Pathogenic mouse hepatitis virus or poly(I:C) induce IL-33 in hepatocytes in murine models of hepatitis
The IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepati...
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| Veröffentlicht in: | PloS one 2013-09, Vol.8 (9), p.e74278 |
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| creator | Arshad, Muhammad Imran Patrat-Delon, Solène Piquet-Pellorce, Claire L'helgoualc'h, Annie Rauch, Michel Genet, Valentine Lucas-Clerc, Catherine Bleau, Christian Lamontagne, Lucie Samson, Michel |
| description | The IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33. |
| doi_str_mv | 10.1371/journal.pone.0074278 |
| format | Article |
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Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0074278</identifier><identifier>PMID: 24058536</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animal models ; Animals ; Antigens ; Antigens, CD1d - genetics ; Antigens, CD1d - immunology ; CD1d antigen ; Cytokines ; D-Galactosamine ; Endothelial cells ; Endothelial Cells - immunology ; Endothelial Cells - pathology ; Endothelial Cells - virology ; Endothelium, Vascular - immunology ; Endothelium, Vascular - pathology ; Endothelium, Vascular - virology ; Galactosamine - administration & dosage ; Gene Deletion ; Gene Expression - immunology ; Health aspects ; Hepatitis ; Hepatitis - etiology ; Hepatitis - genetics ; Hepatitis - immunology ; Hepatitis - pathology ; Hepatitis, Viral, Animal - genetics ; Hepatitis, Viral, Animal - immunology ; Hepatitis, Viral, Animal - pathology ; Hepatitis, Viral, Animal - virology ; Hepatocytes ; Human health and pathology ; Infections ; Infectious diseases ; Inflammation ; Injury prevention ; Interleukin-33 ; Interleukins - genetics ; Interleukins - immunology ; Killer cells ; Killer Cells, Natural - immunology ; Killer Cells, Natural - pathology ; Killer Cells, Natural - virology ; Life Sciences ; Liver ; Liver - immunology ; Liver - pathology ; Liver - virology ; Lymphocytes T ; Mice ; Mice, Knockout ; Murine hepatitis virus - immunology ; Murine hepatitis virus - pathogenicity ; Natural killer cells ; Natural Killer T-Cells - immunology ; Natural Killer T-Cells - pathology ; Natural Killer T-Cells - virology ; Poly (I:C) ; Poly I-C - administration & dosage ; Rodents ; TLR3 protein ; Toll-like receptors ; Tumor necrosis factor-TNF ; Viral infections ; Viruses</subject><ispartof>PloS one, 2013-09, Vol.8 (9), p.e74278</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Arshad 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>Distributed under a Creative Commons Attribution 4.0 International License</rights><rights>2013 Arshad et al 2013 Arshad et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c627t-61bef085a5715e28ae9c0c64e1237038bf0a515641210520669a935d4aed84583</citedby><cites>FETCH-LOGICAL-c627t-61bef085a5715e28ae9c0c64e1237038bf0a515641210520669a935d4aed84583</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/PMC3772926/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772926/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24058536$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00874120$$DView record in HAL$$Hfree_for_read</backlink></links><search><contributor>Leite de Moraes, Maria</contributor><creatorcontrib>Arshad, Muhammad Imran</creatorcontrib><creatorcontrib>Patrat-Delon, Solène</creatorcontrib><creatorcontrib>Piquet-Pellorce, Claire</creatorcontrib><creatorcontrib>L'helgoualc'h, Annie</creatorcontrib><creatorcontrib>Rauch, Michel</creatorcontrib><creatorcontrib>Genet, Valentine</creatorcontrib><creatorcontrib>Lucas-Clerc, Catherine</creatorcontrib><creatorcontrib>Bleau, Christian</creatorcontrib><creatorcontrib>Lamontagne, Lucie</creatorcontrib><creatorcontrib>Samson, Michel</creatorcontrib><title>Pathogenic mouse hepatitis virus or poly(I:C) induce IL-33 in hepatocytes in murine models of hepatitis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33.