Expression of type I pili is abolished in verotoxin-producing Escherichia coli O157

Enami, Mika

doi:10.1016/s0378-1097(99)00438-3

Cited by 13 publications

(12 citation statements)

References 14 publications

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“…Type I fimbriae may play a role in trauma-induced adherence of commensal E. coli to the murine cecum (19). However, modulation of type I fimbriae expression by NE could not explain the increased adherence of E. coli O157:H7 to the bovine ileal mucosa observed in this study, since E. coli O157:H7 strains contain a 16-bp deletion in the promoter region for the major fimbrial subunit and, as such, do not express type I fimbriae (12,37).…”

Section: Vol 72 2004contrasting

confidence: 56%

The Neuroendocrine Stress Hormone Norepinephrine Augments Escherichia coli O157:H7-Induced Enteritis and Adherence in a Bovine Ligated Ileal Loop Model of Infection

et al. 2004

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The role of the neuroendocrine environment in the pathogenesis of enteric bacterial infections is increasingly being recognized. Here we report that norepinephrine augments Escherichia coli O157:H7-induced intestinal inflammatory and secretory responses as well as bacterial adherence to intestinal mucosa in a bovine ligated ileal loop model of infection. Norepinephrine modulation of enteritis and adherence was dependent on the ability of E. coli O157:H7 to form attaching and effacing lesions.Enterohemorrhagic Escherichia coli (EHEC) causes acute gastroenteritis in humans that may be complicated by lifethreatening systemic sequelae depending on serotype-and host-specific factors (35). EHEC strains are defined by their ability to produce one or more Shiga-like toxins and to induce characteristic attaching and effacing (A/E) lesions on intestinal epithelia (33). A/E lesion formation relies on the injection of bacterial effectors via a type III secretion system and is determined by the locus of enterocyte effacement (LEE) (14). The LEE-encoded adhesin intimin is required for the colonization of calves and adult cattle by E. coli O157:H7 (6, 8) and for the colonization of humans by enteropathogenic E. coli (EPEC) (11). Type III secreted proteins also mediate the intestinal colonization of calves by EHEC serotypes O157:H7 and O26:H Ϫ (F. Dziva, P. van Diemen, M. Stevens, and T. Wallis, unpublished data), and EspB is required for the carriage and virulence of EPEC in humans (42).The host factors contributing to the colonization of ruminants and humans by EHEC are poorly understood. Recent studies have suggested that the neuroendocrine environment in the gastrointestinal tract may influence the outcome of infection, since the expression of virulence factors by diarrheagenic E. coli is augmented in vitro by the hormone norepinephrine (NE), which is released by the enteric nervous system under stress (3). NE is taken up by E. coli (23) and stimulates the in vitro expression of the K99 pilus adhesin by enterotoxigenic E. coli (27) as well as growth, iron acquisition, motility, and the expression of Shiga-like toxins and LEE-encoded proteins by EHEC O157:H7 (16,29,30,39). NE also augments the adherence of E. coli O157:H7 to murine cecal explants in vitro (5) and the invasion of the porcine jejunal mucosa (18). NEcontaining neurons innervate all levels of the gastrointestinal tract and terminate in neural plexuses and the mucosa (24). The influence of NE released into the gut on the carriage and virulence of gram-negative bacterial pathogens in vivo has received little attention to date.We have examined the effect of NE on the adherence and enteropathogenicity of E. coli O157:H7 in a bovine ligated ileal loop model of infection. This model permits the simultaneous testing of different treatments in discrete segments of the midileum for their effect on bacterial adherence and the induction of intestinal inflammatory and secretory responses (40). All animal procedures were performed in accordance with the Animals (Scientific P...

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Section: Vol 72 2004contrasting

confidence: 56%

The Neuroendocrine Stress Hormone Norepinephrine Augments Escherichia coli O157:H7-Induced Enteritis and Adherence in a Bovine Ligated Ileal Loop Model of Infection

et al. 2004

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“…Two previous studies indicated that expression of multiple horizontally acquired genes, scattered throughout the E. coli chromosome, is controlled by Ler and H-NS, and several of those genes encode proteins predicted to be associated with adhesion and/or agglutination (1,23). Although the identity of the novel hemagglutinin(s) expressed by the TMS002 (hns lpfA) and TMS003 (hns ler lpfA) mutant strains is currently unknown, our data suggest that in the absence of LPF, the E. coli O157:H7 strain is capable of (8,13,26). The idea of expression of other adhesins is supported by our in vivo studies, where the absence of the lpf genes causes a different pattern of colonization in animal models of infection (14,41), or in our ex vivo studies, where the mutant strain displayed a different tissue tropism in human intestinal biopsies (10).…”

