Enterohemorrhagic Escherichia coli (EHEC) O157:H7 is a food-borne bacterial pathogen that causes various diseases in both humans and animals such as hemorrhagic colitis and hemolytic uremic syndrome. Because cattle are the main reservoir of this microorganism, undercooked meat and meat byproducts contaminated with EHEC O157:H7 are most commonly associated with epidemic disease outbreaks. As an enteric pathogen, EHEC O157:H7 enters the body via a fecal-oral route and must survive passage through the gastric stomach at pH 1.5 to 3.5 to establish an infection within the gastrointestinal tracts. Therefore, the ability to resist such acidic environments is important to the pathogenesis of EHEC O157:H7 during a host infection. In this review, we will discuss on the acid resistance (AR) mechanisms induced by EHEC O157:H7 when E. coli encounters acidic environments.

Shiga toxins (Stxs), some of the most important virulence factors in enterohemorrhagic Escherichia coli (EHEC) O157:H7, are known to be induced and released by various environmental cues, such as DNA damage responses and stress-inducing chemicals. In order to investigate the possible effects of growth media on Stxs expression, we analyzed the growth kinetics and expression of Stxs (Stx1 and 2) in cells grown in Luria-Bertani (LB) and E. coli (EC) media, which are widely used for EHEC O157:H7. Through direct plating and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR), it was revealed that, when EHEC O157:H7 was grown in EC medium, the total bacterial count was reduced significantly and the stx1 transcription was greatly increased during the stationary growth phase than that in LB. Here we report that bile salts and lactose, which are the two only components in EC medium that are absent in LB, function as negative and positive regulatory signals, respectively, for the transcription of both stx1 and stx2. Indeed, stx transcription was significantly increased (~5.7 and ~21.8 fold for stx1 and stx2, respectively; p < 0.05) in an EC medium lacking bile salts when compared to the normal EC. In contrast, EHEC O157:H7 grown in an EC medium lacking lactose did significantly decrease these transcriptions (~93.5 and ~4.3 fold for stx1 and stx2, respectively; p < 0.05). Consistently, stx transcription was drastically increased in an LB medium supplemented with lactose, implying that lactose might be an environmental trigger for the expression of Stxs.

Previously, we demonstrated the presence of a second copy of LPS myristoyl transferase in enterohemorrhagic Escherichia coli O157:H7, an important zoonotic diarrheagenic food-borne pathogen; the pO157-encoded ecf (an eae-conserved fragment) and the chromosomally-encoded lpxM (also referred to as msbM) genes. Although both genes share the same function as an LPS myristoyl transferase, the pO157-encoded ecf is thermoregulated via an intrinsically curved DNA while the chromosomal lpxM is regulated by the PhoP/Q two component regulatory system. However, it is unclear why E. coli O157: H7 carries two copies of LPS myristoyl transferase that are differentially regulated. In this study, a whole genome-scale transcriptome specific to E. coli O157:H7 was carried out for identification of the genes differentially expressed in the amyristoylated E. coli O157:H7. The results identified a total of 110 EHEC genes that were up- or down-regulated in the amyristoylated E. coli O157:H7 strain, including genes associated with virulence (26.36%), metabolism (20.91%), transport (10.91%), signal transduction (4.55%), genetic information processing (3.64%), stress response (2.73%), regulatory function (2.73%), motility/adherence (3.64%), cell envelope (2.73%), cell division (1.82%) and ORFs of unknown function (17.27%). Of particular interest, the expression of LEE pathogenicity island genes was significantly influenced by LPS structural defects.