scholarly journals Lactoferrin inhibits E. coli O157:H7 growth and attachment to intestinal epithelial cells

2010 ◽  
Vol 55 (No. 8) ◽  
pp. 359-368 ◽  
Author(s):  
M. Atef Yekta ◽  
F. Verdonck ◽  
W. Van Den Broeck ◽  
BM Goddeeris ◽  
E. Cox ◽  
...  
Keyword(s):  
Colorectal Adenocarcinoma ◽  
Bacterial Attachment ◽  
Enterohemorrhagic Escherichia Coli ◽  
Intestinal Epithelial ◽  
Antimicrobial Proteins ◽  
Haemolytic Uremic Syndrome ◽  
E Coli ◽  
Uremic Syndrome ◽  
High Concentrations ◽  
Extracellular Environment

Enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 strains are associated with haemorraghic colitis and haemolytic uremic syndrome (HUS) in humans. Cattle are a reservoir of E. coli O157:H7. We studied the ability of bovine and human lactoferrin, two natural antimicrobial proteins present in milk, to inhibit E. coli O157:H7 growth and attachment to a human epithelial colorectal adenocarcinoma cell line (Caco-2). The direct antibacterial effect of bLF on E. coli O157:H7 was stronger than that of hLF. Nevertheless, both lactoferrins had bacteriostatic effects even at high concentrations (10 mg/ml), suggesting blocking of LF activity by a yet undefined bacterial defence mechanism. Additionally, both lactoferrins significantly inhibited E. coli O157:H7 attachment to Caco-2 cells. However, hLF was more effective than bLF, probably due to more efficient binding of bLF to intelectin present on human enterocytes leading to uptake and thus removal of bLF from the extracellular environment. Inhibition of bacterial attachment to Caco-2 cells was at least partly due to the catalytic effect of lactoferrins on the type III secreted proteins EspA and EspB

scholarly journals EnterohemorrhagicEscherichia coliinfection stimulates Shiga toxin 1 macropinocytosis and transcytosis across intestinal epithelial cells

2011 ◽  
Vol 301 (5) ◽  
pp. C1140-C1149 ◽  
Author(s):  
Valeriy Lukyanenko ◽  
Irina Malyukova ◽  
Ann Hubbard ◽  
Michael Delannoy ◽  
Edgar Boedeker ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Shiga Toxin ◽  
Molecular Mechanisms ◽  
Intestinal Epithelial Cells ◽  
Enterohemorrhagic Escherichia Coli ◽  
Intestinal Epithelial ◽  
Systemic Complications ◽  
E Coli ◽  
Systemic Spread ◽  
Uremic Syndrome

Gastrointestinal infection with Shiga toxins producing enterohemorrhagic Escherichia coli causes the spectrum of gastrointestinal and systemic complications, including hemorrhagic colitis and hemolytic uremic syndrome, which is fatal in ∼10% of patients. However, the molecular mechanisms of Stx endocytosis by enterocytes and the toxins cross the intestinal epithelium are largely uncharacterized. We have studied Shiga toxin 1 entry into enterohemorrhagic E. coli-infected intestinal epithelial cells and found that bacteria stimulate Shiga toxin 1 macropinocytosis through actin remodeling. This enterohemorrhagic E. coli-caused macropinocytosis occurs through a nonmuscle myosin II and cell division control 42 (Cdc42)-dependent mechanism. Macropinocytosis of Shiga toxin 1 is followed by its transcytosis to the basolateral environment, a step that is necessary for its systemic spread. Inhibition of Shiga toxin 1 macropinocytosis significantly decreases toxin uptake by intestinal epithelial cells and in this way provides an attractive, antibiotic-independent strategy for prevention of the harmful consequences of enterohemorrhagic E. coli infection.

