Intestines and the ECM: a target to treat?

Intro

Inflammatory bowel disease (IBD) is increasingly being segregated into molecular endotypes characterized either by accelerated tissue formation (fibrostenosis) or by elevated tissue destruction (fistulizing disease). This session will explore which molecular endotypes may be more suitable for specific interventions and how we can detect clinical benefit and remission at an early stage.

From mechanisms to medicines in stricturing Crohn’s Disease

Florian Rieder, Professor and Director of IBD research, Department of Gastroenterology, Hepatology and Nutrition, the Cleveland Clinic, Ohio.

Abstract: Intestinal fibrosis resulting in stricture formation and obstruction in Crohn’s disease (CD) and increased wall stiffness and symptoms in ulcerative colitis (UC) are among the largest unmet needs in inflammatory bowel diseases (IBD). Fibrosis is caused by a multifactorial and complex process involving immune and non-immune cells, their soluble mediators, and exposure to luminal contents, such as microbiota and environmental factors. Creeping fat and matrix bound enzymes are important players in its pathogenesis. To date, no antifibrotic therapy is available. Progress has been made in creating consensus definitions and measurements to quantify stricture morphology for clinical practice and trials, but approaches to determine the degree of fibrosis within a stricture are still lacking. This presentation will describe the current state of stricture pathogenesis, measuring tools, and clinical trial endpoints development.

Title TBD

Bram Verstockt, Assistant Professor at KU Leuven, staff member of the Department of Gastroenterology and Hepatology at the University Hospitals Leuven

Abstract: TBD