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dc.contributor.authorVestad, Beate
dc.contributor.authorUeland, Thor
dc.contributor.authorLerum, Tøri Vigeland
dc.contributor.authorDahl, Tuva Børresdatter
dc.contributor.authorHolm, Kristian
dc.contributor.authorBarratt-Due, Andreas
dc.contributor.authorKåsine, Trine
dc.contributor.authorDyrhol-Riise, Anne Ma
dc.contributor.authorStiksrud, Birgitte
dc.contributor.authorTonby, Kristian
dc.contributor.authorHoel, Hedda
dc.contributor.authorOlsen, Inge Christoffer
dc.contributor.authorHenriksen, Katerina N.
dc.contributor.authorTveita, Anders Aune
dc.contributor.authorManotheepan, Ravinea
dc.contributor.authorHaugli, Mette
dc.contributor.authorEiken, Ragnhild
dc.contributor.authorBerg, Åse
dc.contributor.authorHalvorsen, Bente
dc.contributor.authorLekva, Tove
dc.contributor.authorRanheim, Trine
dc.contributor.authorMichelsen, Annika Elisabeth
dc.contributor.authorKildal, Anders Benjamin
dc.contributor.authorJohannessen, Asgeir
dc.contributor.authorThoresen, Lars
dc.contributor.authorSkudal, Hilde Kristin
dc.contributor.authorKittang, Bård Reiakvam
dc.contributor.authorOlsen, Roy Bjørkholt
dc.contributor.authorYstrøm, Carl Magnus
dc.contributor.authorSkei, Nina Vibeche
dc.contributor.authorHannula, Raisa
dc.contributor.authorAballi, Saad
dc.contributor.authorKvåle, Reidar
dc.contributor.authorSkjønsberg, Ole Henning
dc.contributor.authorAukrust, Pål
dc.contributor.authorHov, Johannes Espolin Roksund
dc.contributor.authorTrøseid, Marius
dc.date.accessioned2023-06-23T08:15:17Z
dc.date.available2023-06-23T08:15:17Z
dc.date.created2022-03-08T14:32:01Z
dc.date.issued2022
dc.identifier.citationJournal of Internal Medicine. 2022, 291 (6), 801-812.en_US
dc.identifier.issn0954-6820
dc.identifier.urihttps://hdl.handle.net/11250/3072843
dc.description.abstractBackground: Although coronavirus disease 2019 (COVID-19) is primarily a respiratory infection, mounting evidence suggests that the gastrointestinal (GI) tract is involved in the disease, with gut barrier dysfunction and gut microbiota alterations being related to disease severity. Whether these alterations persist and are related to long-term respiratory dysfunction remains unknown. Methods: Plasma was collected during hospital admission and after three months from the NOR-Solidarity trial (n = 181) and analysed for markers of gut barrier dysfunction and inflammation. At the three-month follow-up, pulmonary function was assessed by measuring the diffusing capacity of the lungs for carbon monoxide (DLCO ). Rectal swabs for gut microbiota analyses were collected (n = 97) and analysed by sequencing the 16S rRNA gene. Results: Gut microbiota diversity was reduced in COVID-19 patients with respiratory dysfunction, defined as DLCO below the lower limit of normal three months after hospitalisation. These patients also had an altered global gut microbiota composition, with reduced relative abundance of 20 bacterial taxa and increased abundance of five taxa, including Veillonella, potentially linked to fibrosis. During hospitalisation, increased plasma levels of lipopolysaccharide-binding protein (LBP) were strongly associated with respiratory failure, defined as pO2 /fiO2 -(P/F ratio)en_US
dc.description.abstractRespiratory dysfunction three months after severe COVID-19 is associated with gut microbiota alterationsen_US
dc.language.isoengen_US
dc.relation.urihttps://onlinelibrary.wiley.com/doi/10.1111/joim.13458
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/deed.no*
dc.subjectSARS-CoV-2;en_US
dc.subjectmicrobiome;en_US
dc.subjectpulmonary function;en_US
dc.titleRespiratory dysfunction three months after severe COVID-19 is associated with gut microbiota alterationsen_US
dc.title.alternativeRespiratory dysfunction three months after severe COVID-19 is associated with gut microbiota alterationsen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionacceptedVersionen_US
dc.source.pagenumber801-812en_US
dc.source.volume291en_US
dc.source.journalJournal of Internal Medicineen_US
dc.source.issue6en_US
dc.identifier.doi10.1111/joim.13458
dc.identifier.cristin2008297
dc.relation.projectNorges forskningsråd: 2021071en_US
cristin.ispublishedtrue
cristin.fulltextpostprint
cristin.qualitycode2


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Attribution-NonCommercial-NoDerivatives 4.0 Internasjonal
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