Enterohemorrhagic Escherichia coli (EHEC) strains, including E. coli O157:H7, cause severe illness in humans due to the production of
Shiga toxin (Stx) and other
virulence factors. Because Stx is coregulated with lambdoid prophage induction, its expression is especially susceptible to environmental cues.
Infections with Stx-producing E. coli can be difficult to model due to the wide range of disease outcomes: some
infections are relatively mild, while others have serious complications. Probiotic organisms, members of the gut microbiome, and organic
acids can depress Stx production, in many cases by inhibiting the growth of EHEC strains. On the other hand, the factors currently known to amplify Stx act via their effect on the stx-converting phage. Here, we characterize two interactive mechanisms that increase Stx production by O157:H7 strains: first, direct interactions with phage-susceptible E. coli, and second, indirect amplification by secreted factors.
Infection of susceptible strains by the stx-converting phage can expand the Stx-producing population in a human or animal host, and phage
infection has been shown to modulate virulence in vitro and in vivo Acellular factors, particularly
colicins and microcins, can kill O157:H7 cells but may also trigger Stx expression in the process.
Colicins, microcins, and other
bacteriocins have diverse cellular targets, and many such molecules remain uncharacterized. The identification of additional Stx-amplifying microbial interactions will improve our understanding of E. coli O157:H7
infections and help elucidate the intricate regulation of pathogenicity in EHEC strains.