Model

Host-Microbe-Diet interactions and carcinogenesis

Humans have approximately 10 times more bacterial cells than eukaryotic cells, which are in constant interaction. Thus, to a certain degree, we are biologically defined by bacteria. The revolution in the identification of human microbes and their role in health and disease has already begun. For example, intestinal microbes have been linked to various diseases, such as chronic intestinal inflammation and cancer. However the bacterial species responsible and the way they interact with other microbes, the host and the intestinal nutrients remain unclear.

Our laboratory studies the identification of bacterial species and the way they might cause inflammation and colon cancer – the second leading cause of cancer related death in both the United States and Europe. Apart from Helicobacter pylori, no other bacterial species has been confirmed as a causative agent of gastrointestinal cancer. Using the simple model organism, Drosophila melanogaster, we have shown that intestinal bacterial pathogens induce the proliferation of intestinal stem cells and an immune response of the enterocytes, which can be directed by oncogenic mutations towards tumour formation and metastasis.

Using quantitative population genetics, histopathology, microbiology and the fundamental knowledge of Drosophila, but also mice, as model organisms for human infectious diseases and carcinogenesis, we aim to:
1. Identify signaling pathways that link intestinal microbes with tumor formation and tumor cell migration.
2. Identify human intestinal bacteria and dietary conditions that either induce or suppress intestinal disease.
3. Identify host-microbe-diet synergisms that induce and therapeutic interventions that inhibit intestinal disease.