Escherichia coli O157:H7: Epidemiology, Pathogenesis, and Methods for Detection in Food

1992 ◽  
Vol 55 (7) ◽  
pp. 555-565 ◽  
Author(s):  
NISHA V. PADHYE ◽  
MICHAEL P. DOYLE
Keyword(s):  
Escherichia Coli ◽  
Care Center ◽  
Watery Diarrhea ◽  
Clinical Samples ◽  
Escherichia Coli O157 ◽  
Intestinal Epithelial ◽  
Day Care Center ◽  
E Coli ◽  
Life Threatening ◽  
Uremic Syndrome

Escherichia coli O157:H7 is now recognized as an important human pathogen. Illnesses caused by E. coli O157:H7 infection can range from self-limited, watery diarrhea to life-threatening manifestations such as hemolytic uremic syndrome or thrombotic thrombocytopenic purpura. The mode of transmission is primarily through food; however, person-to-person transmission also has been identified in some day-care center and nursing home out-breaks. Studies to date indicate that cattle are an important reservoir of the organism. Although adhesion to intestinal epithelial cells and verotoxins are considered important virulence factors in the pathogenesis of the organism, more research is are necessary to determine the exact mechanism of pathogenicity. There is need for a rapid diagnostic test for the detection of E. coli O157:H7 in food and in clinical samples. Several useful research reagents have been developed for detecting E. coli O157:H7; however, they must be applied to a procedure that is specific, sensitive, rapid, easy to use, and commercially available so that microbiological laboratories can readily use them.

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

2021 ◽  
Vol 17 (2) ◽  
pp. e1009290
Author(s):  
Alyson R. Warr ◽  
Carole J. Kuehl ◽  
Matthew K. Waldor
Keyword(s):  
Escherichia Coli ◽  
Epithelial Cells ◽  
Diarrheal Disease ◽  
Rabbit Model ◽  
Transcriptional Response ◽  
Enterohemorrhagic Escherichia Coli ◽  
Intestinal Epithelial ◽  
Transcriptional Responses ◽  
Gene Encoding ◽  
Uremic Syndrome

Enterohemorrhagic Escherichia coli (EHEC) is a food-borne pathogen that causes diarrheal disease and the potentially lethal hemolytic uremic syndrome. We used an infant rabbit model of EHEC infection that recapitulates many aspects of human intestinal disease to comprehensively assess colonic transcriptional responses to this pathogen. Cellular compartment-specific RNA-sequencing of intestinal tissue from animals infected with EHEC strains containing or lacking Shiga toxins (Stx) revealed that EHEC infection elicits a robust response that is dramatically shaped by Stx, particularly in epithelial cells. Many of the differences in the transcriptional responses elicited by these strains were in genes involved in immune signaling pathways, such as IL23A, and coagulation, including F3, the gene encoding Tissue Factor. RNA FISH confirmed that these elevated transcripts were found almost exclusively in epithelial cells. Collectively, these findings suggest that Stx potently remodels the host innate immune response to EHEC.

scholarly journals Enteroaggregative E. coli O104 from an outbreak of HUS in Germany 2011, could it happen again?

2011 ◽  
Vol 5 (06) ◽  
pp. 425-436 ◽  
Author(s):  
Marie Anne Chattaway ◽  
Tim Dallman ◽  
Iruka N Okeke ◽  
John Wain
Keyword(s):  
Disease Outbreaks ◽  
Surveillance Systems ◽  
Human Gut ◽  
Policy Makers ◽  
Haemolytic Uremic Syndrome ◽  
E Coli ◽  
Routine Surveillance ◽  
Genetic Features ◽  
Uremic Syndrome ◽  
Enterocyte Effacement

Enterohaemorrhagic E. coli (EHEC) particularly O157:H7 (Sequence type 11 complex), is the best documented and most well-known of E. coli that cause diarrhoea. The importance of EHEC lies in the severity of disease. Outbreaks can infect thousands of people causing bloody diarrhoea and haemolytic uremic syndrome (HUS) that in turn can result in protracted illness or even death. The ability of EHEC to colonise the human gut is normally associated with the presence of genes from another group of diarrhoeagenic E. coli, the enteropathogenic E. coli (EPEC), via the locus of enterocyte effacement. However, the massive outbreak in Germany was caused by an EHEC which had acquired virulence genes from yet another group of diarrhoeagenic E. coli, the enteroaggregative E. coli (EAEC). In reality EAEC is probably the most common bacterial cause of diarrhoea but is not identified in most diagnostic laboratories. This outbreak emphasises the importance of being able to detect all diarrhoeagenic E. coli and not to focus on E. coli O157:H7 alone. Routine surveillance systems for EAEC, a once ignored global pathogen, would go a long way to reaching this goal. This review describes methods for identifying non-O157 EHEC and describes the key genetic features of EHEC and EAEC. Our aim is to provide information for laboratories and policy makers which enables them to make informed decisions about the best methods available for detecting newly emergent strains of diarrhoeagenic E. coli.

