RegR Virulence Regulon of Rabbit-Specific Enteropathogenic Escherichia coli Strain E22

Srikhanta, Yogitha N.; Hocking, Dianna M; Praszkier, Judyta; Wakefield, Matthew J.; Robins-Browne, Roy M.; Yang, Jiyeon; Tauschek, Marija

doi:10.1128/iai.01325-12

Cited by 7 publications

(14 citation statements)

References 65 publications

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“…tEPEC microcolonies have been also observed on infected fully differentiated HT-29 Glc Ϫ/ϩ and T84 cells, and the formation of tEPEC microcolonies increases as the brush border develops during the cell differentiation of Caco-2 cells (467). Importantly, animal EPEC-like pathogens such as Citrobacter rodentium (468), rabbit diarrheagenic E. coli (RDEC-1) (469-477), and rabbit EPEC (REPEC) (472,(476)(477)(478)(479)(480)(481)(482)(483)(484), which express virulence factors similar those of human tEPEC, have been shown to produce identical structural and functional damage in animal intestinal barriers and in cultured, fully differentiated human intestinal cells.…”

Section: Cell Interaction Cell Entry and Intracellular Lifestylementioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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SUMMARY Hosts are protected from attack by potentially harmful enteric microorganisms, viruses, and parasites by the polarized fully differentiated epithelial cells that make up the epithelium, providing a physical and functional barrier. Enterovirulent bacteria interact with the epithelial polarized cells lining the intestinal barrier, and some invade the cells. A better understanding of the cross talk between enterovirulent bacteria and the polarized intestinal cells has resulted in the identification of essential enterovirulent bacterial structures and virulence gene products playing pivotal roles in pathogenesis. Cultured animal cell lines and cultured human nonintestinal, undifferentiated epithelial cells have been extensively used for understanding the mechanisms by which some human enterovirulent bacteria induce intestinal disorders. Human colon carcinoma cell lines which are able to express in culture the functional and structural characteristics of mature enterocytes and goblet cells have been established, mimicking structurally and functionally an intestinal epithelial barrier. Moreover, Caco-2-derived M-like cells have been established, mimicking the bacterial capture property of M cells of Peyer's patches. This review intends to analyze the cellular and molecular mechanisms of pathogenesis of human enterovirulent bacteria observed in infected cultured human colon carcinoma enterocyte-like HT-29 subpopulations, enterocyte-like Caco-2 and clone cells, the colonic T84 cell line, HT-29 mucus-secreting cell subpopulations, and Caco-2-derived M-like cells, including cell association, cell entry, intracellular lifestyle, structural lesions at the brush border, functional lesions in enterocytes and goblet cells, functional and structural lesions at the junctional domain, and host cellular defense responses.

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Section: Cell Interaction Cell Entry and Intracellular Lifestylementioning

confidence: 99%

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Moal

Servin

2013

Microbiol Mol Biol Rev

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“…Additionally, recent studies on the RegA homologue RegR, from rabbit-enteropathogenic E. coli strain E22, demonstrated differences in regulatory targets (57). Together, these data suggest that the role of RegA as a key virulence and LEE PAI regulator may be an evolutionary adaptation specific to C. rodentium.…”

mentioning

confidence: 79%

“…RegA homologues were identified by using BLASTP and tBLASTn searches of the NCBI and Broad Institute databases with the C. rodentium RegA protein sequence (here referred to as RegA CR ) and were deemed homologous if they showed a minimum of 60% amino acid identity to RegA CR . From these searches, we identified 19 putative RegA homologues, including the RegR protein from enteropathogenic E. coli strain E22 (57). An additional RegA homologue was identified in the Escherichia clade IV strain H605 (David Gordon, personal communication) (see Table S1 in the supplemental material).…”

Section: Resultsmentioning

confidence: 99%

Evolutionary Adaptation of an AraC-Like Regulatory Protein in Citrobacter rodentium and Escherichia Species

et al. 2015

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dThe evolution of pathogenic bacteria is a multifaceted and complex process, which is strongly influenced by the horizontal acquisition of genetic elements and their subsequent expression in their new hosts. A well-studied example is the RegA regulon of the enteric pathogen Citrobacter rodentium. The RegA regulatory protein is a member of the AraC/XylS superfamily, which coordinates the expression of a gene repertoire that is necessary for full pathogenicity of this murine pathogen. Upon stimulation by an exogenous, gut-associated signal, namely, bicarbonate ions, RegA activates the expression of a series of genes, including virulence factors, such as autotransporters, fimbriae, a dispersin-like protein, and the grlRA operon on the locus of enterocyte effacement pathogenicity island. Interestingly, the genes encoding RegA homologues are distributed across the genus Escherichia, encompassing pathogenic and nonpathogenic subtypes. In this study, we carried out a series of bioinformatic, transcriptional, and functional analyses of the RegA regulons of these bacteria. Our results demonstrated that regA has been horizontally transferred to Escherichia spp. and C. rodentium. Comparative studies of two RegA homologues, namely, those from C. rodentium and E. coli SMS-3-5, a multiresistant environmental strain of E. coli, showed that the two regulators acted similarly in vitro but differed in terms of their abilities to activate the virulence of C. rodentium in vivo, which evidently was due to their differential activation of grlRA. Our data indicate that RegA from C. rodentium has strain-specific adaptations that facilitate infection of its murine host. These findings shed new light on the development of virulence by C. rodentium and on the evolution of virulence-regulatory genes of bacterial pathogens in general. Increases in the amount and availability of DNA sequence data have provided valuable insights into the ongoing speciation and evolution of bacteria. In particular, these data have revealed the frequency and ubiquity of horizontal gene transfer and how these events may have contributed to the development of bacterial pathogens (1-11). For example, the acquisition of the pPla and pMT1 plasmids catalyzed speciation of Yersinia pestis from Yersinia pseudotuberculosis (10), and the recent emergence of a new pathogenic strain of Escherichia coli, which caused a dramatic foodborne disease outbreak in Germany in 2011, is attributed to the horizontal transfer of a number of virulence determinants, including Shiga toxin, various adhesins and autotransporters, and the pESBL C227-11 plasmid (12-14).However, the acquisition of virulence determinants alone is often not sufficient to make a bacterium pathogenic. For example, the murine pathogen Citrobacter rodentium contains a large pathogenicity island known as the locus of enterocyte effacement (LEE PAI), which is required for colonic hyperplasia and the formation of attaching and effacing (A/E) lesions. Evidence indicates that the island has been horizontally mobilized in...

