Figure 2. Modulation of enterohaemorrhagic E. coli virulence through nutrients provided by the microbiota.

a, The microbiota resides in the lumen and outer mucus layer of the intestine. The saccharolytic bacterium Bacteroides thetaiotaomicron is a prominent member of the microbiota. It can release fucose from the mucus and makes the sugar available to other bacteria. When EHEC senses fucose through the FusKR signalling system, it represses both its use of the sugar and the expression of genes that encode the T3SS, a protein-translocation apparatus that enables the bacterium to secrete effector proteins into host cells. This repression prevents EHEC from competing for fucose with commensal E. coli and from expending energy unnecessarily on T3SS expression. b, Metabolites that are provided by B. thetaiotaomicron, such as succinate, lead to an increase in the expression by EHEC of the enzyme mucinase, which obliterates the mucus layers of the intestine. EHEC is then able to reach the intestinal epithelium. B. thetaiotaomicron then begins to secrete succinate and other metabolites that are required for gluconeogenesis into the now nutrient-poor environment. The compounds are sensed by EHEC, which upregulates its expression of the T3SS to enable the bacterium to attach to the epithelial cells of the host intestine and form lesions that cause diarrhoea.