scholarly journals Whole-Genome Sequencing Analysis of a stx-Negative Escherichia coli O63:H6 Isolate Associated with Hemolytic Uremic Syndrome

Diagnostics ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1823
Author(s):  
Tae Yeul Kim ◽  
Tae-Min La ◽  
Taesoo Kim ◽  
Sun Ae Yun ◽  
Sang-Won Lee ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Hemolytic Uremic Syndrome ◽  
Whole Genome Sequencing ◽  
Genome Sequencing ◽  
Virulence Gene ◽  
Enterohemorrhagic Escherichia Coli ◽  
Whole Genome ◽  
Sequencing Analysis ◽  
E Coli ◽  
Uremic Syndrome

Shiga toxin-encoding genes (stx) of enterohemorrhagic Escherichia coli (EHEC) can be lost during infection or in vitro cultivation, and in clinical practice, it is difficult to distinguish EHEC that have lost stx (EHEC-LST) from enteropathogenic E. coli (EPEC), as both are stx-negative and eae-positive. In this study, we performed whole-genome sequencing (WGS) of a stx-negative, eae-positive E. coli O63:H6 isolate from a child with hemolytic uremic syndrome and compared its genome with those of nine E. coli O63:H6 strains in public databases. Virulence gene profiles were analyzed and core-genome multilocus sequence typing (cgMLST) was conducted. The virulence gene profile of our isolate was consistent with EHEC, except for the absence of stx, and the isolate clustered with seven EHEC strains but was distant from two EPEC strains in cgMLST. In genome alignment, our isolate exhibited a high nucleotide identity with EHEC strain 377323_2f but displayed a gap corresponding to the stx-harboring prophage sequence. Overall, our isolate was genetically closely related to EHEC strains, consistent with this being an EHEC-LST strain. As EHEC-LST may be misdiagnosed as EPEC in routine laboratories, comparative genomic analysis using WGS can be useful to determine whether stx-negative and eae-positive isolates are EHEC-LST or EPEC.

scholarly journals Characterization of the role of yadK in the pathogenesis of enterohaemorrhagic E. coli O157:H7

2021 ◽  
Author(s):  
Yijing Yu
Keyword(s):  
Acid Stress ◽  
Haemolytic Uremic Syndrome ◽  
E Coli ◽  
Enterohaemorrhagic Escherichia Coli ◽  
Immunize Rabbit ◽  
Uremic Syndrome ◽  
Adhesion Level ◽  
Fimbrial Adhesin

Enterohaemorrhagic Escherichia coli (EHEC) O157:H7 can use serious diarrhea and haemolytic uremic syndrome. Various factors including adhesins contribute to pathogenesis of EHEC. Previous studies suggested that yadK gene, which encodes a putative fimbrial adhesin in EHEC, may be involved in response of EHEC to acid stress. To characterize role of yadK protein in the pathogenesis of EHEC, recombinant yadK protein was generated and used to immunize rabbit to obtain anti-yadK antiserum, which was able to specifically recognize over-expressed yadK protein in EHEC. Western blotting with anti-yadK revealed a higher level of yadK expression in EHEC under acid adapted-acid stress compared to EHEC under unstressed conditions, which confirmed earlier yadK mRNA studies and indicated that yadK is upregulated in EHEC under acid stress. Finally, we observed that anti-yadK antiserum was able to specifically reduce adhesion of acid stressed EHEC to human epithelial cells compared to adhesion level of unstressed EHEC.

scholarly journals DiarrhoeagenicEscherichia coliandEscherichia albertiiin Brazil: pathotypes and serotypes over a 6-year period of surveillance

2018 ◽  
Vol 147 ◽  
Author(s):  
E. L. Ori ◽  
E. H. Takagi ◽  
T. S. Andrade ◽  
B. T. Miguel ◽  
M. C. Cergole-Novella ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Active Surveillance ◽  
Shiga Toxin ◽  
Control Strategies ◽  
Clinical Samples ◽  
Haemolytic Uremic Syndrome ◽  
E Coli ◽  
Enteric Diseases ◽  
Uremic Syndrome ◽  
And Control

