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Contribution of FliC to epithelial cell invasion by enterohemorrhagic Escherichia coli O113:H21.

ABSTRACT: 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.

SUBMITTER: Luck SN

PROVIDER: S-EPMC1698073 | biostudies-literature | 2006 Dec

REPOSITORIES: biostudies-literature

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Contribution of FliC to epithelial cell invasion by enterohemorrhagic Escherichia coli O113:H21.

Luck Shelley N SN Badea Luminita L Bennett-Wood Vicki V Robins-Browne Roy R Hartland Elizabeth L EL

Infection and immunity 20060918 12

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 b ...[more]

PMID: 16982828

Similar Datasets

Escherichia coli O113:H21

Project description:Transcriptomes of Escherichia coli O113:H21

| PRJNA682189 | ENA

Invasion of epithelial cells by locus of enterocyte effacement-negative enterohemorrhagic Escherichia coli.

Project description:The majority of enterohemorrhagic Escherichia coli (EHEC) strains associated with severe disease carry the locus of enterocyte effacement (LEE) pathogenicity island, which encodes the ability to induce attaching and effacing lesions on the host intestinal mucosa. While LEE is essential for colonization of the host in these pathogens, strains of EHEC that do not carry LEE are regularly isolated from patients with severe disease, although little is known about the way these organisms interact with the host epithelium. In this study, we compared the adherence properties of clinical isolates of LEE-negative EHEC with those of LEE-positive EHEC O157:H7. Transmission electron microscopy revealed that LEE-negative EHEC O113:H21 was internalized by Chinese hamster ovary (CHO-K1) epithelial cells and that intracellular bacteria were located within a membrane-bound vacuole. In contrast, EHEC O157:H7 remained extracellular and intimately attached to the epithelial cell surface. Quantitative gentamicin protection assays confirmed that EHEC O113:H21 was invasive and also showed that several other serogroups of LEE-negative EHEC were internalized by CHO-K1 cells. Invasion by EHEC O113:H21 was significantly reduced in the presence of the cytoskeletal inhibitors cytochalasin D and colchicine and the pan-Rho GTPase inhibitor compactin, whereas the tyrosine kinase inhibitor genistein had no significant impact on bacterial invasion. In addition, we found that EHEC O113:H21 was invasive for the human colonic cell lines HCT-8 and Caco-2. Overall these studies suggest that isolates of LEE-negative EHEC may employ a mechanism of host cell invasion to colonize the intestinal mucosa.

| S-EPMC1087320 | biostudies-literature

Genetic diversity and virulence potential of shiga toxin-producing Escherichia coli O113:H21 strains isolated from clinical, environmental, and food sources.

Project description:Shiga toxin-producing Escherichia coli strains of serotype O113:H21 have caused severe human diseases, but they are unusual in that they do not produce adherence factors coded by the locus of enterocyte effacement. Here, a PCR microarray was used to characterize 65 O113:H21 strains isolated from the environment, food, and clinical infections from various countries. In comparison to the pathogenic strains that were implicated in hemolytic-uremic syndrome in Australia, there were no clear differences between the pathogens and the environmental strains with respect to the 41 genetic markers tested. Furthermore, all of the strains carried only Shiga toxin subtypes associated with human infections, suggesting that the environmental strains have the potential to cause disease. Most of the O113:H21 strains were closely related and belonged in the same clonal group (ST-223), but CRISPR analysis showed a great degree of genetic diversity among the O113:H21 strains.

| S-EPMC4148811 | biostudies-literature

Human intestinal epithelial cell-derived molecule(s) increase enterohemorrhagic Escherichia coli virulence.

Project description:To better understand the role of host cell-derived molecules on enterohemorrhagic Escherichia coli (EHEC) infection, we studied EHEC virulence gene expression when exposed to cell-free spent (conditioned) medium (CM) from HCT-8 intestinal epithelial cells. Exposure to HCT-8 CM for 1 h and 3 h increased the expression of 32 of 41 EHEC locus of enterocyte effacement (LEE) virulence genes compared with fresh medium (FM). Expression of the Shiga toxin 1 (stx1B) gene was up-regulated at 1 h of exposure. Seventeen genes encoded by prophage 933W, including those for Stx2, were also up-regulated at both time-points. The increase in 933W prophage expression was mirrored by a 2.7-fold increase in phage titers. Consistent with the increase in virulence gene expression, we observed a fivefold increase in EHEC attachment to epithelial cells when exposed to CM. The increase in EHEC attachment was abolished when CM was heated to 95 °C or treated with proteinase K to degrade the proteins. The host cell-derived molecule(s) were larger than 3 kDa, which suggests that the molecule(s) that increase EHEC virulence and attachment are protein-based.

| S-EPMC3561499 | biostudies-literature

Sab, a novel autotransporter of locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21, contributes to adherence and biofilm formation.

