topic><topic>Kinases</topic><topic>Laboratories</topic><topic>Life sciences</topic><topic>Livestock</topic><topic>Macrophages</topic><topic>Macrophages, Alveolar - metabolism</topic><topic>Macrophages, Alveolar - virology</topic><topic>MAP kinase</topic><topic>Methyltransferases - antagonists & inhibitors</topic><topic>Monocyte chemoattractant protein 1</topic><topic>p38 Mitogen-Activated Protein Kinases</topic><topic>Pathogenesis</topic><topic>Pathogens</topic><topic>Phosphorylation</topic><topic>Physiological aspects</topic><topic>Porcine reproductive and respiratory syndrome</topic><topic>Porcine Reproductive and Respiratory Syndrome - 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Since 1987, PRRSV has contributed substantial economic losses to the swine industry. Elevation of proinflammatory cytokines in PRRSV-infected pigs is thought to contribute to PRRSV pathogenesis. In this study, PRRSV VR-2385, a Type 2 strain with moderate virulence, was found to induce phosphorylation of signal transducer and activator of transcription 1 (STAT1) at serine 727 (pSTAT1-S727) in MARC-145 cells. No phosphorylated STAT1 at tyrosine 701 was detected, which indicates that the pSTAT1-S727 elevation was interferon-independent. The PRRSV-induced pSTAT1-S727, however, was dose-dependent and its levels increased with infection time. IngelVac PRRS MLV strain had a minimal effect on pSTAT1-S727. Compared to MLV-infected cells, VR-2385 infection caused significantly higher level of expression of proinflammatory cytokines, including interleukin 1 beta (IL-1beta) and IL-8. The VR-2385-induced pSTAT1-S727 and cytokine expression were reduced after SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK), or methylthioadenosine (MTA), a methyl transferase inhibitor, was added to the cells. The SB203580 and MTA-mediated inhibition suggested that the virus-induced pSTAT1-S727 was dependent on p38 MAPK pathway. In primary porcine alveolar macrophages (PAMs), VR-2385 also induced pSTAT1-S727 and expression of proinflammatory cytokines and chemokines, including IL-1beta, IL-8, chemokine ligand 2 (CCL2) and chemokine (C-X-C motif) ligand 10 (CXCL10). Similarly, SB203580 treatment of PAM cells blocked the elevation of pSTAT1-S727 and cytokine expression. Overexpression of individual viral proteins showed that non-structural protein 12 (nsp12) was able to induce elevation of pSTAT1-S727 and the expression of IL-1β and IL-8. These results indicated that PRRSV VR-2385 induces pSTAT1-S727 and the expression of proinflammatory cytokines, which contributes to the insight of PRRSV pathogenesis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23637938</pmid><doi>10.1371/journal.pone.0061967</doi><tpages>e61967</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-04, Vol.8 (4), p.e61967 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1346154585 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Alveoli Animals Biological response modifiers Biology Cell Line Chemokines CXCL10 protein Cytokines Cytokines - genetics Economic impact Enzyme Inhibitors - pharmacology Gene Expression Regulation - drug effects Genomes Health aspects Hogs Humans Illnesses Infections Inflammation Inflammation Mediators - metabolism Inhibitors Interferon Interleukin 1 Interleukin 8 Kinases Laboratories Life sciences Livestock Macrophages Macrophages, Alveolar - metabolism Macrophages, Alveolar - virology MAP kinase Methyltransferases - antagonists & inhibitors Monocyte chemoattractant protein 1 p38 Mitogen-Activated Protein Kinases Pathogenesis Pathogens Phosphorylation Physiological aspects Porcine reproductive and respiratory syndrome Porcine Reproductive and Respiratory Syndrome - genetics Porcine Reproductive and Respiratory Syndrome - metabolism Porcine respiratory and reproductive syndrome virus - physiology Protein kinase Proteins Respiratory diseases Risk factors Rodents Serine Serine - metabolism Signal Transduction Stat1 protein STAT1 Transcription Factor - metabolism Swine Transcription Tumor necrosis factor-TNF Tyrosine Veterinary colleges Veterinary medicine Veterinary Science Viral Proteins - metabolism Virology Virulence Virulence (Microbiology) Viruses |
| title | Induction of STAT1 phosphorylation at serine 727 and expression of proinflammatory cytokines by porcine reproductive and respiratory syndrome virus |
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