Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome

Tarr, Phillip I.; Gordon, C.; Chandler, Wayne L.

doi:10.1016/s0140-6736(05)71144-2

Cited by 1,178 publications

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“…This foodborne enteric pathogen is acquired from contaminated foodstuffs and non-chlorinated drinking water (Karch et al, 2005;Maki, 2006;Rangel et al, 2005). In the severest cases of infection (~10-15 % of cases), the haemolytic uraemic syndrome develops as a systemic complication, leading to patient hospitalization, kidney failure and death (Serna & Boedeker, 2008;Tarr et al, 2005). Renal disease results from bacterial cytotoxin [Shiga-like toxin (Stx)-1 and -2] production in the gut, release into the systemic circulation and damage to vascular endothelial cells in the renal glomerulus (Blackall & Marques, 2004).…”

Section: Introductionmentioning

confidence: 99%

Probiotics prevent enterohaemorrhagic Escherichia coli O157 : H7-mediated inhibition of interferon-γ-induced tyrosine phosphorylation of STAT-1

et al. 2009

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Enterohaemorrhagic Escherichia coli (EHEC) O157 : H7 inhibits interferon (IFN)-c-stimulated tyrosine phosphorylation of signal transducer and activator of transcription (STAT)-1 in epithelial cells. We determined the effects of probiotics on EHEC-mediated disruption of IFN-c-stimulated STAT-1 activation in epithelial cell lines. Confluent Intestine 407, HEp-2 and Caco-2 epithelial cells were pre-treated (3 h) with either probiotics or surface-layer proteins derived from Lactobacillus helveticus R0052 prior to infection with EHEC O157 : H7 strain CL56 (m.o.i. 100 : 1, 6 h, 37 6C in 5 % CO 2 ). Subsequently, cells were washed and stimulated with human recombinant IFN-c (50 ng ml "1 , 0.5 h, 37 6C) followed by whole-cell protein extraction and immunoblotting for tyrosine-phosphorylated STAT-1. Relative to uninfected cells, STAT-1-activation was reduced after EHEC O157 : H7 infection. Pre-incubation with the probiotic L. helveticus R0052 followed by EHEC infection abrogated pathogen-mediated disruption of IFNc-STAT-1 signalling. As determined using Transwell inserts, probiotic-mediated protection was independent of epithelial cell contact. In contrast, pre-incubation with boiled L. helveticus R0052, an equal concentration of viable Lactobacillus rhamnosus R0011, or surface-layer proteins (0.14 mg ml "1 ) did not restore STAT-1 signalling in EHEC-infected cells. The viable probiotic agent L. helveticus R0052 prevented EHEC O157 : H7-mediated subversion of epithelial cell signal transduction responses. INTRODUCTIONOutbreaks of enterohaemorrhagic Escherichia coli (EHEC) serotype O157 : H7 infection occur frequently across the developed world (Serna & Boedeker, 2008). This foodborne enteric pathogen is acquired from contaminated foodstuffs and non-chlorinated drinking water (Karch et al., 2005;Maki, 2006;Rangel et al., 2005). In the severest cases of infection (~10-15 % of cases), the haemolytic uraemic syndrome develops as a systemic complication, leading to patient hospitalization, kidney failure and death (Serna & Boedeker, 2008;Tarr et al., 2005). Renal disease results from bacterial cytotoxin [Shiga-like toxin (Stx)-1 and -2] production in the gut, release into the systemic circulation and damage to vascular endothelial cells in the renal glomerulus (Blackall & Marques, 2004). EHEC pathogenesis is also attributed to intimate bacterial adhesion conferred by the locus of enterocyte effacement (LEE) pathogenicity island, the activity of effector proteins secreted through a type three secretion system (T3SS), and pathogen modulation of host cell signal transduction cascades (Bhavsar et al., 2007;Kaper et al., 2004).EHEC disease pathogenesis includes subversion of epithelial cell signal transduction cascades involved in host innate immune responses to infection (Bhavsar et al., 2007). For instance, EHEC inhibits interferon (IFN)-c-stimulated tyrosine phosphorylation of signal transducer and activator of transcription-1 (STAT-1) in multiple cell lines (Ceponis et al., 2003), which is mediated by a bacterially encoded fac...

