J Biol Chem 1998,273(19):11478–11482.PubMedCrossRef 36. Barbier M, Owings JP, Martinez-Ramos I, Damron FH, Gomila R, Blazquez J, Goldberg JB, Alberti S: Lysine trimethylation of EF-Tu mimics platelet-activating factor to initiate Pseudomonas aeruginosa pneumonia. MBio 2013,4(3):e00207-e00213.PubMedCrossRef 37. Barbier M, Oliver A, Rao J, Hanna SL, Goldberg JB, Alberti S: Novel phosphorylcholine-containing protein of Pseudomonas aeruginosa chronic infection isolates interacts with airway epithelial cells. J Infect Dis 2008,197(3):465–473.PubMedCrossRef

GSK690693 38. Yu H, Boucher JC, Hibler NS, Deretic V: Virulence properties of Pseudomonas aeruginosa lacking the extreme-stress sigma factor AlgU (sigmaE). Infect Immun 1996,64(7):2774–2781.PubMed Authors’ contributions YY designed, performed the experiments, and drafted the manuscript; FHD, TRW and CLP performed the experiments and revised the manuscript; XW and MJS revised the manuscript; HDY designed PF-6463922 manufacturer the experiments and revised the manuscript. All authors read and approved the final manuscript.”
“Background Shiga toxin-producing E. coli (STEC) can cause serious human infections ranging from uncomplicated

watery diarrhea to bloody diarrhea, up to the hemolytic uremic syndrome (HUS), including neurological complications [1]. The production of Shiga toxins (Stx) is considered to be the major virulence factor of STEC [2]. In addition to the production of Stx, the generation of histopathological lesions on host enterocytes, IMP dehydrogenase termed attaching and effacing lesions, which are caused by proteins encoded on the locus of enterocyte effacement (LEE) can lead to serious symptoms of disease [3]. The intimin-encoding E. coli attaching and effacing (eae) gene is located on the LEE. Intimin is involved in the intimate attachment of STEC to the enterocytes, and the corresponding eae gene has been used as a marker for the presence of the LEE [4]. In contrast, eae-negative E. coli of various serotypes were described to cause serious diseases. Examples

of these are the learn more outbreak of hemolytic-uremic syndrome (HUS) caused by a STEC strain of serotype O113:H21 in South Australia in 1998 [5], and more recently, the serious outbreak of diarrhea and HUS in Germany in 2011 with STEC of serotype O104:H4 [6]. Such strains may harbor other important virulence markers than the LEE. Whereas the O104:H4 outbreak strain had an enteroaggregative E. coli backbone, the O113:H21 outbreak strain expressed a subtilase cytotoxin (SubAB) with cytotoxic and apoptotic properties, in addition to Stx [7]. Paton et al. [8] described this novel AB5 cytotoxin occurring in the eae-negative STEC O113:H21 outbreak strain. This toxin caused cell death in a number of animal and human cells and enhanced survival of pathogenic E. coli strains in macrophages [9]. The initially described subtilase cytotoxin SubAB is encoded by the closely linked subA and subB genes organized in an operon structure on the megaplasmid pO113 [7, 8].