</description><subject>Animal models</subject><subject>Animals</subject><subject>Antigens</subject><subject>Antigens, CD1d - genetics</subject><subject>Antigens, CD1d - immunology</subject><subject>CD1d antigen</subject><subject>Cytokines</subject><subject>D-Galactosamine</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - immunology</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelial Cells - virology</subject><subject>Endothelium, Vascular - immunology</subject><subject>Endothelium, Vascular - pathology</subject><subject>Endothelium, Vascular - virology</subject><subject>Galactosamine - administration & dosage</subject><subject>Gene Deletion</subject><subject>Gene Expression - immunology</subject><subject>Health aspects</subject><subject>Hepatitis</subject><subject>Hepatitis - etiology</subject><subject>Hepatitis - genetics</subject><subject>Hepatitis - immunology</subject><subject>Hepatitis - pathology</subject><subject>Hepatitis, Viral, Animal - genetics</subject><subject>Hepatitis, Viral, Animal - immunology</subject><subject>Hepatitis, Viral, Animal - pathology</subject><subject>Hepatitis, Viral, Animal - virology</subject><subject>Hepatocytes</subject><subject>Human health and pathology</subject><subject>Infections</subject><subject>Infectious diseases</subject><subject>Inflammation</subject><subject>Injury prevention</subject><subject>Interleukin-33</subject><subject>Interleukins - genetics</subject><subject>Interleukins - immunology</subject><subject>Killer cells</subject><subject>Killer Cells, Natural - immunology</subject><subject>Killer Cells, Natural - pathology</subject><subject>Killer Cells, Natural - virology</subject><subject>Life Sciences</subject><subject>Liver</subject><subject>Liver - immunology</subject><subject>Liver - pathology</subject><subject>Liver - virology</subject><subject>Lymphocytes T</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Murine hepatitis virus - immunology</subject><subject>Murine hepatitis virus - pathogenicity</subject><subject>Natural killer cells</subject><subject>Natural Killer T-Cells - immunology</subject><subject>Natural Killer T-Cells - pathology</subject><subject>Natural Killer T-Cells - virology</subject><subject>Poly (I:C)</subject><subject>Poly I-C - administration & dosage</subject><subject>Rodents</subject><subject>TLR3 protein</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor-TNF</subject><subject>Viral infections</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>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNp1UsuO0zAUjRCIecAfIIjEhlmk-BE_MgukqgKmUiVYwNpynZvUVRIHO6nUv8edZIYpAnlh3-vz8LVOkrzBaIGpwB_3bvSdbha962CBkMiJkM-SS1xQknGC6PMn54vkKoQ9QoxKzl8mFyRHTDLKL5P6ux52robOmrR1Y4B0B70e7GBDerB-DKnzae-a44f17eomtV05GkjXm4zSWExgZ44DhFPZjt52EIVKaCKz-iP2KnlR6SbA63m_Tn5--fxjdZdtvn1dr5abzHAihozjLVRIMs0EZkCkhsIgw3PAhApE5bZCmmHGc0wwYgRxXuiCsjLXUMqcSXqdvJt0-8YFNf9RUDinhBQCERER6wlROr1Xvbet9kfltFX3Dedrpf1gTQOqEgxTSaINg-iAZUkk2lasZBgkz3XU-jS7jdsWSgPd4HVzJnp-09mdqt1BUSFIQXgUuJkEdn_R7pYbdeohJEUcFh1wxL6fzbz7NUIY_jPejKp1nMB2lYvGprXBqGUuJJFSFCyiFv9AxVVCa01MVGVj_4yQTwTjXQgeqsfXYqROeXx4jDrlUc15jLS3Tz_okfQQQPob4-faig</recordid><startdate>20130913</startdate><enddate>20130913</enddate><creator>Arshad, Muhammad Imran</creator><creator>Patrat-Delon, Solène</creator><creator>Piquet-Pellorce, Claire</creator><creator>L'helgoualc'h, Annie</creator><creator>Rauch, Michel</creator><creator>Genet, Valentine</creator><creator>Lucas-Clerc, Catherine</creator><creator>Bleau, Christian</creator><creator>Lamontagne, Lucie</creator><creator>Samson, Michel</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>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>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>COVID</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>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130913</creationdate><title>Pathogenic