dc.contributor.author | Genster, Ninette | |
dc.contributor.author | Østrup, Olga | |
dc.contributor.author | Schjalm, Camilla | |
dc.contributor.author | Mollnes, Tom Eirik | |
dc.contributor.author | Cowland, Jack B. | |
dc.contributor.author | Garred, Peter | |
dc.date.accessioned | 2017-11-08T08:04:28Z | |
dc.date.available | 2017-11-08T08:04:28Z | |
dc.date.created | 2017-09-12T10:47:55Z | |
dc.date.issued | 2017 | |
dc.identifier.issn | 2045-2322 | |
dc.identifier.uri | http://hdl.handle.net/11250/2464780 | |
dc.description.abstract | Ficolins are a family of pattern recognition molecules that are capable of activating the lectin pathway of complement. A limited number of reports have demonstrated a protective role of ficolins in animal models of infection. In addition, an immune modulatory role of ficolins has been suggested. Yet, the contribution of ficolins to inflammatory disease processes remains elusive. To address this, we investigated ficolin deficient mice during a lipopolysaccharide (LPS)-induced model of systemic inflammation. Although murine serum ficolin was shown to bind LPS in vitro, there was no difference between wildtype and ficolin deficient mice in morbidity and mortality by LPS-induced inflammation. Moreover, there was no difference between wildtype and ficolin deficient mice in the inflammatory cytokine profiles after LPS challenge. These findings were substantiated by microarray analysis revealing an unaltered spleen transcriptome profile in ficolin deficient mice compared to wildtype mice. Collectively, results from this study demonstrate that ficolins are not involved in host response to LPS-induced systemic inflammation. | nb_NO |
dc.language.iso | eng | nb_NO |
dc.publisher | Nature Publishing Group | nb_NO |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.title | Ficolins do not alter host immune responses to lipopolysaccharide-induced inflammation in vivo | nb_NO |
dc.type | Journal article | nb_NO |
dc.type | Peer reviewed | nb_NO |
dc.description.version | publishedVersion | nb_NO |
dc.source.volume | 7 | nb_NO |
dc.source.journal | Scientific Reports | nb_NO |
dc.source.issue | 1 | nb_NO |
dc.identifier.doi | 10.1038/s41598-017-04121-w | |
dc.identifier.cristin | 1492924 | |
dc.description.localcode | © 2017 The Authors. Published by Nature Publishing Group. This is an open access article licensed under a Creative Commons Attribution 4.0 International License | nb_NO |
cristin.unitcode | 194,65,15,0 | |
cristin.unitname | Institutt for klinisk og molekylær medisin | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |