Enterohemorrhagic Escherichia coli , a hound for signals

(EHEC) is a major cause of severe diarrhea worldwide and can produce Shiga toxin, leading to hemolytic uremic syndrome and resulting in high morbidity and mortality. EHEC colonizes the human colon but must overcome multiple barriers before reaching its infection niche. The gut microbiota is known as a first line of defense against pathogen colonization by depleting the microenvironment of nutrients and limiting pathogen expansion. To overcome this limitation, EHEC can sense various signals to identify its infection niche and successfully colonize its host. Here, we review the signals that regulate the locus of enterocyte effacement, or LEE, which encodes EHEC's major virulence factor, a type 3 secretion system (T3SS) that allows EHEC to attach to the host colon epithelium. Over the years, EHEC has been found to sense a variety of signals, from carbon sources to microbiota-derived signals and even host communication factors. These signals are mostly perceived by two-component systems (TCSs) and can regulate LEE expression. Since antibiotics trigger Shiga toxin production, developing anti-virulence approaches to treat EHEC infection is the best alternative. Identifying the signals that regulate LEE expression and the underlying mechanistic pathways can enable new strategies to treat EHEC or enteric pathogens more broadly.