title: Impact of the rpoS genotype for acid resistance patterns of pathogenic and probiotic Escherichia coli.
abstract: BACKGROUND
  Enterohemorrhagic E. coli (EHEC), a subgroup of Shiga toxin (Stx) producing E. coli (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 E. coli strains used for therapeutic purposes such as the probiotic E. coli Nissle 1917 (EcN). In E. coli and related enteric bacteria it has been extensively demonstrated, that the alternative sigma factor sigmaS, encoded by the rpoS gene, acts as a master regulator mediating resistance to various environmental stress factors.
  
  
  METHODS
  Using rpoS 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 rpoS gene for orchestrating a satisfactory response to acid stress in these strains. We then functionally characterized rpoS of probiotic EcN and five rpoS genes selected from STEC isolates pre-investigated for acid resistance.
  
  
  RESULTS
  First, we found out that ATCC isolate 700927 of EHEC EDL933 has a point mutation in rpoS, 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 rpoS genes could effectively complement acid sensitivity of an rpoS deletion mutant.
  
  
  CONCLUSIONS
  The attenuation of sequenced EHEC EDL933 might be of importance for anyone planning to do either in vitro or in vivo studies with this prototype strain. Furthermore our data supports recently published observations, that individual E. coli isolates are able to significantly modulate their acid resistance phenotype independent of their rpoS genotype.
authors: Institute for Medical Microbiology and Hospital Epidemiology, Hannover Medical School, Hannover, Germany. sina.coldewey@web.de <sina.coldewey@web.de>
authors: Sina M
authors: SM
authors: Coldewey
authors: Maike
authors: M
authors: Hartmann
authors: Dorothea S
authors: DS
authors: Schmidt
authors: Uta
authors: U
authors: Engelking
authors: Sya N
authors: SN
authors: Ukena
authors: Florian
authors: F
authors: Gunzer
mesh_terms: D000143:Acids / Q000494:pharmacology*; D001483:Base Sequence; D024881:Drug Resistance, Bacterial / Q000235:genetics*; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development; D019453:Escherichia coli O157 / Q000187:drug effects / Q000235:genetics / Q000254:growth & development; D029968:Escherichia coli Proteins / Q000235:genetics* / Q000502:physiology; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D005816:Genetic Complementation Test; D005838:Genotype; D006863:Hydrogen-Ion Concentration; D008969:Molecular Sequence Data; D017354:Point Mutation; D019936:Probiotics; D016415:Sequence Alignment; D012808:Sigma Factor / Q000235:genetics* / Q000502:physiology
chemical_list: D000143:Acids; D029968:Escherichia coli Proteins; D012808:Sigma Factor