AbstractDiarrhoeagenicEscherichia coli(DEC) is a leading cause of infectious diarrhoea worldwide. In recent years,Escherichia albertiihas also been implicated as a cause of human enteric diseases. This study describes the occurrence ofE. colipathotypes and serotypes associated with enteric illness and haemolytic uremic syndrome (HUS) isolated in Brazil from 2011 to 2016. Pathotypes isolated included enteropathogenicE. coli(EPEC), enteroaggregativeE. coli(EAEC), enterotoxigenicE. coli(ETEC), enteroinvasiveE. coli(EIEC) and Shiga toxin-producingE. coli(STEC). PCR of stool enrichments for DEC pathotypes was employed, andE. albertiiwas also sought. O:H serotyping was performed on all DEC isolates. A total of 683 DEC and 10E. albertiistrains were isolated from 5047 clinical samples. The frequencies of DEC pathotypes were 52.6% (359/683) for EPEC, 32.5% for EAEC, 6.3% for ETEC, 4.4% for EIEC and 4.2% for STEC. DEC strains occurred in patients from 3 months to 96 years old, but EPEC, EAEC and STEC were most prevalent among children. Both typical and atypical isolates of EPEC and EAEC were recovered and presented great serotype heterogeneity. HUS cases were only associated with STEC serotype O157:H7. TwoE. albertiiisolates belonged to serogroup O113 and one had thestx2f gene. The higher prevalence of atypical EPEC in relation to EAEC in community-acquired diarrhoea in Brazil suggests a shift in the trend of DEC pathotypes circulation as previously EAEC predominated. This is the first report ofE. albertiiisolation from active surveillance. These results highlight the need of continuing DEC andE. albertiisurveillance, as a mean to detect changes in the pattern of pathotypes and serotypes circulation and provide useful information for intervention and control strategies.

scholarly journals Structure and Function of Plasmid pColD157 of Enterohemorrhagic Escherichia coli O157 and Its Distribution among Strains from Patients with Diarrhea and Hemolytic-Uremic Syndrome

1998 ◽  
Vol 36 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Clemens Hofinger ◽  
Helge Karch ◽  
Herbert Schmidt
Keyword(s):  
Escherichia Coli ◽  
Nucleotide Sequence ◽  
Hemolytic Uremic Syndrome ◽  
Enterohemorrhagic Escherichia Coli ◽  
E Coli ◽  
Uremic Syndrome ◽  
And Function ◽  
High Degree ◽  
Degree Of Similarity

In this study, pColD157, a 6.7-kb colicinogenic plasmid of enterohemorrhagic Escherichia coli (EHEC) O157:H7 strain CL40cu, was characterized by restriction mapping and determination of its complete nucleotide sequence. The sequence consists of 6,675 bp and shows a high degree of similarity to the nucleotide sequence of colicinogenic plasmids pColD-CA23 and pColK. Seven potential genes were located on pColD157, three of which were closely related (>97.9%) to the colicin D structural gene and the corresponding immunity and lysis genes of plasmid pColD-CA23, and these were therefore designatedcda, cdi, and cdl, respectively, using the reference extension -CL40 for differentiation. The adjacent 3′ region is related to the origin of replication of pColD-CA23. In contrast, the remaining part of the plasmid harbors a cluster of genes, closely related to the mobilization genes of pColK, which is followed by a 0.3-kb stretch homologous to the pColK resolution function. These determinants were designated mbdA, mbdB,mbdC, and mbdD and cdr, respectively. Southern blot analysis was performed with a probe specific for the cda gene of pColD157 and two groups of EHEC O157:H7 isolates from patients with diarrhea or hemolytic-uremic syndrome resident in Germany. Whereas 16 of 46 E. coli O157 strains isolated between 1987 and 1991 harbored plasmid pColD157, only 1 of 50 strains isolated during 1996 carried this plasmid. In addition, all strains harboring plasmid pColD157 were shown to have colicinogenic activity.

scholarly journals The Intimin-Like Protein FdeC Is Regulated by H-NS and Temperature in Enterohemorrhagic Escherichia coli

