Epigenetic processes are involved in tissue differentiation, maintenance and homeostasis. It was conceived early that deregulated epigenetic mechanisms might not only be linked to developmental processes, but also to manifestation and progression of human diseases. Furthermore, exposure to toxins like tobacco smoke as well as other environmental cues including the resident microbiota leave epigenetic imprints on the DNA. This type of memory, which is partially heritable, is currently being discussed as disease relevant. Specific epigenetic signatures and genetic variants in genes encoding parts of the epigenetic machinery (e.g. DNMT3A/B) have been associated with inflammatory bowel disease. Thus, we hypothesize that alterations of the epigenome in different cellular compartments may link genetic susceptibility and environmental influences and could represent "decision points" in the progression towards disease onset (i.e. manifestation) and/or progression of IBD. The group is part of the International Human Epigenome Consortium. Our research aims are  

• To understand the function of DNMT3A/B in specific cell types of the intestinal mucosa with a focus on epithelial and myeloid cells

• To investigate cellular mechanisms, which are deregulated by disease-associated DNA methylation patterns  

• To identify actionable targets for therapeutic epigenome editing. Various CRISPR/Cas9 strategies, such as Cas9 guided DNA-(de)methylation are investigated 

• To explore how epigenetic regulation influences the pathophysiological switch between acute and chronic inflammatory processes. 

• To assess how external stressors like tobacco smoke, nutrition or microbiota can impact the epigenome and subsequently influence the IBD risk of an individual and its children.