Section: Discussionmentioning

confidence: 84%

Contribution of the Ler- and H-NS-Regulated Long Polar Fimbriae of Escherichia coli O157:H7 during Binding to Tissue-Cultured Cells

et al. 2008

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The expression of the long polar fimbriae (LPF) of enterohemorrhagic Escherichia coli (EHEC) O157:H7 is controlled by a tightly regulated process, and, therefore, the role of these fimbriae during binding to epithelial cells has been difficult to establish. We recently found that histone-like nucleoid-structuring protein (H-NS) binds to the regulatory sequence of the E. coli O157:H7 lpf1 operon and "silences" its transcription, while Ler inhibits the action of the H-NS protein and allows lpf1 to be expressed. In the present study, we determined how the deregulated expression of LPF affects binding of EHEC O157:H7 to tissue-cultured cells, correlating the adherence phenotype with lpf1 expression. We tested the adherence properties of EHEC hns mutant and found that this strain adhered 2.8-fold better than the wild type. In contrast, the EHEC ler mutant adhered 2.1-fold less than the wild type. The EHEC hns ler mutant constitutively expressed the lpf genes, and, therefore, we observed that the double mutant adhered 5.6-fold times better than the wild type. Disruption of lpfA in the EHEC hns and hns ler mutants or the addition of anti-LpfA serum caused a reduction in adhesion, demonstrating that the increased adherence was due to the expression of LPF. Immunogold-labeling electron microscopy showed that LPF is present on the surface of EHEC lpfA ؉ strains. Furthermore, we showed that EHEC expressing LPF agglutinates red blood cells from different species and that the agglutination was blocked by the addition of anti-LpfA serum. Overall, our data confirmed that expression of LPF is a tightly regulated process and, for the first time, demonstrated that these fimbriae are associated with adherence and hemagglutination phenotypes in EHEC O157:H7.

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“…coli O157:H7 strains carry the fimA genes for the type 1 fimbrial subunit but do not appear to be able to express fimA (14). A 16-bp deletion in the fim switch locks the expression phase in the "off" orientation only in VTEC O157 (45).…”

Section: Discussionmentioning

confidence: 99%

Identification of Four Fimbria-Encoding Genomic Islands That Are Highly Specific for Verocytotoxin-Producing Escherichia coli Serotype O157 Strains

et al. 2005

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Verocytotoxin-producing Escherichia coli causes zoonotic food-or waterborne infection that may be associated with massive outbreaks and with the serious complication of hemolytic uremic syndrome (HUS). Serotypes O157:H7 and O157:NM are more commonly associated with HUS and outbreaks than other serotypes, such as O26:H11. To determine whether a genetic basis exists for why serotype O157:H7/NM causes HUS and outbreaks more often than other serotypes, such as O26:H11, we conducted suppression subtractive hybridization (SSH) between the genomes of the sequenced O157:H7 strain EDL933 and CL1, a clinical serotype O26:H11 isolate. Genes from four EDL933 fimbria-encoding genomic O islands (OIs) (OI-1, -47, -141, and -154) were identified in the SSH library. OI-47 encodes several additional putative virulence factors, including secreted and signaling proteins, a hemolysin locus, a lipoprotein, an ABC transport system, and a lipid biosynthesis locus. The distribution of the OIs was investigated by PCR and Southern hybridization (when PCR was negative) with 69 VTEC strains belonging to 39 different serotypes corresponding to 5 seropathotypes that differ in their disease and epidemic potential. The four OIs described here were distributed almost exclusively in serotypes O157:H7 and O157:NM, which indicates that they may be associated with the ability of these strains to colonize human and/or animal intestinal tracts and to cause epidemic and serious disease more frequently than other serotypes. The occurrence of the four OIs in enteropathogenic E. coli O55:H7 strains is consistent with their vertical inheritance by VTEC O157:H7/NM from this clonally related ancestor.Verocytotoxin-producing Escherichia coli (VTEC) (31), also referred to as Shiga toxin-producing E. coli (8), is a major cause of zoonotic food-or waterborne infection that may be associated with massive outbreaks and with the serious complication of hemolytic uremic syndrome (HUS) (15,27,29,30,39). More than 200 serotypes of VTEC have been isolated from humans (65), but their incidence and association with serious or epidemic disease are highly variable, suggesting differences in epidemicity and virulence between VTEC serotypes (28). To determine why some serotypes are more common and cause serious and epidemic disease more frequently than other serotypes, we have classified VTEC serotypes in the following five "seropathotypes" based on their relative incidence and their association with epidemic and/or serious disease, such as HUS (28). Serotypes O157:H7 and O157:NM, which are associated most commonly with outbreaks and HUS (3,15,16,22,26,39), are classified as seropathotype A. Seropathotype B comprises serotypes O26:H11, O103:H2, O111: NM, O121:H19, and O145:NM, which are associated with outbreaks and HUS but much less frequently than serotypes O157:H7 and O157: NM (6,16,22,34,65). Serotypes such as O91:H21 and O113:H21, which have an occasional association with sporadic HUS but not with outbreaks (6,22,39), are classified as seropathotype C. Seropathotype D c...

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Expression of type I pili is abolished in verotoxin-producing Escherichia coli O157

Cited by 13 publications

References 14 publications

The Neuroendocrine Stress Hormone Norepinephrine Augments Escherichia coli O157:H7-Induced Enteritis and Adherence in a Bovine Ligated Ileal Loop Model of Infection

The Neuroendocrine Stress Hormone Norepinephrine Augments Escherichia coli O157:H7-Induced Enteritis and Adherence in a Bovine Ligated Ileal Loop Model of Infection

Contribution of the Ler- and H-NS-Regulated Long Polar Fimbriae of Escherichia coli O157:H7 during Binding to Tissue-Cultured Cells

Identification of Four Fimbria-Encoding Genomic Islands That Are Highly Specific for Verocytotoxin-Producing Escherichia coli Serotype O157 Strains

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