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dc.contributor.authorKaarbø, Mari
dc.contributor.authorYang, Mingyi
dc.contributor.authorHov, Johannes Espolin Roksund
dc.contributor.authorHolm, Kristian
dc.contributor.authorSousa, Mirta
dc.contributor.authorMacpherson, Magnhild Eide
dc.contributor.authorReims, Henrik Mikael
dc.contributor.authorKran, Anne-Marte Bakken
dc.contributor.authorHalvorsen, Bente
dc.contributor.authorKarlsen, Tom Hemming
dc.contributor.authorAukrust, Pål
dc.contributor.authorLundin, Knut
dc.contributor.authorFevang, Børre
dc.contributor.authorBjørås, Magnar
dc.contributor.authorJørgensen, Silje Fjellgård
dc.date.accessioned2022-12-23T10:23:43Z
dc.date.available2022-12-23T10:23:43Z
dc.date.created2022-12-06T15:22:53Z
dc.date.issued2022
dc.identifier.citationJournal of Allergy and Clinical Immunology. 2022, .en_US
dc.identifier.issn0091-6749
dc.identifier.urihttps://hdl.handle.net/11250/3039369
dc.description.abstractBackground A substantial proportion of common variable immunodeficiency (CVID) patients has duodenal inflammation of largely unknown etiology. However, because of its histologic similarities with celiac disease, gluten sensitivity has been proposed as a potential mechanism. Objective We aimed to elucidate the role of the duodenal microenvironment in the pathogenesis of duodenal inflammation in CVID by investigating the transcriptional, proteomic, and microbial signatures of duodenal biopsy samples in CVID. Methods DNA, total RNA, and protein were isolated from snap-frozen pieces of duodenal biopsy samples from CVID (with and without duodenal inflammation), healthy controls, and patients with celiac disease (untreated). RNA sequencing, mass spectrometry–based proteomics, and 16S ribosomal DNA sequencing (bacteria) were then performed. Results CVID separated from controls in regulation of transcriptional response to lipopolysaccharide and cellular immune responses. These differences were independent of mucosal inflammation. Instead, CVID patients with duodenal inflammation displayed alterations in transcription of genes involved in response to viral infections. Four proteins were differently regulated between CVID patients and healthy controls—DBNL, TRMT11, GCHFR, and IGHA2—independent of duodenal inflammation. Despite similar histology, there were major differences in CVID with duodenal inflammation and celiac disease both at the RNA and protein level. No significant difference was observed in the bacterial gut microbial signature between CVID, celiac, and healthy controls. Conclusion Our findings suggest the existence of altered functions of the duodenal epithelium, particularly in response to lipopolysaccharide and viruses. The latter finding was related to duodenal inflammation, suggesting that viruses, not gluten sensitivity, could be related to duodenal inflammation in CVID. Key words CVID RNA sequencing proteomics microbiome gut microbiota microbiota gastrointestinal tract duodenum celiac disease Primary immunodeficiency IgAen_US
dc.language.isoengen_US
dc.publisherElsevieren_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleDuodenal inflammation in common variable immunodeficiency has altered transcriptional response to virusesen_US
dc.title.alternativeDuodenal inflammation in common variable immunodeficiency has altered transcriptional response to virusesen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.pagenumber0en_US
dc.source.journalJournal of Allergy and Clinical Immunologyen_US
dc.identifier.doi10.1016/j.jaci.2022.09.029
dc.identifier.cristin2089582
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode2


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