Please use this identifier to cite or link to this item:
http://doi.org/10.25358/openscience-254
Authors: | Khandagale, Avinash Kittner, Jens M. Mann, Amrit Ascher, Stefanie Kollar, Bettina Reinhardt, Christoph |
Title: | Coagulation factor 9-deficient mice are protected against dextran sulfate sodium-induced colitis |
Online publication date: | 19-Dec-2018 |
Year of first publication: | 2018 |
Language: | english |
Abstract: | Patients 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. |
DDC: | 610 Medizin 610 Medical sciences |
Institution: | Johannes Gutenberg-Universität Mainz |
Department: | FB 04 Medizin |
Place: | Mainz |
ROR: | https://ror.org/023b0x485 |
DOI: | http://doi.org/10.25358/openscience-254 |
URN: | urn:nbn:de:hebis:77-publ-587104 |
Version: | Published version |
Publication type: | Zeitschriftenaufsatz |
License: | CC BY |
Information on rights of use: | https://creativecommons.org/licenses/by/3.0/ |
Journal: | Biology open 7 7 |
Pages or article number: | bio034140 |
Publisher: | Company |
Publisher place: | Cambridge |
Issue date: | 2018 |
ISSN: | 2046-6390 |
Publisher URL: | http://dx.doi.org/10.1242/bio.034140 |
Publisher DOI: | 10.1242/bio.034140 |
Appears in collections: | JGU-Publikationen |