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dc.date.accessioned2016-02-29T08:46:09Z
dc.date.available2016-02-29T08:46:09Z
dc.date.created2015-08-17T11:56:25Z
dc.date.issued2015
dc.identifier.citationLau, Corinna Olstad, Ole Kristoffer Holden, Marit Nygård, Ståle Fure, Hilde Lappegård, Knut Tore Brekke, Ole Lars Espevik, Terje Hovig, Johannes Eivind Mollnes, Tom Eirik . Gene expression profiling of Gram-negative bacteria-induced inflammation in human whole blood: The role of complement and CD14-mediated innate immune response. Genomics Data. 2015, 5, 176-183
dc.identifier.urihttp://hdl.handle.net/10852/49251
dc.description.abstractNon-sterile pathogen-induced sepsis and sterile inflammation like in trauma or ischemia–reperfusion injury may both coincide with the life threatening systemic inflammatory response syndrome and multi-organ failure. Consequently, there is an urgent need for specific biomarkers in order to distinguish sepsis from sterile conditions. The overall aim of this study was to uncover putative sepsis biomarkers and biomarker pathways, as well as to test the efficacy of combined inhibition of innate immunity key players complement and Toll-like receptor co-receptor CD14 as a possible therapeutic regimen for sepsis. We performed whole blood gene expression analyses using microarray in order to profile Gram-negative bacteria-induced inflammatory responses in an ex vivo human whole blood model. The experiments were performed in the presence or absence of inhibitors of complement proteins (C3 and CD88 (C5a receptor 1)) and CD14, alone or in combination. In addition, we used blood from a C5-deficient donor. Anti-coagulated whole blood was challenged with heat-inactivated Escherichia coli for 2 h, total RNA was isolated and microarray analyses were performed on the Affymetrix GeneChip Gene 1.0 ST Array platform. The initial experiments were performed in duplicates using blood from two healthy donors. C5-deficiency is very rare, and only one donor could be recruited. In order to increase statistical power, a technical replicate of the C5-deficient samples was run. Subsequently, log2-transformed intensities were processed by robust multichip analysis and filtered using a threshold of four. In total, 73 microarray chips were run and analyzed. The normalized and filtered raw data have been deposited in NCBI's Gene Expression Omnibus (GEO) and are accessible with GEO Series accession number GSE55537. Linear models for microarray data were applied to estimate fold changes between data sets and the respective multiple testing adjusted p-values (FDR q-values). The interpretation of the data has been published by Lau et al. in an open access article entitled “CD14 and Complement Crosstalk and Largely Mediate the Transcriptional Response to Escherichia coli in Human Whole Blood as revealed by DNA Microarray” (Lau et al., 2015).en_US
dc.languageEN
dc.language.isoenen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.titleGene expression profiling of Gram-negative bacteria-induced inflammation in human whole blood: The role of complement and CD14-mediated innate immune responseen_US
dc.typeJournal articleen_US
dc.creator.authorLau, Corinna
dc.creator.authorOlstad, Ole Kristoffer
dc.creator.authorHolden, Marit
dc.creator.authorNygård, Ståle
dc.creator.authorFure, Hilde
dc.creator.authorLappegård, Knut Tore
dc.creator.authorBrekke, Ole Lars
dc.creator.authorEspevik, Terje
dc.creator.authorHovig, Johannes Eivind
dc.creator.authorMollnes, Tom Eirik
cristin.unitcode185,15,5,35
cristin.unitnameForskningsgruppen for biomedisinsk informatikk
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.cristin1258334
dc.identifier.bibliographiccitationinfo:ofi/fmt:kev:mtx:ctx&ctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Genomics Data&rft.volume=5&rft.spage=176&rft.date=2015
dc.identifier.jtitleGenomics Data
dc.identifier.volume5
dc.identifier.startpage176
dc.identifier.endpage183
dc.identifier.doihttp://dx.doi.org/10.1016/j.gdata.2015.05.019
dc.identifier.urnURN:NBN:no-53014
dc.type.documentTidsskriftartikkelen_US
dc.type.peerreviewedPeer reviewed
dc.source.issn2213-5960
dc.identifier.fulltextFulltext https://www.duo.uio.no/bitstream/handle/10852/49251/1/article91969.pdf
dc.type.versionPublishedVersion


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