The interplay between the microbiota and enterohemorrhagic Escherichia coli

The gastrointestinal tract of mammals is home to a plethora of microbial species that comprise the microbiota. The role of the microbiota in human health is at the forefront of science in recent years, because it is now appreciated that this intricate microbe-host association shapes the host's immune response and physiology. Many diseases are associated with changes in the microbiota, called dysbiosis. Dysbiosis is associated with obesity, metabolic syndromes, inflammatory bowel-disease, inflammatory bowel syndrome, cancer, diabetes, allergies, and autism. The microbiota is largely regarded as a barrier to enteric infections, such as with enterohemorrhagic Escherichia coli (EHEC). However, the interactions between pathogens and the microbiota are largely unknown, as is how these interactions influence the outcome of enteric disease. The microbial composition of the gastrointestinal tract shapes the landscape in which EHEC survives within the host. This organism competes for nutrients derived from the host diet, liberates additional resources from dietary and host sources, and produces signaling molecules sensed by EHEC to direct gene expression. To successfully colonize the recto-anal junction of a ruminant, the EHEC reservoir, or the colon of a human, an accidental host, EHEC must alter its physiology to survive within the host digestive tract. In this article, we explore the classes of molecules produced or modified by the microbiota that appear to be instrumental in governing virulence gene expression of EHEC. We also explore how interaction with different microbiotas influences EHEC infectivity and host interaction.