Consolidated Researcher Details:
I studied medicine in Kiel and Boston and graduated in 2001. During my studies I was awarded a research scholarship from the BMEP. I spent this time at the laboratories of Patsy Nishina (Jackson Lab, Maine) and Jeffrey Isner (St. Elisabeth Medical Center, Tufts University) working on mouse genetics and gene therapy. I received my MD degree on the characterization of Angiotensin II as a neurotrophic factor in 2003. After graduating I went to the Dept. of Internal Medicine in Kiel for medical training / a postdoc position in Internal Medicine/Mucosal Immunology with Ulrich Fölsch and Stefan Schreiber. Currently, I hold a professorship in Molecular and Evolutionary Medicine. I serve as member on the steering committees of several large-scale research initiatives in human diseases (e.g. gEUVADIS, ICGC MMML-Seq, Excellence Cluster Inflammation at Interfaces) and animal immunity (Excellence Cluster Future Ocean and Priority Program SPP1399).
My main scientific interest is to contribute to an understanding of the complex interactions between human intestinal mucosa and the environment in health and disease. Emphasis is given to the translation of positional genetic signals in inflammatory bowel disease into distinct, functional molecular effects in underlying cellular pathways and networks. We are beginning to understand that in intestinal inflammation the human host together with its associated gut microbiome must be regarded as a functional unit. Disease mechanisms can thus only be described when taking both sides of this “metaorganism” into account. For these questions, we also develop novel tools and techniques using large-scale sequencing and bioinformatics to understand regulatory events and cellular/bacterial response profiles in model systems of chronic inflammatory diseases.
Inflammatory bowel disease is a prime example for a complex polygenic disease in which a comprehensive understanding of the genetic etiology has been achieved, and we are beginning to link this genetic map to environmental risk factors as it is clear that the steeply rising incidence of inflammatory disease in industrialized countries cannot solely be explained by genetics. Therefore, the mechanisms that precipitate individual (poly)genetic susceptibility into disease manifestation are an important research focus to design interventions that could help to maintain health despite an existing genetic risk constellation. The RTG combines different skill sets and excellent young researchers. I am excited to be part of this group and I am convinced that it will significantly contribute to this major question in today´s medicine.