The mammalian intestinal tract harbours a high diversity of resident microbes, fungi, parasites and viruses comprising the human gut microbiota. Maintaining a balance between tolerance and defence shapes the healthy gut barrier and licenses immune responses beyond the intestinal mucosa. The host’s ability to discriminate “friend and foe” and establish a precise crosstalk and co-metabolism with its associated microbiota is crucial for fitness and survival. Disturbed host-microbial interactions have been implicated in the etiology of numerous human diseases including chronic inflammatory bowel disease and colorectal cancer. The hypothesis that microbial and environmental challenges might be among the main causative factors of disease manifestation in genetically susceptible individuals clearly connotes a potential therapeutic and/or preventive exploitation.

The group focuses on understanding metabolic pathways and related signalling events evoked by physiological and pathological host-microbe interaction at the intestinal mucosal interface. We postulate that the failure to mount adequate responses to temporal variation of the intestinal microbiota destabilizes the intestinal ecosystem, which -finally- is associated with failing resilience phenomena and changes in microbial community functions. We hypothesize that frequently dual-use principles exist where key metabolites of the host-microbe co-metabolic network such as tryptophan derivatives serve at the same time as important recognition cues. In vitro and in vivo model-systems established in our group allow us to focus in on the effect of IBD susceptibility genes such as NOD2 and ATG16L1 on the microbiome or investigate the crosstalk between specific symbiotic bacteria, metabolic principles (glycolysis) epithelial organ development and immune priming.  

Our research aims are: 

We apply innovative methods (phylogenomics, meta-genomics and meta-transcriptomics and metabolomics), to study the microbiota and host functional networks.