Abstract
Enterohaemorrhagic Escherichia coli (EHEC) mediates disease using a type 3 secretion system (T3SS), which is encoded on the locus of enterocyte effacement (LEE) and is tightly controlled by master regulators. This system is further modulated by a number of signals that help to fine-tune virulence, including metabolic, environmental and chemical signals. Since the LEE and its master regulator, Ler, were established, there have been numerous scientific advancements in understanding the regulation and expression of virulence factors in EHEC. This review will discuss the recent advancements in this field since our previous review, with a focus on the transcriptional regulation of the LEE.
Highlights
Escherichia coli is a Gram-negative bacterium, highly adapted to survive within the gastrointestinal tract of multiple hosts [1]
Several pathotypes are classed as enteric diarrheal pathogens, such as Enterohaemorrhagic E. coli (EHEC) and most notably the O157:H7 serotype
EHEC is a subset of Shiga-toxin E. coli (STEC) that can cause diarrheal infections and in severe cases lead to haemolytic uraemic syndrome (HUS)
Summary
Enterohaemorrhagic Escherichia coli (EHEC) mediates disease using a type 3 secretion system (T3SS), which is encoded on the locus of enterocyte effacement (LEE) and is tightly controlled by master regulators. This system is further modulated by a number of signals that help to fine-tune virulence, including metabolic, environmental and chemical signals. Since the LEE and its master regulator, Ler, were established, there have been numerous scientific advancements in understanding the regulation and expression of virulence factors in EHEC. This review will discuss the recent advancements in this field since our previous review, with a focus on the transcriptional regulation of the LEE
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