mouse hepatitis virus or poly(I:C) induce IL-33 in hepatocytes in murine models of hepatitis</title><author>Arshad, Muhammad Imran ; Patrat-Delon, Solène ; Piquet-Pellorce, Claire ; L'helgoualc'h, Annie ; Rauch, Michel ; Genet, Valentine ; Lucas-Clerc, Catherine ; Bleau, Christian ; Lamontagne, Lucie ; Samson, Michel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c627t-61bef085a5715e28ae9c0c64e1237038bf0a515641210520669a935d4aed84583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Antigens</topic><topic>Antigens, CD1d - genetics</topic><topic>Antigens, CD1d - immunology</topic><topic>CD1d antigen</topic><topic>Cytokines</topic><topic>D-Galactosamine</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - immunology</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelial Cells - virology</topic><topic>Endothelium, Vascular - immunology</topic><topic>Endothelium, Vascular - pathology</topic><topic>Endothelium, Vascular - virology</topic><topic>Galactosamine - administration & dosage</topic><topic>Gene Deletion</topic><topic>Gene Expression - immunology</topic><topic>Health aspects</topic><topic>Hepatitis</topic><topic>Hepatitis - etiology</topic><topic>Hepatitis - genetics</topic><topic>Hepatitis - immunology</topic><topic>Hepatitis - pathology</topic><topic>Hepatitis, Viral, Animal - genetics</topic><topic>Hepatitis, Viral, Animal - immunology</topic><topic>Hepatitis, Viral, Animal - pathology</topic><topic>Hepatitis, Viral, Animal - virology</topic><topic>Hepatocytes</topic><topic>Human health and pathology</topic><topic>Infections</topic><topic>Infectious diseases</topic><topic>Inflammation</topic><topic>Injury prevention</topic><topic>Interleukin-33</topic><topic>Interleukins - genetics</topic><topic>Interleukins - immunology</topic><topic>Killer cells</topic><topic>Killer Cells, Natural - immunology</topic><topic>Killer Cells, Natural - pathology</topic><topic>Killer Cells, Natural - virology</topic><topic>Life Sciences</topic><topic>Liver</topic><topic>Liver - immunology</topic><topic>Liver - pathology</topic><topic>Liver - virology</topic><topic>Lymphocytes T</topic><topic>Mice</topic><topic>Mice, Knockout</topic><topic>Murine hepatitis virus - immunology</topic><topic>Murine hepatitis virus - pathogenicity</topic><topic>Natural killer cells</topic><topic>Natural Killer T-Cells - immunology</topic><topic>Natural Killer T-Cells - pathology</topic><topic>Natural Killer T-Cells - virology</topic><topic>Poly (I:C)</topic><topic>Poly I-C - administration & dosage</topic><topic>Rodents</topic><topic>TLR3 protein</topic><topic>Toll-like receptors</topic><topic>Tumor necrosis factor-TNF</topic><topic>Viral infections</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Arshad, Muhammad Imran</creatorcontrib><creatorcontrib>Patrat-Delon, Solène</creatorcontrib><creatorcontrib>Piquet-Pellorce, Claire</creatorcontrib><creatorcontrib>L'helgoualc'h, Annie</creatorcontrib><creatorcontrib>Rauch, Michel</creatorcontrib><creatorcontrib>Genet, Valentine</creatorcontrib><creatorcontrib>Lucas-Clerc, Catherine</creatorcontrib><creatorcontrib>Bleau, Christian</creatorcontrib><creatorcontrib>Lamontagne, Lucie</creatorcontrib><creatorcontrib>Samson, Michel</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Arshad, Muhammad Imran</au><au>Patrat-Delon, Solène</au><au>Piquet-Pellorce, Claire</au><au>L'helgoualc'h, Annie</au><au>Rauch, Michel</au><au>Genet, Valentine</au><au>Lucas-Clerc, Catherine</au><au>Bleau, Christian</au><au>Lamontagne, Lucie</au><au>Samson, Michel</au><au>Leite de Moraes, Maria</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pathogenic mouse hepatitis virus or poly(I:C) induce IL-33 in hepatocytes in murine models of