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“…The PsrB protein belongs to the AraC superfamily of transcriptional regulators which control the expression of genes involved in diverse cellular functions such as carbon metabolism, stress responses, and virulence (35,36). In enteric bacterial pathogens, a number of AraC-like activators including AggR of enteroaggregative E. coli (37), Rns of enterotoxigenic E. coli (38), PerA, RegR, and RalR of enteropathogenic E. coli (39)(40)(41), RegA of Citrobacter rodentium (42,43), and ToxT of Vibrio cholerae (44) play a critical role in bacterial virulence. The genes encoding these virulence activators appear to have coevolved with their principal target virulence genes, which code for secreted factors and surface proteins responsible for intestinal colonization (40,41,45,46).…”

Section: Discussionmentioning

confidence: 99%

Control of Acid Resistance Pathways of Enterohemorrhagic Escherichia coli Strain EDL933 by PsrB, a Prophage-Encoded AraC-Like Regulator

et al. 2015

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bEnterohemorrhagic Escherichia coli (EHEC) O157:H7 causes bloody diarrhea and hemolytic-uremic syndrome (HUS) and is the most prevalent E. coli serotype associated with food-borne illness worldwide. This pathogen is transmitted via the fecal-oral route and has a low infectious dose that has been estimated to be between 10 and 100 cells. We and others have previously identified three prophage-encoded AraC-like transcriptional regulators, PatE, PsrA, and PsrB in the EHEC O157:H7 EDL933 strain. Our analysis showed that PatE plays an important role in facilitating survival of EHEC under a number of acidic conditions, but the contribution of PsrA and PsrB to acid resistance (AR) was unknown. Here, we investigated the involvement of PsrA and PsrB in the survival of E. coli O157:H7 in acid. Our results showed that PsrB, but not PsrA, enhanced the survival of strain EDL933 under various acidic conditions. Transcriptional analysis using promoter-lacZ reporters and electrophoretic mobility shift assays demonstrated that PsrB activates transcription of the hdeA operon, which encodes a major acid stress chaperone, by interacting with its promoter region. Furthermore, using a mouse model, we showed that expression of PsrB significantly enhanced the ability of strain EDL933 to overcome the acidic barrier of the mouse stomach. Taken together, our results indicate that EDL933 acquired enhanced acid tolerance via horizontally acquired regulatory genes encoding transcriptional regulators that activate its AR machinery. Enterohemorrhagic Escherichia coli (EHEC) strains of serotype O157:H7 are associated with epidemic and sporadic infection worldwide. EHEC is a food-and waterborne pathogen that can cause hemorrhagic colitis and hemolytic-uremic syndrome (1-4). The main reservoir of EHEC is cattle and other ruminants that shed the microorganism in feces. Many outbreaks have been associated with contaminated beef products, milk, vegetables, and fruits (5, 6). The infectious dose of EHEC is extremely low (ϳ10 to 100 cells), which significantly increases the risk of infection (7).EHEC expresses one or two cytotoxins, Shiga toxin 1 (Stx1) and/or Shiga toxin 2 (Stx2), which are responsible for the lifethreatening manifestations of infection (8, 9). In addition, EHEC (O157:H7) strains carry a pathogenicity island known as the locus of enterocyte effacement pathogenicity island (LEE PAI), which encodes portions of a type III secretion pathway, the adhesin intimin, and its translocated receptor (Tir) (10, 11). Together, these virulence factors enable EHEC to adhere to intestinal epithelial cells and form attaching-and-effacing lesions, which cause the destruction of microvilli and the rearrangement of cytoskeletal proteins (11, 12). Expression of the five operons within the LEE PAI is tightly regulated by a number of transcriptional regulators including H-NS, Ler, GrlA, integration host factor (IHF), GadE, and QseA, which allows the various virulence factors to be expressed when EHEC enters its preferred environmental niches in the host int...

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RegR Virulence Regulon of Rabbit-Specific Enteropathogenic Escherichia coli Strain E22

Cited by 7 publications

References 65 publications

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Pathogenesis of Human Enterovirulent Bacteria: Lessons from Cultured, Fully Differentiated Human Colon Cancer Cell Lines

Evolutionary Adaptation of an AraC-Like Regulatory Protein in Citrobacter rodentium and Escherichia Species

Control of Acid Resistance Pathways of Enterohemorrhagic Escherichia coli Strain EDL933 by PsrB, a Prophage-Encoded AraC-Like Regulator

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