Genetic basis involved in host interaction and adaption of Escherichia coli: impact on commensalism, symptomatic and asymptomatic infection

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The comparison of commensal and pathogenic bacteria improves our understanding of the molecular basis for pathogenicity and commensalism as well as for the occurrence of symptomatic or asymptomatic infections. We use Escherichia coli (E. coli) as a model organism because non-pathogenic commensal as well as pathogenic variants of this species belong to the normal intestinal flora of humans. The comparison of isolates from symptomatic or asymptomatic infection with commensals will promote the identification of bacterial properties and the molecular mechanisms involved in different forms of host-bacterium interaction, thus leading to different types of infection. Successful colonization of a niche requires bacterial adaptation to the growth conditions encountered including the host response during infection. Bacterial adaptation results from genome plasticity and positive selection. To correlate genetic flexibility and virulence potential of the bacteria with host response, we plan to investigate the (i) complex host-pathogen interaction, (ii) bacterial evolution/adaptation of E. coli in the human host on the population scale, (iii) bacterial traits required for symptomatic infection, and (iv) driving forces behind bacterial adaptation in vivo. Our results will contribute to the full comprehension of the molecular context between prokaryotic microorganisms, their hosts and commensalism or pathogenicity.