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dc.contributor.authorBrekke, Ole-Lars
dc.contributor.authorChristiansen, Dorte
dc.contributor.authorKisserli, Aymric
dc.contributor.authorFure, Hilde
dc.contributor.authorDahl, Jim André
dc.contributor.authorDonvito, Béatrice
dc.contributor.authorReveil, Brigitte
dc.contributor.authorLudviksen, Judith K
dc.contributor.authorTabary, Thierry
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorCohen, Jacques H.M.
dc.date.accessioned2020-04-14T12:44:33Z
dc.date.available2020-04-14T12:44:33Z
dc.date.created2019-09-09T11:53:06Z
dc.date.issued2019
dc.identifier.citationMolecular Immunology. 2019, 114 139-148.en_US
dc.identifier.issn0161-5890
dc.identifier.urihttps://hdl.handle.net/11250/2651008
dc.description.abstractAim To study the role of complement receptor 1 (CR1) for binding of Escherichia coli (E. coli) to erythrocytes, for leukocyte phagocytosis, oxidative burst and complement activation in human whole blood from a CR1 deficient (CR1D) patient and healthy controls with low, medium and high CR1 numbers. Methods Alexa-labelled bacteria were used to quantify erythrocyte-bound bacteria, free bacteria in plasma and phagocytosis using flow cytometry. Complement activation in plasma was measured by enzyme-linked immunosorbent assay. The CR1 numbers as well as C3bc and C4bc deposition on erythrocytes were measured by flow cytometry. Cytokines were measured using multiplex technology, and bacterial growth was measured by colony forming units. CR1 was blocked using the anti-CR1 blocking mAb 3D9. Results Approximately 85% of E. coli bound to erythrocytes after 15 min incubation in donor blood with high and medium CR1 numbers, 50% in the person with low CR1 numbers and virtually no detectable binding in the CR1D (r2 = 0.87, P < 0.0007). The number of free bacteria in plasma was inversely related to erythrocyte CR1 numbers (r2 = 0.98, P < 0.0001). E. coli-induced phagocytosis and oxidative burst were significantly enhanced by the anti-CR1 mAb 3D9 and in the CR1D and the donor with low CR1 numbers. E. coli-induced complement activation in plasma, C3bc and C4bc deposition on erythrocytes, and bacterial growth were similar in all four cases. Conclusions CR1D and low CR1 numbers prevented E. coli binding to erythrocytes, increased free bacteria in plasma, phagocytosis and oxidative burst, but did not affect plasma or surface complement activation and bacterial growth.en_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.titleKey role of the number of complement receptor 1 on erythrocytes for binding of Escherichia coli to erythrocytes and for leukocyte phagocytosis and oxidative burst in human whole blooden_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionacceptedVersionen_US
dc.source.pagenumber139-148en_US
dc.source.volume114en_US
dc.source.journalMolecular Immunologyen_US
dc.identifier.doi10.1016/j.molimm.2019.07.014
dc.identifier.cristin1722749
dc.description.localcode© 2019. This is the authors’ accepted and refereed manuscript to the article. Locked until 25.7.2020 due to copyright restrictions. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ "en_US
cristin.unitcode194,65,15,0
cristin.unitnameInstitutt for klinisk og molekylær medisin
cristin.ispublishedtrue
cristin.fulltextpreprint
cristin.qualitycode1


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
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