Acute experimental barrier injury triggers ulcerative colitis specific innate hyper-responsiveness and ulcerative colitis-type microbiome changes in humans

Jakob Benedict Seidelin*, Martin Iain Bahl, Tine Rask Licht, Benjamin E Mead, Jeffrey M Karp, Jens Vilstrup Johansen, Lene Buhl Riis, Marina Ramírez Galera, Anders Woetmann, Jacob Tveiten Bjerrum

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

10 Downloads (Pure)

Abstract

The trigger hypothesis opens the possibility of anti-flare-initiation therapies by stating that ulcerative colitis (UC) flares originates from inadequate responses to acute mucosal injuries. However, experimental evidence is restricted by a limited use of suitable human models. We thus aimed to investigate the acute mucosal barrier injury responses in humans with and without UC using an experimental injury model. A standardized mucosal break was inflicted in the sigmoid colon of 19 patients with UC in endoscopic and histological remission and 20 control subjects. Post-injury responses were assessed repeatedly by high resolution imaging and sampling to perform Geboes scoring, RNA sequencing, and injury niche microbiota 16S rRNA gene sequencing. UC patients had more severe endoscopic post-injury inflammation than controls (p
Original languageEnglish
JournalCellular and Molecular Gastroenterology and Hepatology
ISSN2352-345X
DOIs
Publication statusAccepted/In press - 2021

Fingerprint

Dive into the research topics of 'Acute experimental barrier injury triggers ulcerative colitis specific innate hyper-responsiveness and ulcerative colitis-type microbiome changes in humans'. Together they form a unique fingerprint.

Cite this