The complete sequence of the locus of enterocyte effacement (LEE) from enteropathogenic <i>Escherichia coli</i> E2348/69

Elliott, Simon J.; Wainwright, Leslie A.; McDaniel, Timothy K.; Jarvis, Karen G.; Deng, Yulin; Lai, Li-Ching; McNamara, Barry P.; Donnenberg, Michael S.; Kaper, James B.

doi:10.1046/j.1365-2958.1998.00783.x

Cited by 607 publications

(507 citation statements)

References 30 publications

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“…The pathogenesis of EPEC depends on the locus of enterocyte effacement (LEE), a chromosomal pathogenicity island. The LEE contains a number of different genes, including eae, which has an essential role in inducing a characteristic lesion formation in the intestinal epithelium, termed an attaching and effacing (A/E) lesion (Elliott et al, 1998;Vallance & Finlay 2000;Kaper et al, 2004). The eae gene encodes intimin, a 94 kDa outer-membrane protein that is responsible for the intimate adherence between bacterial and enterocyte membranes (Vallance & Finlay, 2000;Trabulsi et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Molecular analysis of typical and atypical enteropathogenic Escherichia coli (EPEC) isolated from children with diarrhoea

Nakhjavani

Emaneini

Hosseini

et al. 2013

Journal of Medical Microbiology

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Diarrhoea continues to be one of the most common causes of morbidity and mortality among infants and children in developing countries. To investigate the incidence, antimicrobial resistance and genetic relationships of enteropathogenic Escherichia coli (EPEC) in children with diarrhoea, a total of 612 stool specimens were collected in Tehran, Iran, and cultured to isolate strains of EPEC. The disc diffusion method was used to determine the susceptibility of the isolates according to the Clinical and Laboratory Standards Institute (CLSI) guidelines. The presence of eae, stx and bfp-A genes was determined by PCR. The genetic relationships between EPEC isolates were determined by pulsed-field gel electrophoresis (PFGE). Out of the 412 strains of E. coli obtained from 612 diarrhoeal stool specimens, 23 (5.6 %) were identified as EPEC, of which seven (30.4 %) were classified as typical strains of EPEC and 16 (69.6 %) were classified as atypical. Out of the 23 EPEC isolates, 69.5 % were resistant to ampicillin, 39.1 % were resistant to tetracycline and cotrimoxazole, 30.4 % were resistant to cefpodoxime, ceftazidime, ceftriaxone and aztreonam, and 26.1 % were resistant to imipenem. The isolates were classified into 21 pulsotypes by PFGE profiles. The present study shows that typical and atypical EPEC isolates displayed considerable heterogeneity in PFGE profiles and EPEC infections were only sporadic in Tehran. Overall 69 % of isolates were resistant to at least one of the antibiotics tested. INTRODUCTIONEnteropathogenic Escherichia coli (EPEC) is one of the major causes of diarrhoea among children in developing countries (Hernandes et al., 2009;Moura et al., 2009). The pathogenesis of EPEC depends on the locus of enterocyte effacement (LEE), a chromosomal pathogenicity island. The LEE contains a number of different genes, including eae, which has an essential role in inducing a characteristic lesion formation in the intestinal epithelium, termed an attaching and effacing (A/E) lesion (Elliott et al., 1998;Vallance & Finlay 2000;Kaper et al., 2004). The eae gene encodes intimin, a 94 kDa outer-membrane protein that is responsible for the intimate adherence between bacterial and enterocyte membranes (Vallance & Finlay, 2000;Trabulsi et al., 2002). EPEC strains are classified as typical or atypical, according to the presence or absence of the E. coli adherence factor plasmid (EAF) that carries the bfpA gene, which encodes the bundle-forming pili (Hernandes et al., 2009). The most typical EPEC strains belong to the classic O : H serotypes and are eae-and bfpA-positive (Ochoa et al., 2008). The atypical EPEC isolates are eaepositive and bfpA-and stx (the gene encoding shiga-like toxin)-negative. EPEC are among the most important pathogens infecting children under 2 years of age in the developing world (Ochoa et al., 2008). Recent studies indicate that atypical EPEC is more prevalent than typical Abbreviations: EPEC, enteropathogenic Escherichia coli; LEE, locus of enterocyte effacement; PFGE, pulsed-field gel electrophore...

