Faulty digestion within intestinal epithelial cells promotes inflammation

Organoide, hier mit 400facher Vergrößerung unter dem Mikroskop
© Konrad Aden/IKMBOrganoids, here with 400x magnification under a microscope, function partially like real bowels. The mini-bowel for research is made from stem cells in the laboratory, which were previously removed from the bowel tissue of humans or lab animals by means of colonoscopy.

A study by the Cluster of Excellence "Inflammation at Interfaces" finds a new approach for personalised treatment of chronic inflammatory bowel diseases.

20 percent of all patients with Crohn's disease, a clinical subtype of inflammatory bowel disease, have a mutation in the gene ATG16L1. This gene is involved in a cellular process called autophagy, which functions as a recycling mechanisms of aged organelles and macromolecules within cells. The delineation of the molecular consequences of Atg16l1 mutations on host immune system has been investigated in the Cluster of Excellence "Inflammation at Interfaces" for a long time. Now, a team led by Cluster Board Member Professor Philip Rosenstiel and Dr Konrad Aden from the Institute of Clinical Molecular Biology (IKMB) at Kiel University and the Department of Internal Medicine I, UKSH Kiel have made a discovery with on a novel function of Atg16l1, which sheds a new light on the pathogenesis of IBD and might help to refine future treatment of IBD patients.

to the press release of I@I