The subject of our work is the physiology and pathophysiology of the intestine.
The main focus is on the development of chronic inflammatory bowel diseases.
Specifically, our group studies how the immune system controls homeostasis, i.e. cell division, cell differentiation and cell death in the intestinal epithelium and what effects this in turn has on the mucosal immune system in the intestine. Excessive cell death creates gaps in the epithelial layer - a cell layer that is actually supposed to protect the intestinal wall from invasion by harmful bacteria. Inflammation of the intestinal mucosa is the result. However, if individual epithelial cells do not die at all, colorectal cancer can develop in the long term. Our research investigates the molecular processes and the organic consequences of a malfunction of these processes and derives models for the development of inflammatory bowel diseases and colorectal cancer.
Our work is dedicated to understanding the intestinal epithelium as a barrier, as well as the regulation of cell death in the intestinal epithelium and its importance in the development of inflammatory bowel disease. Our work shows, among other things, that misregulation of programmed cell death in the intestinal epithelium leads to the loss of the intestinal barrier, the invasion of bacteria, the overactivation of immune cells in the intestine and ultimately to chronic intestinal inflammation. Further work has elucidated how the immune system controls cell death in the intestinal epithelium during inflammatory responses, what role bacteria and viruses play in this process in the intestine, and what cellular signaling pathways cause or prevent programmed cell death in the intestinal epithelium. The aim of our work is to find starting points for new therapeutic procedures in the treatment and prevention of Crohn's disease and ulcerative colitis, as well as colorectal cancer.