Yanfei Yu

PhD Student

Michael Naumann

Project Leader

Chronic gastric diseases are characterized by maladaptive processes in the gastric mucosa. Colonisation of the gastric epithelium by Helicobacter pylori is a risk factor for the development of gastric diseases, including gastric cancer. Dysregulation of a number of cellular processes may contribute to impaired barrier function including unfolded protein response (UPR) and autophagy. We hypothesize that H. pylori triggers coordinated regulation of these processes. Specifically, we investigate the mechanisms of intracellular signaling of the UPR and/or the autophagy and their functional consequences for the control of H. pylori-associated apoptotic cell death. (cooperation Project 1-2, Project 11-2 and Medical Doctor Project 8). The functional relevance of the UPR and autophagy for maladaptive processes in the gastric mucosa is investigated by co-culture of gastric epithelial carcinoma cells (NCI-N87) and fibroblasts in the Boyden chamber. Factors relevant for maladaptation are identified in the secretome of the cells and assessed in knockout cells (cooperation Project P11-2).

H. pylori-induced UPR and autophagy in the gastric mucosa. The studies in gastric carcinoma cells (NCI-N87) address the role of the unfolded protein response (UPR, ATF6, IRE1a) and autophagy (AMPK1, p62) in H. pylori-associated apoptotic cell death. Maladaptive processes in the gastric microenvironment are investigated by co-culture of NCI-N87 cells and fibroblasts in the Boyden chamber. Factors relevant for the maladaptation are identified in the secretome of the cells.