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Research > Medical Microbiology and Hospital Epidemiology > WG Prof. B. Stecher > 

The intestinal microbiota and enteric infections

A microbial ecosystem of unsurpassed diversity, termed microbiota, colonizes the healthy human intestine, where various bacterial members engage in a physiological network of cooperation and competition. A normal and healthy microbiota is able to block colonization of enteric pathogens in a process termed colonization resistance. However, antibiotics, immunosuppression and inflammation can disrupt colonization resistance and introduce microbiota imbalances (dysbiosis), with increased susceptibility to pathogen infections. A dysbiotic microbiota is characterized by depletion of the obligate anaerobic species (e.g. Clostridia and Bacteroidetes) and a relative enrichment in facultative anaerobic bacteria, in particular members of the Enterobacteriaceae, leading to the definition of “Enterobacterial blooming”. The mechanisms driving inflammation-induced blooms include generation of alternative electron acceptors (e.g. NO3-), production of antimicrobial effectors and iron depletion. Inflammation-induced blooms can be considered as a potential threat to the human health by promoting horizontal spread of fitness- and virulence factors, as well as antibiotic-resistances among potential pathogenic species.
Due to the enormous complexity of the intestinal microbiota and the lack of appropriate animal models, the mechanisms governing colonization resistance, i.e. interaction between microbiota, host immune system and pathogens, remain largely unclear. We focus on infections with Gram negative enteric pathogens including Salmonella enterica, Yersinia enterocolitica and pathogenic Escherichia coli, with the following aims:
1)    Understanding interaction of commensal bacteria with each other and with enteric pathogens;
2)    Analysing how bacterial evolution and horizontal gene transfer in the intestinal ecosystem is shaped by microbial interaction, environmental factors and interaction with the host´s mucosa;
3)    Elucidating how inflammatory immune responses and antibiotics affect the microbiota and pathogens, their interaction and gene expression.