2014 ◽  
Vol 80 (23) ◽  
pp. 7337-7347 ◽  
Author(s):  
Donna M. Easton ◽  
Luke P. Allsopp ◽  
Minh-Duy Phan ◽  
Danilo Gomes Moriel ◽  
Guan Kai Goh ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Culture Conditions ◽  
Enterohemorrhagic Escherichia Coli ◽  
Infection Model ◽  
Content Type ◽  
E Coli ◽  
Uremic Syndrome ◽  
Animal Hosts ◽  
And Function

ABSTRACTEnterohemorrhagicEscherichia coli(EHEC) is a Shiga-toxigenic pathogen capable of inducing severe forms of enteritis (e.g., hemorrhagic colitis) and extraintestinal sequelae (e.g., hemolytic-uremic syndrome). The molecular basis of colonization of human and animal hosts by EHEC is not yet completely understood, and an improved understanding of EHEC mucosal adherence may lead to the development of interventions that could disrupt host colonization. FdeC, also referred to by its IHE3034 locus tag ECOK1_0290, is an intimin-like protein that was recently shown to contribute to kidney colonization in a mouse urinary tract infection model. The expression of FdeC is tightly regulatedin vitro, and FdeC shows promise as a vaccine candidate against extraintestinalE. colistrains. In this study, we characterized the prevalence, regulation, and function offdeCin EHEC. We showed that thefdeCgene is conserved in both O157 and non-O157 EHEC and encodes a protein that is expressed at the cell surface and promotes biofilm formation under continuous-flow conditions in a recombinantE. colistrain background. We also identified culture conditions under which FdeC is expressed and showed that minor alterations of these conditions, such as changes in temperature, can significantly alter the level of FdeC expression. Additionally, we demonstrated that the transcription of thefdeCgene is repressed by the global regulator H-NS. Taken together, our data suggest a role for FdeC in EHEC when it grows at temperatures above 37°C, a condition relevant to its specialized niche at the rectoanal junctions of cattle.

scholarly journals EnterohemorrhagicEscherichia colisuppresses inflammatory response to cytokines and its own toxin

2009 ◽  
Vol 297 (3) ◽  
pp. G576-G581 ◽  
Author(s):  
Amy Bellmeyer ◽  
Cynthia Cotton ◽  
Rajani Kanteti ◽  
Athanasia Koutsouris ◽  
V. K. Viswanathan ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Intestinal Epithelial Cells ◽  
Enterohemorrhagic Escherichia Coli ◽  
Receptor Expression ◽  
Intestinal Epithelial ◽  
Potent Inducer ◽  
Life Threatening ◽  
Uremic Syndrome

Infection with the enteric pathogen enterohemorrhagic Escherichia coli (EHEC) causes a variety of symptoms ranging from nonbloody diarrhea to more severe sequelae including hemorrhagic colitis, altered sensorium and seizures, and even life-threatening complications, such as hemolytic uremic syndrome and thrombotic thrombocytopenic purpura. The more severe consequences of EHEC infection are attributable to the production of Shiga toxin (Stx) and its subsequent effects on the vasculature, which expresses high levels of the Stx receptor, Gb3. Interestingly, the intestinal epithelium does not express Gb3. Despite the lack of Gb3 receptor expression, intestinal epithelial cells translocate Stx. The effect of Stx on intestinal epithelial cells is controversial with some studies demonstrating induction of inflammation and others not. This may be difficult to resolve because EHEC expresses both proinflammatory molecules, such as flagellin, and factor(s) that dampen the inflammatory response of epithelial cells. The goal of our study was to define the effect of Stx on the inflammatory response of intestinal epithelial cells and to determine whether infection by EHEC modulates this response. Here we show that Stx is a potent inducer of the inflammatory response in intestinal epithelial cells and confirm that EHEC attenuates the induction of IL-8 by host-derived proinflammatory cytokines. More importantly, however, we show that infection with EHEC attenuates the inflammatory response by intestinal epithelial cells to its own toxin. We speculate that the ability of EHEC to dampen epithelial cell inflammatory responses to Stx and cytokines facilitates intestinal colonization.

Sign in / Sign up

Export Citation Format

Share Document