hepatitis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-09-13</date><risdate>2013</risdate><volume>8</volume><issue>9</issue><spage>e74278</spage><pages>e74278-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The IL-33/ST2 axis is known to be involved in liver pathologies. Although, the IL-33 levels increased in sera of viral hepatitis patients in human, the cellular sources of IL-33 in viral hepatitis remained obscure. Therefore, we aimed to investigate the expression of IL-33 in murine fulminant hepatitis induced by a Toll like receptor (TLR3) viral mimetic, poly(I:C) or by pathogenic mouse hepatitis virus (L2-MHV3). The administration of poly(I:C) plus D-galactosamine (D-GalN) in mice led to acute liver injury associated with the induction of IL-33 expression in liver sinusoidal endothelial cells (LSEC) and vascular endothelial cells (VEC), while the administration of poly(I:C) alone led to hepatocyte specific IL-33 expression in addition to vascular IL-33 expression. The hepatocyte-specific IL-33 expression was down-regulated in NK-depleted poly(I:C) treated mice suggesting a partial regulation of IL-33 by NK cells. The CD1d KO (NKT deficient) mice showed hepatoprotection against poly(I:C)-induced hepatitis in association with increased number of IL-33 expressing hepatocytes in CD1d KO mice than WT controls. These results suggest that hepatocyte-specific IL-33 expression in poly(I:C) induced liver injury was partially dependent of NK cells and with limited role of NKT cells. In parallel, the L2-MHV3 infection in mice induced fulminant hepatitis associated with up-regulated IL-33 expression as well as pro-inflammatory cytokine microenvironment in liver. The LSEC and VEC expressed inducible expression of IL-33 following L2-MHV3 infection but the hepatocyte-specific IL-33 expression was only evident between 24 to 32h of post infection. In conclusion, the alarmin cytokine IL-33 was over-expressed during fulminant hepatitis in mice with LSEC, VEC and hepatocytes as potential sources of IL-33.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24058536</pmid><doi>10.1371/journal.pone.0074278</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-09, Vol.8 (9), p.e74278 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1432297027 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animal models Animals Antigens Antigens, CD1d - genetics Antigens, CD1d - immunology CD1d antigen Cytokines D-Galactosamine Endothelial cells Endothelial Cells - immunology Endothelial Cells - pathology Endothelial Cells - virology Endothelium, Vascular - immunology Endothelium, Vascular - pathology Endothelium, Vascular - virology Galactosamine - administration & dosage Gene Deletion Gene Expression - immunology Health aspects Hepatitis Hepatitis - etiology Hepatitis - genetics Hepatitis - immunology Hepatitis - pathology Hepatitis, Viral, Animal - genetics Hepatitis, Viral, Animal - immunology Hepatitis, Viral, Animal - pathology Hepatitis, Viral, Animal - virology Hepatocytes Human health and pathology Infections Infectious diseases Inflammation Injury prevention Interleukin-33 Interleukins - genetics Interleukins - immunology Killer cells Killer Cells, Natural - immunology Killer Cells, Natural - pathology Killer Cells, Natural - virology Life Sciences Liver Liver - immunology Liver - pathology Liver - virology Lymphocytes T Mice Mice, Knockout Murine hepatitis virus - immunology Murine hepatitis virus - pathogenicity Natural killer cells Natural Killer T-Cells - immunology Natural Killer T-Cells - pathology Natural Killer T-Cells - virology Poly (I:C) Poly I-C - administration & dosage Rodents TLR3 protein Toll-like receptors Tumor necrosis factor-TNF Viral infections Viruses |
| title | Pathogenic mouse hepatitis virus or poly(I:C) induce IL-33 in hepatocytes in murine models of hepatitis |
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