EHEC is a normal resident of cattle, but can cause disease in humans following the ingestion of contaminated food or water. EHEC attaches intimately to intestinal epithelial cells and triggers extensive cytoskeletal rearrangements resulting in attaching and effacing (AE) lesions and formation of a characteristic pedestal structure. Most of the genes involved in AE lesion formation are encoded within a chromosomal pathogenicity island called the locus of enterocyte effacement (LEE). The mortality associated with EHEC infections is due to the production and release of a Shiga toxin (Stx) by these bacteria. Stx is a potent inhibitor of protein synthesis that binds to receptors found in the kidneys and the central nervous system, thus causing the complications associated with EHEC disease.

In order to successfully cause disease, EHEC must compete with the indigenous microbiota for nutrients. Ethanolamine (EA) is present in the large intestine due to the turnover of intestinal cells as well as through the host diet. EHEC uses EA as a nitrogen source and thus gains a competitive advantage for colonization over the indigenous microbiota. Recently, we have shown that EA is not only important for nitrogen metabolism, but that it is also used as a signaling molecule to activate genes involved in inter-kingdom signaling, AE lesion formation, and Stx production (Kendall et al., 2012).

We use genetic, biochemical, and bioinformatics approaches to address questions about host-pathogen interactions. Altogether, our aim is to obtain a detailed, mechanistic understanding of how EHEC assimilates environmental information and modulates expression of virulence genes.