Bacterial endotoxin induces the release of high mobility group box 1 via the IFN-beta signaling pathway
Sepsis is a devastating condition characterized by a systemic inflammatory response. Recently, high mobility group box 1 (HMGB1) was identified as a necessary and sufficient mediator of the lethal systemic inflammation caused by sepsis. However, despite its clinical importance, the mechanism of HMGB...
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| Veröffentlicht in: | The Journal of immunology (1950) 2009-02, Vol.182 (4), p.2458-2466 |
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| container_title | The Journal of immunology (1950) |
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| creator | Kim, Ju-Hyun Kim, Seon-Ju Lee, Im-Soon Lee, Myung-Shik Uematsu, Satoshi Akira, Shizuo Oh, Kwon Ik |
| description | Sepsis is a devastating condition characterized by a systemic inflammatory response. Recently, high mobility group box 1 (HMGB1) was identified as a necessary and sufficient mediator of the lethal systemic inflammation caused by sepsis. However, despite its clinical importance, the mechanism of HMGB1 release has remained to be elusive. In this study, we demonstrate that the IFN-beta-mediated JAK/STAT pathway is essential for LPS or Escherichia coli-induced HMGB1 release, which is dependent on Toll/IL-1R domain-containing adapter-inducing IFN-beta adaptor. Additionally, we show that NO acts as a downstream molecule of the IFN-beta signaling. Furthermore, the JAK inhibitor treatment as well as the STAT-1 or IFN-beta receptor deficiency reduced HMGB1 release in a murine model of endotoxemia. Our results suggest that HMGB1 release in sepsis is dependent on the IFN-beta signaling axis; thus, therapeutic agents that selectively inhibit IFN-beta signaling could be beneficial in the treatment of sepsis. |
| doi_str_mv | 10.4049/jimmunol.0801364 |
| format | Article |
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Recently, high mobility group box 1 (HMGB1) was identified as a necessary and sufficient mediator of the lethal systemic inflammation caused by sepsis. However, despite its clinical importance, the mechanism of HMGB1 release has remained to be elusive. In this study, we demonstrate that the IFN-beta-mediated JAK/STAT pathway is essential for LPS or Escherichia coli-induced HMGB1 release, which is dependent on Toll/IL-1R domain-containing adapter-inducing IFN-beta adaptor. Additionally, we show that NO acts as a downstream molecule of the IFN-beta signaling. Furthermore, the JAK inhibitor treatment as well as the STAT-1 or IFN-beta receptor deficiency reduced HMGB1 release in a murine model of endotoxemia. Our results suggest that HMGB1 release in sepsis is dependent on the IFN-beta signaling axis; thus, therapeutic agents that selectively inhibit IFN-beta signaling could be beneficial in the treatment of sepsis.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.0801364</identifier><identifier>PMID: 19201901</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Blotting, Western ; Endotoxemia - immunology ; Endotoxemia - metabolism ; Endotoxins - immunology ; Endotoxins - metabolism ; Enzyme-Linked Immunosorbent Assay ; Escherichia coli - immunology ; HMGB1 Protein - immunology ; HMGB1 Protein - metabolism ; Interferon-beta - immunology ; Interferon-beta - metabolism ; Janus Kinases - immunology ; Janus Kinases - metabolism ; Lipopolysaccharides - immunology ; Macrophages - immunology ; Macrophages - metabolism ; Mice ; Nitric Oxide - immunology ; Nitric Oxide - metabolism ; Signal Transduction - immunology ; STAT1 Transcription Factor - immunology ; STAT1 Transcription Factor - metabolism ; Toll-Like Receptor 4 - immunology ; Toll-Like Receptor 4 - metabolism</subject><ispartof>The Journal of immunology (1950), 2009-02, Vol.182 (4), p.2458-2466</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c339t-8a0c07fa6c8d1ef14d712c8ad6b8bea6913f2d302bbfb494e19a79a8fdf007173</citedby><cites>FETCH-LOGICAL-c339t-8a0c07fa6c8d1ef14d712c8ad6b8bea6913f2d302bbfb494e19a79a8fdf007173</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19201901$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Ju-Hyun</creatorcontrib><creatorcontrib>Kim, Seon-Ju</creatorcontrib><creatorcontrib>Lee, Im-Soon</creatorcontrib><creatorcontrib>Lee, Myung-Shik</creatorcontrib><creatorcontrib>Uematsu, Satoshi</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Oh, Kwon Ik</creatorcontrib><title>Bacterial endotoxin induces the release of high mobility group box 1 via the IFN-beta signaling pathway</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Sepsis is a devastating condition characterized by a systemic inflammatory response. Recently, high mobility group box 1 (HMGB1) was identified as a necessary and sufficient mediator of the lethal systemic inflammation caused by sepsis. However, despite its clinical importance, the mechanism of HMGB1 release has remained to be elusive. In this study, we demonstrate that the IFN-beta-mediated JAK/STAT pathway is essential for LPS or Escherichia coli-induced HMGB1 release, which is dependent on Toll/IL-1R domain-containing adapter-inducing IFN-beta adaptor. Additionally, we show that NO acts as a downstream molecule of the IFN-beta signaling. Furthermore, the JAK inhibitor treatment as well as the STAT-1 or IFN-beta receptor deficiency reduced HMGB1 release in a murine model of endotoxemia. Our results suggest that HMGB1 release in sepsis is dependent on the IFN-beta signaling axis; thus, therapeutic agents that selectively inhibit IFN-beta signaling could be beneficial in the treatment of sepsis.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Endotoxemia - immunology</subject><subject>Endotoxemia - metabolism</subject><subject>Endotoxins - immunology</subject><subject>Endotoxins - metabolism</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>Escherichia coli - immunology</subject><subject>HMGB1 Protein - immunology</subject><subject>HMGB1 Protein - metabolism</subject><subject>Interferon-beta - immunology</subject><subject>Interferon-beta - metabolism</subject><subject>Janus Kinases - immunology</subject><subject>Janus Kinases - metabolism</subject><subject>Lipopolysaccharides - immunology</subject><subject>Macrophages - immunology</subject><subject>Macrophages - metabolism</subject><subject>Mice</subject><subject>Nitric Oxide - immunology</subject><subject>Nitric Oxide - metabolism</subject><subject>Signal Transduction - immunology</subject><subject>STAT1 Transcription Factor - immunology</subject><subject>STAT1 Transcription Factor - metabolism</subject><subject>Toll-Like Receptor 4 - immunology</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkLFOwzAURS0EoqWwMyFPbCnPSerEI1QUKlWwwBw9J8-pqyQucQLt31NoENNdzj3DYexawDSGWN1tbF33jaumkIKIZHzCxmI2g0BKkKdsDBCGgUhkMmIX3m8AQEIYn7ORUCEIBWLMygfMO2otVpyawnVuZxtum6LPyfNuTbylitATd4avbbnmtdO2st2el63rt1y7HRf80-IvvFy8BJo65N6WDVa2KfkWu_UX7i_ZmcHK09WwE_a-eHybPwer16fl_H4V5FGkuiBFyCExKPO0EGREXCQizFMspE41oVQiMmERQai10bGKSShMFKamMACJSKIJuz16t6376Ml3WW19TlWFDbneZ1KmSkVSHEA4gnnrvG_JZNvW1tjuMwHZT9zsL242xD1cbgZ3r2sq_g9DzegbCjJ4uQ</recordid><startdate>20090215</startdate><enddate>20090215</enddate><creator>Kim, Ju-Hyun</creator><creator>Kim, Seon-Ju</creator><creator>Lee, Im-Soon</creator><creator>Lee, Myung-Shik</creator><creator>Uematsu, Satoshi</creator><creator>Akira, Shizuo</creator><creator>Oh, Kwon Ik</creator><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>20090215</creationdate><title>Bacterial endotoxin induces the release of high mobility group box 1 via the IFN-beta signaling pathway</title><author>Kim, Ju-Hyun ; Kim, Seon-Ju ; Lee, Im-Soon ; Lee, Myung-Shik ; Uematsu, Satoshi ; Akira, Shizuo ; Oh, Kwon Ik</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c339t-8a0c07fa6c8d1ef14d712c8ad6b8bea6913f2d302bbfb494e19a79a8fdf007173</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Blotting, Western</topic><topic>Endotoxemia - immunology</topic><topic>Endotoxemia - metabolism</topic><topic>Endotoxins - immunology</topic><topic>Endotoxins - metabolism</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>Escherichia coli - immunology</topic><topic>HMGB1 Protein - immunology</topic><topic>HMGB1 Protein - metabolism</topic><topic>Interferon-beta - immunology</topic><topic>Interferon-beta - metabolism</topic><topic>Janus Kinases - immunology</topic><topic>Janus Kinases - metabolism</topic><topic>Lipopolysaccharides - immunology</topic><topic>Macrophages - immunology</topic><topic>Macrophages - metabolism</topic><topic>Mice</topic><topic>Nitric Oxide - immunology</topic><topic>Nitric Oxide - metabolism</topic><topic>Signal Transduction - immunology</topic><topic>STAT1 Transcription Factor - immunology</topic><topic>STAT1 Transcription Factor - metabolism</topic><topic>Toll-Like Receptor 4 - immunology</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Ju-Hyun</creatorcontrib><creatorcontrib>Kim, Seon-Ju</creatorcontrib><creatorcontrib>Lee, Im-Soon</creatorcontrib><creatorcontrib>Lee, Myung-Shik</creatorcontrib><creatorcontrib>Uematsu, Satoshi</creatorcontrib><creatorcontrib>Akira, Shizuo</creatorcontrib><creatorcontrib>Oh, Kwon Ik</creatorcontrib><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>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Ju-Hyun</au><au>Kim, Seon-Ju</au><au>Lee, Im-Soon</au><au>Lee, Myung-Shik</au><au>Uematsu, Satoshi</au><au>Akira, Shizuo</au><au>Oh, Kwon Ik</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bacterial endotoxin induces the release of high mobility group box 1 via the IFN-beta signaling pathway</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2009-02-15</date><risdate>2009</risdate><volume>182</volume><issue>4</issue><spage>2458</spage><epage>2466</epage><pages>2458-2466</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Sepsis is a devastating condition characterized by a systemic inflammatory response. Recently, high mobility group box 1 (HMGB1) was identified as a necessary and sufficient mediator of the lethal systemic inflammation caused by sepsis. However, despite its clinical importance, the mechanism of HMGB1 release has remained to be elusive. In this study, we demonstrate that the IFN-beta-mediated JAK/STAT pathway is essential for LPS or Escherichia coli-induced HMGB1 release, which is dependent on Toll/IL-1R domain-containing adapter-inducing IFN-beta adaptor. Additionally, we show that NO acts as a downstream molecule of the IFN-beta signaling. Furthermore, the JAK inhibitor treatment as well as the STAT-1 or IFN-beta receptor deficiency reduced HMGB1 release in a murine model of endotoxemia. Our results suggest that HMGB1 release in sepsis is dependent on the IFN-beta signaling axis; thus, therapeutic agents that selectively inhibit IFN-beta signaling could be beneficial in the treatment of sepsis.</abstract><cop>United States</cop><pmid>19201901</pmid><doi>10.4049/jimmunol.0801364</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Blotting, Western Endotoxemia - immunology Endotoxemia - metabolism Endotoxins - immunology Endotoxins - metabolism Enzyme-Linked Immunosorbent Assay Escherichia coli - immunology HMGB1 Protein - immunology HMGB1 Protein - metabolism Interferon-beta - immunology Interferon-beta - metabolism Janus Kinases - immunology Janus Kinases - metabolism Lipopolysaccharides - immunology Macrophages - immunology Macrophages - metabolism Mice Nitric Oxide - immunology Nitric Oxide - metabolism Signal Transduction - immunology STAT1 Transcription Factor - immunology STAT1 Transcription Factor - metabolism Toll-Like Receptor 4 - immunology Toll-Like Receptor 4 - metabolism |
| title | Bacterial endotoxin induces the release of high mobility group box 1 via the IFN-beta signaling pathway |
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