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dc.contributor.authorHellerud, Bernt C
dc.contributor.authorOrrem, Hilde L.
dc.contributor.authorDybwik, Knut Gustav
dc.contributor.authorPischke, Søren Erik
dc.contributor.authorBarratt-Due, Andreas
dc.contributor.authorCastellheim, Albert
dc.contributor.authorFure, Hilde
dc.contributor.authorBergseth, Grete
dc.contributor.authorChristiansen, Dorte
dc.contributor.authorNunn, Miles A.
dc.contributor.authorEspevik, Terje
dc.contributor.authorLau, Corinna
dc.contributor.authorBrandtzæg, Petter
dc.contributor.authorNielsen, Erik Waage
dc.contributor.authorMollnes, Tom Eirik
dc.date.accessioned2017-11-22T14:56:18Z
dc.date.available2017-11-22T14:56:18Z
dc.date.created2017-11-17T09:59:29Z
dc.date.issued2017
dc.identifier.citationJournal of Intensive Care. 2017, 5:21 1-9.nb_NO
dc.identifier.issn2052-0492
dc.identifier.urihttp://hdl.handle.net/11250/2467631
dc.description.abstractBackground Fulminant meningococcal sepsis, characterized by overwhelming innate immune activation, mostly affects young people and causes high mortality. This study aimed to investigate the effect of targeting two key molecules of innate immunity, complement component C5, and co-receptor CD14 in the Toll-like receptor system, on the inflammatory response in meningococcal sepsis. Methods Meningococcal sepsis was simulated by continuous intravenous infusion of an escalating dose of heat-inactivated Neisseria meningitidis administered over 3 h. The piglets were randomized, blinded to the investigators, to a positive control group (n = 12) receiving saline and to an interventional group (n = 12) receiving a recombinant anti-CD14 monoclonal antibody together with the C5 inhibitor coversin. Results A substantial increase in plasma complement activation in the untreated group was completely abolished in the treatment group (p = 0.006). The following inflammatory mediators were substantially reduced in plasma in the treatment group: Interferon-γ by 75% (p = 0.0001), tumor necrosis factor by 50% (p = 0.01), Interleukin (IL)-8 by 50% (p = 0.03), IL-10 by 40% (p = 0.04), IL-12p40 by 50% (p = 0.03), and granulocyte CD11b (CR3) expression by 20% (p = 0.01). Conclusion Inhibition of C5 and CD14 may be beneficial in attenuating the detrimental effects of complement activation and modulating the cytokine storm in patients with fulminant meningococcal sepsis.nb_NO
dc.language.isoengnb_NO
dc.publisherBioMed Centralnb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleCombined inhibition of C5 and CD14 efficiently attenuated the inflammatory response in a porcine model of meningococcal sepsisnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.description.versionpublishedVersionnb_NO
dc.source.pagenumber1-9nb_NO
dc.source.volume5:21nb_NO
dc.source.journalJournal of Intensive Carenb_NO
dc.identifier.doi10.1186/s40560-017-0217-0
dc.identifier.cristin1515136
dc.description.localcode© The Author(s). 2017 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise statednb_NO
cristin.unitcode194,65,15,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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