Project description:Shiga-toxigenic Escherichia coli (STEC) strains cause serious gastrointestinal disease, which can lead to potentially life-threatening systemic complications such as hemolytic-uremic syndrome. Although the production of Shiga toxin has been considered to be the main virulence trait of STEC for many years, the capacity to colonize the host intestinal epithelium is a crucial step in pathogenesis. In this study, we have characterized a novel megaplasmid-encoded outer membrane protein in locus of enterocyte effacement (LEE)-negative O113:H21 STEC strain 98NK2, termed Sab (for STEC autotransporter [AT] contributing to biofilm formation). The 4,296-bp sab gene encodes a 1,431-amino-acid protein with the features of members of the AT protein family. When expressed in E. coli JM109, Sab contributed to the diffuse adherence to human epithelial (HEp-2) cells and promoted biofilm formation on polystyrene surfaces. A 98NK2 sab deletion mutant was also defective in biofilm formation relative to its otherwise isogenic wild-type parent, and this was complemented by transformation with a sab-carrying plasmid. Interestingly, an unrelated O113:H21 STEC isolate that had a naturally occurring deletion in sab was similarly defective in biofilm formation. PCR analysis indicated that sab is present in LEE-negative STEC strains belonging to serotypes/groups O113:H21, O23, and O82:H8. These findings raise the possibility that Sab may contribute to colonization in a subset of LEE-negative STEC strains.

| S-EPMC2715694 | biostudies-literature

Escherichia coli O113:H21 str. CL-3

Project description:Escherichia coli O113:H21 str. CL-3 Genome Sequencing

| PRJNA72243 | ENA

Evidence for a hybrid genomic island in verocytotoxin-producing Escherichia coli CL3 (serotype O113:H21) containing segments of EDL933 (serotype O157:H7) O islands 122 and 48.

Project description:Genomic O island 122 (OI-122) of the verocytotoxin-producing Escherichia coli (VTEC) strain EDL933 contains four putative virulence genes, Z4321, Z4326, Z4332, and Z4333. However, strain CL3 (serotype O113:H21) contains only Z4321, not the other three genes. To determine whether Z4321 is part of a different genomic island in CL3, a region of 27,293 bp up- and downstream of Z4321 was sequenced and found to contain elements of two different EDL933 genomic islands (OI-48 and OI-122) and a Yersinia pestis-like hemolysin/adhesin gene cluster. The region contained OI-48 genes Z1635, Z1636, and Z1637 at the left terminus and Z1641, Z1642, Z1643, and Z1644 at the right. The middle portion consisted of OI-48 gene Z1640, which was separated into three fragments by genomic segments including the Y. pestis cluster and EDL933 OI-122 genes Z4322, Z4321, and Z4318. In a PCR investigation of 36 VTEC strains of different serotypes, intact Z1640 was present in strains of serotypes O157:H7, O26:H11, O103:H2, O111:NM, and O145:NM, which are associated with hemolytic uremic syndrome and outbreaks. In contrast, fragmented Z1640 was seen in strains of nonepidemic serotypes, such as O91:H21 and O113:H21, and in animal serotypes that have not been associated with human disease, indicating that Z1640 might be a virulence gene.

| S-EPMC355994 | biostudies-literature

Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli.

| S-EPMC7880444 | biostudies-literature

Molecular characterization of a Shiga toxigenic Escherichia coli O113:H21 strain lacking eae responsible for a cluster of cases of hemolytic-uremic syndrome.

Project description:Shiga toxigenic Escherichia coli (STEC) strains are a diverse group of organisms capable of causing severe gastrointestinal disease in humans. Within the STEC family, certain strains appear to have greater virulence for humans. STEC strains carrying eae and belonging to serogroup O157 or O111 have been responsible for the vast majority of outbreaks of STEC disease reported to date. Here we describe a STEC O113:H21 strain lacking eae that was responsible for a cluster of three cases of hemolytic-uremic syndrome. This strain produces a single Stx2-related toxin and adheres efficiently to Henle 407 cells.

| S-EPMC85566 | biostudies-other

Shiga toxin remodels the intestinal epithelial transcriptional response to Enterohemorrhagic Escherichia coli

Project description:Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. Here, we used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess the host colonic epithelial and lamina propria cell transcriptional responses to EHEC infection. Furthermore, comparisons of colonic pathology and intestinal transcriptomic profiles in animals infected with EHEC strains containing or lacking Shiga toxins (∆∆stx) were carried out to investigate how these potent toxins shape the host response to the pathogen. We found that Stx is required for severe, multi-focal hemorrhage and extensive apoptosis in the colon. RNA-sequencing revealed that EHEC infection elicits a robust innate immune response in the colonic epithelium that is dramatically shaped by Stx. Over 1400 genes were differentially expressed in animals infected with WT versus ∆∆stx EHEC strains. Several pathways linked to innate immune responses were dependent on Stx. Upregulated genes in the presence of toxin included cytokines IL23a and CXCL8, as well as F3, the gene encoding the coagulation initiator Tissue Factor. RNA FISH revealed that these elevated transcripts were found almost exclusively in epithelial cells, suggesting that Stx remodels the transcriptional profile of the epithelium. Collectively, these findings reveal that Stx potently modulates the innate immune response to EHEC in the intestine, and suggest that Stx drives the response to infection towards type 3 immunity.

2021-01-14 | GSE156056 | GEO

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