Abstract
Escherichia coli O157:H7 pathogenesis is due to Shiga toxin (Stx) production, though variation in virulence has been observed. Clade 8 strains, for instance, were shown to overproduce Stx and were more common among hemolytic uremic syndrome cases. One candidate gene, norV, which encodes a nitric oxide (NO) reductase found in a clade 8 O157:H7 outbreak strain (TW14359), was thought to impact virulence. Hence, we screened for norV in 303 O157 isolates representing multiple clades, examined stx2 expression following NO exposure in TW14359 for comparison to an isogenic mutant (ΔnorV), and evaluated survival in THP-1 derived macrophages. norV was intact in strains representing clades 6–9, whereas a 204 bp deletion was found in clades 2 and 3. During anaerobic growth, NO induced stx2 expression in TW14359. A similar increase in stx2 expression was observed for the ΔnorV mutant in anaerobiosis, though it was not impaired in its ability to survive within macrophages relative to TW14359. Altogether, these data suggest that NO enhances virulence by inducing Stx2 production in TW14359, and that toxin production is inhibited by NorV encoded by a gene found in most clade 8 strains. The mechanism linked to these responses, however, remains unclear and likely varies across genotypes.
Highlights
Received: 3 November 2021Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a leading cause of gastrointestinal illness linked to food and waterborne outbreaks worldwide
STEC O157 often present with hemorrhagic colitis, some can develop hemolytic uremic syndrome (HUS) [1] that can lead to kidney failure and death
We previously showed that a diverse set of O157 strains could be classified into nine distinct clades based on the phylogenetic analysis of 96 single nucleotide polymorphisms (SNPs) [10]
Summary
Received: 3 November 2021Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a leading cause of gastrointestinal illness linked to food and waterborne outbreaks worldwide. STEC pathogenesis is mainly due to the production of one or more Shiga toxins (Stx) encoded by genes carried on lambda-like bacteriophages [5]. STEC strains possessing genes like eae (intimin) found on the locus of enterocyte effacement (LEE) pathogenicity island [6], contribute to attaching and effacing lesion formation on intestinal epithelial cells. E. coli strains possessing stx as well as the LEE island are classified as enterohemorrhagic E. coli. (EHEC), which were found to be more virulent than STEC strains lacking these factors [7]. EHEC strains producing the Stx2a and/or Stx2c variants were observed to be more virulent causing a higher frequency of HUS than strains producing the Stx variant alone or with
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