Combined inhibition of complement and CD14 improved outcome in porcine polymicrobial sepsis
Sepsis is an exaggerated and dysfunctional immune response to infection. Activation of innate immunity recognition systems including complement and the Toll-like receptor family initiate this disproportionate inflammatory response. The aim of this study was to explore the effect of combined inhibiti...
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| Veröffentlicht in: | Critical care (London, England) England), 2015-11, Vol.19 (1), p.415-415, Article 415 |
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| creator | Skjeflo, Espen W Sagatun, Caroline Dybwik, Knut Aam, Sturla Urving, Sven H Nunn, Miles A Fure, Hilde Lau, Corinna Brekke, Ole-Lars Huber-Lang, Markus Espevik, Terje Barratt-Due, Andreas Nielsen, Erik W Mollnes, Tom E |
| description | Sepsis is an exaggerated and dysfunctional immune response to infection. Activation of innate immunity recognition systems including complement and the Toll-like receptor family initiate this disproportionate inflammatory response. The aim of this study was to explore the effect of combined inhibition of the complement component C5 and the Toll-like receptor co-factor CD14 on survival, hemodynamic parameters and systemic inflammation including complement activation in a clinically relevant porcine model of polymicrobial sepsis.
Norwegian landrace piglets (4 ± 0.5 kg) were blindly randomized to a treatment group (n = 12) receiving the C5 inhibitor coversin (OmCI) and anti-CD14 or to a positive control group (n = 12) receiving saline. Under anesthesia, sepsis was induced by a 2 cm cecal incision and the piglets were monitored in standard intensive care for 8 hours. Three sham piglets had a laparotomy without cecal incision or treatment. Complement activation was measured as sC5b-9 using enzyme immunoassay. Cytokines were measured with multiplex technology.
Combined C5 and CD14 inhibition significantly improved survival (p = 0.03). Nine piglets survived in the treatment group and four in the control group. The treatment group had significantly lower pulmonary artery pressure (p = 0.04) and ratio of pulmonary artery pressure to systemic artery pressure (p |
| doi_str_mv | 10.1186/s13054-015-1129-9 |
| format | Article |
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Norwegian landrace piglets (4 ± 0.5 kg) were blindly randomized to a treatment group (n = 12) receiving the C5 inhibitor coversin (OmCI) and anti-CD14 or to a positive control group (n = 12) receiving saline. Under anesthesia, sepsis was induced by a 2 cm cecal incision and the piglets were monitored in standard intensive care for 8 hours. Three sham piglets had a laparotomy without cecal incision or treatment. Complement activation was measured as sC5b-9 using enzyme immunoassay. Cytokines were measured with multiplex technology.
Combined C5 and CD14 inhibition significantly improved survival (p = 0.03). Nine piglets survived in the treatment group and four in the control group. The treatment group had significantly lower pulmonary artery pressure (p = 0.04) and ratio of pulmonary artery pressure to systemic artery pressure (p < 0.001). Plasma sC5b-9 levels were significantly lower in the treatment group (p < 0.001) and correlated significantly with mortality (p = 0.006). IL-8 and IL-10 were significantly (p < 0.05) lower in the treatment group.
Combined inhibition of C5 and CD14 significantly improved survival, hemodynamic parameters and inflammation in a blinded, randomized trial of porcine polymicrobial sepsis.</description><identifier>ISSN: 1364-8535</identifier><identifier>ISSN: 1466-609X</identifier><identifier>EISSN: 1466-609X</identifier><identifier>EISSN: 1364-8535</identifier><identifier>EISSN: 1366-609X</identifier><identifier>DOI: 10.1186/s13054-015-1129-9</identifier><identifier>PMID: 26612199</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Clinical medical disciplines: 750 ; Complement C5 - antagonists & inhibitors ; Critical care ; Cytokines ; Enzymes ; Epidemiology ; Infection ; Inflammation ; Inflammation - blood ; Inflammation - mortality ; Klinisk medisinske fag: 750 ; Laboratories ; Lipopolysaccharide Receptors - metabolism ; Medical disciplines: 700 ; Medical prognosis ; Medisinske Fag: 700 ; Multiple organ dysfunction syndrome ; Neutrophils ; Patient outcomes ; Pulmonary arteries ; Rodents ; Sepsis ; Sepsis - drug therapy ; Sepsis - metabolism ; Sepsis - microbiology ; Sepsis - mortality ; Swine ; Toll-Like Receptors - immunology ; Toll-Like Receptors - metabolism ; Tumor necrosis factor-TNF ; VDP</subject><ispartof>Critical care (London, England), 2015-11, Vol.19 (1), p.415-415, Article 415</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>info:eu-repo/semantics/openAccess</rights><rights>Skjeflo et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c615t-a4167e8786fc0491efe2faa50296615e9319acee5bf46795916c636e8d4da32e3</citedby><cites>FETCH-LOGICAL-c615t-a4167e8786fc0491efe2faa50296615e9319acee5bf46795916c636e8d4da32e3</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/PMC4662001/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4662001/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,26548,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26612199$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Skjeflo, Espen W</creatorcontrib><creatorcontrib>Sagatun, Caroline</creatorcontrib><creatorcontrib>Dybwik, Knut</creatorcontrib><creatorcontrib>Aam, Sturla</creatorcontrib><creatorcontrib>Urving, Sven H</creatorcontrib><creatorcontrib>Nunn, Miles A</creatorcontrib><creatorcontrib>Fure, Hilde</creatorcontrib><creatorcontrib>Lau, Corinna</creatorcontrib><creatorcontrib>Brekke, Ole-Lars</creatorcontrib><creatorcontrib>Huber-Lang, Markus</creatorcontrib><creatorcontrib>Espevik, Terje</creatorcontrib><creatorcontrib>Barratt-Due, Andreas</creatorcontrib><creatorcontrib>Nielsen, Erik W</creatorcontrib><creatorcontrib>Mollnes, Tom E</creatorcontrib><title>Combined inhibition of complement and CD14 improved outcome in porcine polymicrobial sepsis</title><title>Critical care (London, England)</title><addtitle>Crit Care</addtitle><description>Sepsis is an exaggerated and dysfunctional immune response to infection. Activation of innate immunity recognition systems including complement and the Toll-like receptor family initiate this disproportionate inflammatory response. The aim of this study was to explore the effect of combined inhibition of the complement component C5 and the Toll-like receptor co-factor CD14 on survival, hemodynamic parameters and systemic inflammation including complement activation in a clinically relevant porcine model of polymicrobial sepsis.
Norwegian landrace piglets (4 ± 0.5 kg) were blindly randomized to a treatment group (n = 12) receiving the C5 inhibitor coversin (OmCI) and anti-CD14 or to a positive control group (n = 12) receiving saline. Under anesthesia, sepsis was induced by a 2 cm cecal incision and the piglets were monitored in standard intensive care for 8 hours. Three sham piglets had a laparotomy without cecal incision or treatment. Complement activation was measured as sC5b-9 using enzyme immunoassay. Cytokines were measured with multiplex technology.
Combined C5 and CD14 inhibition significantly improved survival (p = 0.03). Nine piglets survived in the treatment group and four in the control group. The treatment group had significantly lower pulmonary artery pressure (p = 0.04) and ratio of pulmonary artery pressure to systemic artery pressure (p < 0.001). Plasma sC5b-9 levels were significantly lower in the treatment group (p < 0.001) and correlated significantly with mortality (p = 0.006). IL-8 and IL-10 were significantly (p < 0.05) lower in the treatment group.
Combined inhibition of C5 and CD14 significantly improved survival, hemodynamic parameters and inflammation in a blinded, randomized trial of porcine polymicrobial sepsis.</description><subject>Analysis</subject><subject>Animals</subject><subject>Clinical medical disciplines: 750</subject><subject>Complement C5 - antagonists & inhibitors</subject><subject>Critical care</subject><subject>Cytokines</subject><subject>Enzymes</subject><subject>Epidemiology</subject><subject>Infection</subject><subject>Inflammation</subject><subject>Inflammation - blood</subject><subject>Inflammation - mortality</subject><subject>Klinisk medisinske fag: 750</subject><subject>Laboratories</subject><subject>Lipopolysaccharide Receptors - metabolism</subject><subject>Medical disciplines: 700</subject><subject>Medical prognosis</subject><subject>Medisinske Fag: 700</subject><subject>Multiple organ dysfunction