| Summary: | <p>Abstract</p> <p>Background</p> <p>Enterohemorrhagic <it>E. coli </it>(EHEC), a subgroup of Shiga toxin (Stx) producing <it>E. coli </it>(STEC), may cause severe enteritis and hemolytic uremic syndrome (HUS) and is transmitted orally via contaminated foods or from person to person. The infectious dose is known to be very low, which requires most of the bacteria to survive the gastric acid barrier. Acid resistance therefore is an important mechanism of EHEC virulence. It should also be a relevant characteristic of <it>E. coli </it>strains used for therapeutic purposes such as the probiotic <it>E. coli </it>Nissle 1917 (EcN). In <it>E. coli </it>and related enteric bacteria it has been extensively demonstrated, that the alternative sigma factor σ<sup>S</sup>, encoded by the <it>rpoS </it>gene, acts as a master regulator mediating resistance to various environmental stress factors.</p> <p>Methods</p> <p>Using <it>rpoS </it>deletion mutants of a highly virulent EHEC O26:H11 patient isolate and the sequenced prototype EHEC EDL933 (ATCC 700927) of serotype O157:H7 we investigated the impact of a functional <it>rpoS </it>gene for orchestrating a satisfactory response to acid stress in these strains. We then functionally characterized <it>rpoS </it>of probiotic EcN and five r<it>poS </it>genes selected from STEC isolates pre-investigated for acid resistance.</p> <p>Results</p> <p>First, we found out that ATCC isolate 700927 of EHEC EDL933 has a point mutation in <it>rpoS</it>, not present in the published sequence, leading to a premature stop codon. Moreover, to our surprise, one STEC strain as well as EcN was acid sensitive in our test environment, although their cloned <it>rpoS </it>genes could effectively complement acid sensitivity of an <it>rpoS </it>deletion mutant.</p> <p>Conclusion</p> <p>The attenuation of sequenced EHEC EDL933 might be of importance for anyone planning to do either <it>in vitro </it>or <it>in vivo </it>studies with this prototype strain. Furthermore our data supports recently published observations, that individual <it>E. coli </it>isolates are able to significantly modulate their acid resistance phenotype independent of their <it>rpoS </it>genotype.</p>
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