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dc.contributor.authorBakke, Ingunn
dc.contributor.authorWalaas, Gunnar Andreas
dc.contributor.authorBruland, Torunn
dc.contributor.authorRøyset, Elin Synnøve
dc.contributor.authorGranlund, Atle van Beelen
dc.contributor.authorEscudero-Hernandez, Celia
dc.contributor.authorThorsvik, Silje
dc.contributor.authorMünch, Andreas
dc.contributor.authorSandvik, Arne Kristian
dc.contributor.authorØstvik, Ann Elisabet
dc.date.accessioned2021-09-28T13:03:54Z
dc.date.available2021-09-28T13:03:54Z
dc.date.created2021-08-20T08:53:10Z
dc.date.issued2021
dc.identifier.issn0944-1174
dc.identifier.urihttps://hdl.handle.net/11250/2784145
dc.description.abstractBackground Collagenous colitis (CC) is an inflammatory bowel disease where chronic diarrhoea is the main symptom. Diagnostic markers distinguishing between CC and other causes of chronic diarrhoea remain elusive. This study explores neutrophil gelatinase-associated lipocalin (NGAL) and its mRNA lipocalin2 (LCN2) as histological and faecal disease markers in CC. Methods NGAL/LCN2 were studied in colonic biopsies from CC patients before and during budesonide treatment using RNA sequencing (n = 9/group), in situ hybridization (ISH) (n = 13–22/group) and immunohistochemistry (IHC) (n = 14–25/group). Faecal samples from CC (n = 3–28/group), irritable bowel syndrome diarrhoea (IBS-D) (n = 14) and healthy controls (HC) (n = 15) were assayed for NGAL and calprotectin. Results NGAL/LCN2 protein and mRNA expression were upregulated in active CC vs HC, and vs paired samples of treated CC in clinical remission. IHC and ISH localized increased NGAL/LCN2 mainly to epithelium of active CC, compared to almost absence in HC and treated CC. In contrast, calprotectin was solely expressed in immune cells. Despite great individual differences, faecal NGAL was significantly increased in active CC compared to HC, IBS-D and treated CC and had high test sensitivity. Faecal calprotectin levels were variably increased in active CC, but the values remained below usual clinical cut-offs. Conclusion NGAL/LCN2 is upregulated in the epithelium of active CC and reduced during budesonide-induced clinical remission to the level of HC and IBD-S. This was reflected in NGAL faecal concentrations. We propose NGAL as an IHC marker for disease activity in CC and a potential faecal biomarker discriminating CC from HC and IBS-D.en_US
dc.language.isoengen_US
dc.publisherSpringeren_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleMucosal and faecal neutrophil gelatinase-associated lipocalin as potential biomarkers for collagenous colitisen_US
dc.typePeer revieweden_US
dc.typeJournal articleen_US
dc.description.versionpublishedVersionen_US
dc.source.journalJournal of gastroenterologyen_US
dc.identifier.doi10.1007/s00535-021-01814-y
dc.identifier.cristin1927509
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1


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