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Section: Introductionmentioning

confidence: 99%

Probiotics prevent enterohaemorrhagic Escherichia coli O157 : H7-mediated inhibition of interferon-γ-induced tyrosine phosphorylation of STAT-1

et al. 2009

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“…STEC is a serologically diverse group of foodborne, zoonotic pathogens. Serotype O157 : H7 has been the predominant type worldwide (Tarr et al, 2005). However, altogether more than 200 STEC serotypes have been reported and more than 100 have been linked with human infection (Eklund et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Shiga toxin-producing Escherichia coli isolated from patients with diarrhoea in Bangladesh

Islam

Heuvelink

Boer

et al. 2007

Journal of Medical Microbiology

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“…Shiga toxin-producing Escherichia coli (STEC) strains associated with hemorrhagic colitis or the hemolytic-uremic syndrome (HUS) in humans are commonly referred to as enterohemorrhagic E. coli (EHEC) (32). Most EHEC strains carry the locus for enterocyte effacement (LEE), which is essential for intestinal colonization (12,14,19,27,34).…”

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Contribution of FliC to Epithelial Cell Invasion by Enterohemorrhagic Escherichia coli O113:H21

et al. 2006

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Enterohemorrhagic Escherichia coli (EHEC) O113:H21 can invade epithelial cells. In this study, we found that invasion but not adherence was inhibited by anti-FliC H21 specific antibodies. In addition, deletion of fliC H21 from EHEC O113:H21 resulted in an eightfold decrease in invasion that was restored upon transcomplementation with fliC H21 but not with fliC H6 . These results suggested that FliC plays an important role in the pathogenesis of infections caused by EHEC O113:H21 by allowing bacteria to penetrate the intestinal epithelium.Shiga toxin-producing Escherichia coli (STEC) strains associated with hemorrhagic colitis or the hemolytic-uremic syndrome (HUS) in humans are commonly referred to as enterohemorrhagic E. coli (EHEC) (32). Most EHEC strains carry the locus for enterocyte effacement (LEE), which is essential for intestinal colonization (12,14,19,27,34). Nevertheless, strains of EHEC that do not carry LEE are regularly isolated from patients with severe disease, and these isolates have been termed eae-or LEE-negative EHEC or STEC (2,4,11,13,17,20,24,25). We have shown previously that clinical isolates of LEE-negative EHEC have the ability to invade Chinese Hamster Ovary (CHO-K1) cells and the human colonic cell lines HCT-8 and Caco-2 (21). We speculate that this atypical subgroup of EHEC may use a mechanism of host cell invasion to colonize the intestinal mucosa.Recently, Rogers et al. used the streptomycin-treated mouse model to show that LEE-negative EHEC O113:H21 strain 98NK2 was closely associated with the colonic mucosa during infection (30). In addition, bacteria were observed to penetrate the gut epithelium, and this close interaction was dependent on fliC. Although there was no difference in the fecal shedding of wild-type 98NK2 and a 98NK2⌬fliC mutant, fliC was required for full lethality in mice mediated by Shiga toxin, suggesting that a close interaction of 98NK2 with the intestinal mucosa was important for virulence. In the present study, we have extended these findings to examine the contribution of FliC to invasion of HCT-8 epithelial cells by EHEC O113:H21.FliC H21 -mediated invasion of HCT-8 cells. Previous work has shown that FliC is more highly expressed at temperatures below 37°C in the invasive pathogens Yersinia enterocolitica and Listeria monocytogenes (3, 9, 18). We therefore examined FliC H21 expression by wild-type STEC O113:H21 strain EH41 at two different growth temperatures. EH41 is a clinical isolate that has been described previously (10). Bacteria were grown in Luria-Bertani (LB) broth to the same optical density (i.e., an optical density at 600 nm of 0.8 [mid-log phase]) at 25 and 37°C, and whole-cell lysates were analyzed by immunoblotting with anti-H21 antibodies (Statens Serum Institut, Copenhagen, Denmark). The results showed that FliC H21 production by EH41 was more abundant at 25°C than at 37°C (Fig. 1A). To determine whether increased expression of FliC H21 correlated with increased invasion, we performed invasion assays with EH41 grown in LB broth overnight ...

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Shiga-toxin-producing Escherichia coli and haemolytic uraemic syndrome

Cited by 1,178 publications

References 167 publications

Probiotics prevent enterohaemorrhagic Escherichia coli O157 : H7-mediated inhibition of interferon-γ-induced tyrosine phosphorylation of STAT-1

Probiotics prevent enterohaemorrhagic Escherichia coli O157 : H7-mediated inhibition of interferon-γ-induced tyrosine phosphorylation of STAT-1

Shiga toxin-producing Escherichia coli isolated from patients with diarrhoea in Bangladesh

Contribution of FliC to Epithelial Cell Invasion by Enterohemorrhagic Escherichia coli O113:H21

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