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Section: Introductionmentioning

confidence: 99%

Molecular analysis of typical and atypical enteropathogenic Escherichia coli (EPEC) isolated from children with diarrhoea

Nakhjavani

Emaneini

Hosseini

et al. 2013

Journal of Medical Microbiology

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“…One of the secreted proteins, the translocated intimin receptor (Tir), inserts into the host membrane and interacts with intimin on the bacterial surface, leading to intimate attachment, actin polymerization within host cells, and the formation of a pedestal-like structure (38). The homologous loci of enterocyte effacement (LEE) in these pathogens share the same overall organization and encode the TTSS as well as various effector proteins required to form A/E lesions and mediate other host effects (11,27).…”

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Comparative Analysis of EspF from Enteropathogenic and Enterohemorrhagic Escherichia coli in Alteration of Epithelial Barrier Function

et al. 2004

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Enteropathogenic Escherichia coli (EPEC) and enterohemorrhagic E. coli (EHEC) are related intestinal pathogens that harbor highly similar pathogenicity islands known as the locus of enterocyte effacement (LEE). Despite their genetic similarity, these two pathogens disrupt epithelial tight junction barrier function with distinct kinetics. EHEC-induced reduction in transepithelial electrical resistance (TER), a measure of barrier function disruption, is significantly slower and more modest in comparison to that induced by EPEC. The variation in bacterial adherence only partially accounted for these differences. The LEE-encoded effector protein EspF has been shown to be critical for EPEC-induced alterations in TER. EspF from both EPEC and EHEC is expressed and secreted upon growth in tissue culture medium. The mutation of EHEC cesF suggested that the optimal expression and secretion of EHEC EspF required its chaperone CesF, as has been shown for EPEC. In contrast to EPEC espF and cesF, mutation of the corresponding EHEC homologs did not dramatically alter the decrease in TER. These differences could possibly be explained by the presence of additional espF-like sequences (designated U-and M-espF, where the letter designations refer to the specific cryptic prophage sequences on the EHEC chromosome closest to the respective genes) in EHEC. Reverse transcription-PCR analyses revealed coordinate regulation of EHEC U-espF and the LEE-encoded espF, with enhanced expression in bacteria grown in Dulbecco-Vogt modified Eagle's medium compared to bacteria grown in Luria broth. Both EHEC espF and U-espF complemented an EPEC espF deletion strain for barrier function alteration. The overexpression of U-espF, but not espF, in wild-type EHEC potentiated the TER response. These studies reveal further similarities and differences in the pathogenesis of EPEC and EHEC.

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“…The formation of A/E lesions is dependent on a type III secretion system (TTSS) encoded by a unique 35 kbp chromosomal pathogenicity island, termed the locus of enterocyte effacement (LEE; Elliott et al, 1998). The TTSS mediates the secretion of proteins to the medium and also the translocation of bacterial virulence proteins (effectors) into the membrane and cytoplasm of infected host cells.…”

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Enteropathogenic Escherichia coli induces modification of the focal adhesions of infected host cells

et al. 2002

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SummaryEnteropathogenic Escherichia coli (EPEC) is a human-specific pathogen that causes severe diarrhoea in young children. The disease involves intimate interaction between the pathogen and the brush border of enterocytes. During infection, EPEC uses a type III secretion system (TTSS) to inject several proteins into the infected cells, and these effector proteins modify specific processes in the host cell. We show that, upon infection, EPEC induces detachment of the infected host cells from the substratum, modification of focal adhesions (FA) in the infected cells and specific dephosphorylation of focal adhesion kinase (FAK). We also show that EPEC-induced cell detachment is dependent on FAK expression by the infected cells. Finally, we demonstrate that cell detachment, FA modification and FAK dephosphorylation are dependent on functional TTSS in the infecting EPEC. These results suggest that EPEC is using its TTSS to inject protein(s) into the infected cells, which can induce FAK dephosphorylation, as well as FAK-dependent FA modification and cell detachment. These processes are specific and probably play an important role in EPEC virulence.

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The complete sequence of the locus of enterocyte effacement (LEE) from enteropathogenic Escherichia coli E2348/69

Cited by 607 publications

References 30 publications

Molecular analysis of typical and atypical enteropathogenic Escherichia coli (EPEC) isolated from children with diarrhoea

Molecular analysis of typical and atypical enteropathogenic Escherichia coli (EPEC) isolated from children with diarrhoea

Comparative Analysis of EspF from Enteropathogenic and Enterohemorrhagic Escherichia coli in Alteration of Epithelial Barrier Function

Enteropathogenic Escherichia coli induces modification of the focal adhesions of infected host cells

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