Research aims

(1) Search for competition-factors of commensal E. coli and their role in inhibition of enteropathogens in the inflamed intestine
We found that certain commensal E. coli strains can out-compete Salmonella Typhimurium in a mouse colitis model (Stecher et al., PNAS 2012). In this project we investigate the molecular mechanisms of competitive E. coli overgrowth and pathogen suppression in the inflamed gut. We aim at identifying traits that contribute to the competitive phenotype of this type of E. coli strains to enhance our understanding of the role of competitive E. coli in enteropathogen infection and may be exploited for the improvement of probiotics in the future.

(2) Establishing a gnotobiotic mouse model for analysing the impact of infection on the microbiota
Infections with enteropathogenic bacteria are a major insult for the intestinal mucosa and the gut ecosystem. A vigorous inflammatory response is triggered by the intestinal immune system involving effector cell infiltration (i.e. neutrophils) and induction of an array of host defenses (i.e. toxic oxygen/nitrogen radicals, proteases and antimicrobial peptides). Naturally, this immune response affects both, the pathogen and, as 'collateral damage' also the beneficial commensal flora within the intestine (Stecher & Hardt, Current Opinion in Microbiology, 2011). Indeed, infections with Helicobacter hepaticus, Citrobacter rodentium and Salmonella enterica serovar Typhimurium (S.Typhimurium) were accompanied by gut flora alterations. We are using gnotobiotic mice having a standardized commensal flora to address the impact of inflammation on a microbial consortium in the gut.