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The Presence of the pAA Plasmid in the German O104:H4 Shiga Toxin Type 2a (Stx2a)–Producing Enteroaggregative Escherichia coli Strain Promotes the Translocation of Stx2a Across an Epithelial Cell Monolayer
- Source :
- The Journal of Infectious Diseases. 210:1909-1919
- Publication Year :
- 2014
- Publisher :
- Oxford University Press (OUP), 2014.
-
Abstract
- (See the editorial commentary by Steiner on pages 1860–2.) Enteroaggregative Escherichia coli (EAEC) is a pathotype of diarrheagenic Escherichia coli that is a cause of acute and persistent diarrhea in many settings [1–7]. EAEC strains express a heterogeneous array of putative virulence factors [8–12] encoded on the bacterial chromosome or on the EAEC-specific pAA plasmid. EAEC strains often harbor a transcriptional activator of the AraC/XylS class, called “AggR” [13], which controls genes on both the plasmid and the chromosome. Among the genes under AggR control include those that encode the aggregative adherence fimbriae (AAF), of which at least 4 variants exist [14–18]. AAF adhesins have been shown to be essential for EAEC adherence to human intestinal explants and to elicit both cytokine release and opening of epithelial tight junctions in a polarized epithelial model [19, 20]. EAEC strains also often harbor a variable number of serine protease autotransporters of Enterobacteriaceae (SPATEs) that are implicated in immune evasion, mucosal damage, secretogenicity, and colonization [21]. In 2011, an outbreak of foodborne hemorrhagic colitis originated in Germany, spreading to other European countries. Over 4000 individuals were affected, including primary and secondary cases [22]. Hemolytic uremic syndrome (HUS) developed in approximately 22% of the cases [22], and 54 people died [23, 24]. The implicated pathogen was an EAEC strain of the rare serotype O104:H4 [23], which was lysogenized with an Stx2a-converting phage. Genomic analysis [25] demonstrated that the outbreak strain contained the genes required to produce the AAF/I variant and 3 SPATEs (Pic, SigA, and SepA). Although much is known about the pathogenesis of serotype O157:H7 Shiga toxin (Stx)–producing E. coli, it is unclear how an EAEC strain would be able to elicit severe hemorrhagic colitis and HUS, even when harboring an Stx-encoding gene. In this study, we tested the hypothesis that the plasmid-borne virulence factors of EAEC contributed to the high pathogenicity of the German outbreak strain by promoting strong adherence to the epithelium and/or by opening epithelial tight junctions.
- Subjects :
- Genotype
Virulence Factors
Fimbria
Virulence
Serogroup
medicine.disease_cause
Shiga Toxin 2
Bacterial Adhesion
Cell Line
Microbiology
Plasmid
Germany
Escherichia coli
medicine
Humans
Immunology and Allergy
Escherichia coli Infections
biology
Escherichia coli Proteins
Interleukin-8
Epithelial Cells
Shiga toxin
biology.organism_classification
Enterobacteriaceae
Virology
Bacterial adhesin
Protein Transport
Infectious Diseases
Enteroaggregative Escherichia coli
Trans-Activators
biology.protein
Gene Deletion
Plasmids
Subjects
Details
- ISSN :
- 15376613 and 00221899
- Volume :
- 210
- Database :
- OpenAIRE
- Journal :
- The Journal of Infectious Diseases
- Accession number :
- edsair.doi.dedup.....ebd74a68e8a7d76639481697f7b0dbc6