syndrome</subject><subject>Neutrophils</subject><subject>Patient outcomes</subject><subject>Pulmonary arteries</subject><subject>Rodents</subject><subject>Sepsis</subject><subject>Sepsis - drug therapy</subject><subject>Sepsis - metabolism</subject><subject>Sepsis - microbiology</subject><subject>Sepsis - mortality</subject><subject>Swine</subject><subject>Toll-Like Receptors - immunology</subject><subject>Toll-Like Receptors - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>VDP</subject><issn>1364-8535</issn><issn>1466-609X</issn><issn>1466-609X</issn><issn>1364-8535</issn><issn>1366-609X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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>3HK</sourceid><recordid>eNp9Ul1rFTEQXUSxtfoDfJEFX3zZmtl8bPIilNtWhYIvCoIPIZudbVN2kzXZW-i_dy63H1RE8jAhc2bmzMmpqrfAjgG0-liAMykaBrIBaE1jnlWHIJRqFDM_n9OdK9FoyeVB9aqUa8ag04q_rA5apaAFYw6rX5s09yHiUId4FfqwhhTrNNY-zcuEM8a1dnGoN6cg6jAvOd0QNG1XyiOV1EvKnsopTrdz8Dn1wU11waWE8rp6Mbqp4Ju7eFT9OD_7vvnSXHz7_HVzctF4BXJtnADVoSZqo2fCAI7Yjs5J1hqiKdFwMM4jyn4UqjPSgPKKK9SDGBxvkR9Vn_Z9l20_4-CJdHaTXXKYXb61yQX7NBPDlb1MN5akakkUavBu38DnUNYQbUzZWWCMd1ZL3RHgw92EnH5vsax2DsXjNLmIaVssdFwL3RqtCfr-L-h12uZI-1swEmRHe_H_oroOjAIt4RF16Sa0IY6J6PvdaHsilIGWM6MIdfwPFJ0B6UdSxDHQ-5MCuF83lZJxfJAKmN0Zy-6NZclYdmcsax4l2iv5UHHvJP4H5X7GAg</recordid><startdate>20151127</startdate><enddate>20151127</enddate><creator>Skjeflo, Espen W</creator><creator>Sagatun, Caroline</creator><creator>Dybwik, Knut</creator><creator>Aam, Sturla</creator><creator>Urving, Sven H</creator><creator>Nunn, Miles A</creator><creator>Fure, Hilde</creator><creator>Lau, Corinna</creator><creator>Brekke, Ole-Lars</creator><creator>Huber-Lang, Markus</creator><creator>Espevik, Terje</creator><creator>Barratt-Due, Andreas</creator><creator>Nielsen, Erik W</creator><creator>Mollnes, Tom E</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>3HK</scope><scope>5PM</scope></search><sort><creationdate>20151127</creationdate><title>Combined inhibition of complement and CD14 improved outcome in porcine polymicrobial sepsis</title><author>Skjeflo, Espen W ; Sagatun, Caroline ; Dybwik, Knut ; Aam, Sturla ; Urving, Sven H ; Nunn, Miles A ; Fure, Hilde ; Lau, Corinna ; Brekke, Ole-Lars ; Huber-Lang, Markus ; Espevik, Terje ; Barratt-Due, Andreas ; Nielsen, Erik W ; Mollnes, Tom E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c615t-a4167e8786fc0491efe2faa50296615e9319acee5bf46795916c636e8d4da32e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Analysis</topic><topic>Animals</topic><topic>Clinical medical disciplines: 750</topic><topic>Complement C5 - antagonists & inhibitors</topic><topic>Critical care</topic><topic>Cytokines</topic><topic>Enzymes</topic><topic>Epidemiology</topic><topic>Infection</topic><topic>Inflammation</topic><topic>Inflammation - blood</topic><topic>Inflammation - mortality</topic><topic>Klinisk medisinske fag: 750</topic><topic>Laboratories</topic><topic>Lipopolysaccharide Receptors - metabolism</topic><topic>Medical disciplines: 700</topic><topic>Medical prognosis</topic><topic>Medisinske Fag: 700</topic><topic>Multiple organ dysfunction syndrome</topic><topic>Neutrophils</topic><topic>Patient outcomes</topic><topic>Pulmonary arteries</topic><topic>Rodents</topic><topic>Sepsis</topic><topic>Sepsis - drug therapy</topic><topic>Sepsis - metabolism</topic><topic>Sepsis - microbiology</topic><topic>Sepsis - mortality</topic><topic>Swine</topic><topic>Toll-Like Receptors - immunology</topic><topic>Toll-Like Receptors - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>VDP</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Skjeflo, Espen W</creatorcontrib><creatorcontrib>Sagatun, Caroline</creatorcontrib><creatorcontrib>Dybwik, Knut</creatorcontrib><creatorcontrib>Aam, Sturla</creatorcontrib><creatorcontrib>Urving, Sven H</creatorcontrib><creatorcontrib>Nunn, Miles A</creatorcontrib><creatorcontrib>Fure, Hilde</creatorcontrib><creatorcontrib>Lau, Corinna</creatorcontrib><creatorcontrib>Brekke, Ole-Lars</creatorcontrib><creatorcontrib>Huber-Lang, Markus</creatorcontrib><creatorcontrib>Espevik, Terje</creatorcontrib><creatorcontrib>Barratt-Due, Andreas</creatorcontrib><creatorcontrib>Nielsen, Erik W</creatorcontrib><creatorcontrib>Mollnes, Tom E</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>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>ProQuest Central