Please use this identifier to cite or link to this item: http://doi.org/10.25358/openscience-254
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dc.contributor.authorKhandagale, Avinash-
dc.contributor.authorKittner, Jens M.-
dc.contributor.authorMann, Amrit-
dc.contributor.authorAscher, Stefanie-
dc.contributor.authorKollar, Bettina-
dc.contributor.authorReinhardt, Christoph-
dc.date.accessioned2018-12-19T12:48:47Z-
dc.date.available2018-12-19T13:48:47Z-
dc.date.issued2018-
dc.identifier.urihttps://openscience.ub.uni-mainz.de/handle/20.500.12030/256-
dc.description.abstractPatients with inflammatory bowel disease (IBD) are susceptible to thromboembolism. Interestingly, IBD occurs less frequently in patients with inherited bleeding disorders. Therefore, we analyzed whether F9-deficiency is protective against the onset of acute colitis in a genetic hemophilia B mouse model. In the 3.5% dextran sulfate sodium (DSS)-induced colitis model, F9 deficient mice were protected from body-weight loss and had a reduced disease activity score. We detected decreased colonic myeloperoxidase activity and decreased CXCL1 levels in DSS-treated F9 deficient mice compared with wild-type (WT) littermate controls, indicating decreased neutrophil infiltration. Remarkably, we identified expression of coagulation factor IX (FIX) protein in small intestinal epithelial cells (MODE-K). In epithelial cell cultures, cellular FIX protein expression was increased following stimulation with the bacterial Toll-like receptor agonists lipopolysaccharide, macrophage-activating lipopeptide-2 and Pam3CSK4. Thus, we revealed a protective role of F9-deficiency in DSS-induced colitis and identified the intestinal epithelium as a site of ectopic FIX.This article has an associated First Person interview with the first author of the paper.en_GB
dc.description.sponsorshipDFG, Open Access-Publizieren Universität Mainz / Universitätsmedizin-
dc.language.isoeng-
dc.rightsCC BYde_DE
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/-
dc.subject.ddc610 Medizinde_DE
dc.subject.ddc610 Medical sciencesen_GB
dc.titleCoagulation factor 9-deficient mice are protected against dextran sulfate sodium-induced colitisen_GB
dc.typeZeitschriftenaufsatzde_DE
dc.identifier.urnurn:nbn:de:hebis:77-publ-587104-
dc.identifier.doihttp://doi.org/10.25358/openscience-254-
jgu.type.dinitypearticle-
jgu.type.versionPublished versionen_GB
jgu.type.resourceText-
jgu.organisation.departmentFB 04 Medizin-
jgu.organisation.number2700-
jgu.organisation.nameJohannes Gutenberg-Universität Mainz-
jgu.rights.accessrightsopenAccess-
jgu.journal.titleBiology open-
jgu.journal.volume7-
jgu.journal.issue7-
jgu.pages.alternativebio034140-
jgu.publisher.year2018-
jgu.publisher.nameCompany-
jgu.publisher.placeCambridge-
jgu.publisher.urihttp://dx.doi.org/10.1242/bio.034140-
jgu.publisher.issn2046-6390-
jgu.organisation.placeMainz-
jgu.subject.ddccode610-
opus.date.accessioned2018-12-19T12:48:47Z-
opus.date.modified2019-01-10T11:01:33Z-
opus.date.available2018-12-19T13:48:47-
opus.subject.dfgcode00-000-
opus.organisation.stringFB 04: Medizin: Centrum für Thrombose und Hämostase (CTH)de_DE
opus.organisation.stringFB 04: Medizin: I. Medizinische Klinik und Poliklinikde_DE
opus.identifier.opusid58710-
opus.institute.number0463-
opus.institute.number0425-
opus.metadataonlyfalse-
opus.type.contenttypeKeinede_DE
opus.type.contenttypeNoneen_GB
opus.affiliatedKittner, Jens M.-
opus.affiliatedReinhardt, Christoph-
jgu.publisher.doi10.1242/bio.034140
jgu.organisation.rorhttps://ror.org/023b0x485
Appears in collections:JGU-Publikationen

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