Essentials</collection><collection>ProQuest Central</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 Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</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>MEDLINE - Academic</collection><collection>NORA - Norwegian Open Research Archives</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Critical care (London, England)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Skjeflo, Espen W</au><au>Sagatun, Caroline</au><au>Dybwik, Knut</au><au>Aam, Sturla</au><au>Urving, Sven H</au><au>Nunn, Miles A</au><au>Fure, Hilde</au><au>Lau, Corinna</au><au>Brekke, Ole-Lars</au><au>Huber-Lang, Markus</au><au>Espevik, Terje</au><au>Barratt-Due, Andreas</au><au>Nielsen, Erik W</au><au>Mollnes, Tom E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Combined inhibition of complement and CD14 improved outcome in porcine polymicrobial sepsis</atitle><jtitle>Critical care (London, England)</jtitle><addtitle>Crit Care</addtitle><date>2015-11-27</date><risdate>2015</risdate><volume>19</volume><issue>1</issue><spage>415</spage><epage>415</epage><pages>415-415</pages><artnum>415</artnum><issn>1364-8535</issn><issn>1466-609X</issn><eissn>1466-609X</eissn><eissn>1364-8535</eissn><eissn>1366-609X</eissn><abstract>Sepsis is an exaggerated and dysfunctional immune response to infection. Activation of innate immunity recognition systems including complement and the Toll-like receptor family initiate this disproportionate inflammatory response. The aim of this study was to explore the effect of combined inhibition of the complement component C5 and the Toll-like receptor co-factor CD14 on survival, hemodynamic parameters and systemic inflammation including complement activation in a clinically relevant porcine model of polymicrobial sepsis.
Norwegian landrace piglets (4 ± 0.5 kg) were blindly randomized to a treatment group (n = 12) receiving the C5 inhibitor coversin (OmCI) and anti-CD14 or to a positive control group (n = 12) receiving saline. Under anesthesia, sepsis was induced by a 2 cm cecal incision and the piglets were monitored in standard intensive care for 8 hours. Three sham piglets had a laparotomy without cecal incision or treatment. Complement activation was measured as sC5b-9 using enzyme immunoassay. Cytokines were measured with multiplex technology.
Combined C5 and CD14 inhibition significantly improved survival (p = 0.03). Nine piglets survived in the treatment group and four in the control group. The treatment group had significantly lower pulmonary artery pressure (p = 0.04) and ratio of pulmonary artery pressure to systemic artery pressure (p < 0.001). Plasma sC5b-9 levels were significantly lower in the treatment group (p < 0.001) and correlated significantly with mortality (p = 0.006). IL-8 and IL-10 were significantly (p < 0.05) lower in the treatment group.
Combined inhibition of C5 and CD14 significantly improved survival, hemodynamic parameters and inflammation in a blinded, randomized trial of porcine polymicrobial sepsis.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26612199</pmid><doi>10.1186/s13054-015-1129-9</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Critical care (London, England), 2015-11, Vol.19 (1), p.415-415, Article 415 |
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| source | MEDLINE; NORA - Norwegian Open Research Archives; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Springer Nature OA Free Journals; PubMed Central; Alma/SFX Local Collection; SpringerLink Journals - AutoHoldings |
| subjects | Analysis Animals Clinical medical disciplines: 750 Complement C5 - antagonists & inhibitors Critical care Cytokines Enzymes Epidemiology Infection Inflammation Inflammation - blood Inflammation - mortality Klinisk medisinske fag: 750 Laboratories Lipopolysaccharide Receptors - metabolism Medical disciplines: 700 Medical prognosis Medisinske Fag: 700 Multiple organ dysfunction syndrome Neutrophils Patient outcomes Pulmonary arteries Rodents Sepsis Sepsis - drug therapy Sepsis - metabolism Sepsis - microbiology Sepsis - mortality Swine Toll-Like Receptors - immunology Toll-Like Receptors - metabolism Tumor necrosis factor-TNF VDP |
| title | Combined inhibition of complement and CD14 improved outcome in porcine polymicrobial sepsis |
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