Ontology highlight
ABSTRACT:
PROVIDER: PRJNA477322 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Staphylococcus aureus isolate:Robert Koch Institute, Berlin Genome sequencing
| PRJNA737330 | ENA
Project description:Whole genome trancription study of Citrobacter rodentium grown in rich media. Publication Title: Citrobacter rodentium is an Unstable Pathogen Showing Evidence of Significant Genomic Flux Publication Author List: Nicola K. Petty, Theresa Feltwell, Derek Pickard, Simon Clare, Ana L. Toribio, Maria Fookes, Kevin Roberts, Rita Monson, Satheesh Nair, Robert A. Kingsley, Richard Bulgin, Siouxsie Wiles, David Goulding, Craig Corton, Nicola Lennard, David Harris, David Willey, Richard Rance, Lu Yu, Jyoti S. Choudhary, Carol Churcher, Michael A. Quail, Julian Parkhill, Gad Frankel, Gordon Dougan, George P.C. Salmond, Nicholas R. Thomson ArrayExpress Release Date: 2011-02-12 Person Roles: investigator Person Last Name: Thomson Person First Name: Nicholas Person Mid Initials: Person Email: nrt@sanger.ac.uk Person Phone: Person Address: Wellcome Trust Genome Campus, Hinxton, Cambridge, UK Person Affiliation: Wellcome Trust Sanger Institute Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30610 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) are transmitted from cattle to human by means of contaminated food products resulting from fecal contamination. Transcriptome analysis was performed to gain further insight into the metabolic pathways required for persistence and growth of EHEC in the bovine intestine. Understanding the physiology of EHEC in the gut of ruminants is critical to identifying the potential nutritional basis to limiting EHEC shedding. A global transcriptome analysis was performed to gain further insight into the metabolic pathways required for persistence and growth of EHEC in the bovine intestine. DNA microarrays were performed using RNA from EHEC O157:H7 EDL933 incubated in bovine small intestine content (BSIC) compared with cells incubated in M9-minimal media.
2013-08-01 | GSE49468 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) is a gram negative enteric bacterial pathogen that can cause hemorrhagic colitis and heamolytic uremic syndrome (HUS) in humans and is the cause of bloody diarrhoea and acute renal failure in children. We have studied the transcriptional response of a colon cell line (CaCo2) to infection by EHEC and compared its profile to infection by EHEC shocked in acid at pH 2.5. We carried out microarray analysis on CaCo2 infected with EHEC O157H:7 EDL933 and EHEC shocked at pH 2.5 at 4 hours post infection.
2016-09-01 | GSE13404 | GEO
Project description:Regulation of EHEC gene expression by the gut commensal bacterium B. thetaiotaomicron. EHEC is a human pathogen that colonizes in the colon where B. thetaiotaomicron is a predominant commensal. We used microarrays to evaluate global regulation of EHEC when cultured with B. thetaiotaomicron.
2013-05-29 | GSE47418 | GEO
Project description:Enterohemorrhagic Escherichia coli (EHEC) induces the attachment and effacement of intestinal microvilli. While the molecular mechanisms contributed to the attachment of EHEC have been thoroughly studied, the underlying mechanisms for the effacement of intestinal microvilli induced by EHEC remained elusive. By focus RNAi screening and genetic analysis in C. elegans and further reconfirmed in human Caco-2 intestinal epithelial cells, we demonstrate that the CDK1-formin signal axis is required for this EHEC-induced microvillar effacement in vitro and in vivo.
2020-11-11 | GSE142507 | GEO
Project description:Contamination with enterohemorrhagic Escherichia coli O157:H7 (EHEC) is a worldwide problem but there is no effective therapy available for EHEC infection. Biofilm formation is closely related with EHEC infection and is one of the mechanisms of antimicrobial resistance. Antibiofilm screening of 560 plant secondary metabolites against EHEC shows that ginkgolic acids C15:1 and C17:1 at 5 μg/ml and Ginko biloba extract at 100 μg/ml significantly inhibited EHEC biofilm formation on the surface of polystyrene, nylon membrane, and glass. Importantly, the working concentration of ginkgolic acids and G. biloba extract did not affect bacterial growth and has been known to be non-toxic to human. Transcriptional analyses showed that ginkgolic acid C15:1 repressed curli genes and prophage genes in EHEC, which were corroborated by reduced fimbriae production and biofilm reduction in EHEC. Interestingly, ginkgolic acids and G. biloba extract did not inhibit the biofilm formation of commensal E. coli K-12 strain. The current study suggests that plant secondary metabolites are important resource of biofilm inhibitors, as well as other bioactive compounds.
2015-07-29 | GSE49367 | GEO
Project description:Previous experiments have shown that E. feacalis increases EHEC virulence by secreting adenine, this RNAseq aims to understand the molecular mechanism underlaying adenine role on EHEC
2024-05-01 | GSE244178 | GEO
Project description:While significant advances have been made in EHEC pathogenesis, we still do not fully understand the impact of environmental stress on EHEC virulence. During the course of infection, EHEC must evade or overcome several biological barriers, the first of which is the gastric acidity encountered during passage through the stomach. EHEC is remarkable in its ability to tolerate this acidity. There are four different acid resistance systems that provide E. coli O157:H7 protection against exposure to low pH (2-2.5). Interestingly, EHEC uses these acid resistance systems differentially for survival in foods versus the bovine intestinal tract. The glutamate-dependent acid-resistance system is thought to offer the best protection below pH 3. Since the infectious dose of EHEC is so low (50-100 organisms), acid resistance becomes an important virulence trait. Studies of EHEC response to acid stress have focused primarily on levels of acid tolerance and the molecular basis of tolerance. However, the impact of acid stress on EHEC virulence is less well understood. In the related pathogen, EPEC, the plasmid-encoded regulator, Per, that regulates expression of many EPEC virulence factors, is regulated negatively at pH 5.5 and positively at pH 8.0, suggesting that virulence gene expression is repressed during mild acid stress and enhanced in alkaline pH typical of the small intestine. Expression of EPEC type III secreted factors involved in A/E lesion formation has been shown to be influenced by factors including culture media, iron and calcium levels. Protein secretion was inhibited at pH 6 and 8. In a third study, a gadE (encoding acid resistance regulator) mutation resulted in increased adhesion of E.coli O157:H7 to colonic epithelial cells, suggesting negative regulation of one or more adhesins. Other studies have reported that shiga toxin production is sensitive to culture conditions including pH. However, there are no studies of EHEC virulence changes after more severe acid stress nor studies linking stressed EHEC virulence phenotype with transcriptional changes. The goal of this study was to determine how acid stress affects EHEC virulence properties and through microarray analysis, define the genetic basis for these changes. Understanding how acid stress modulates the virulence potential of this pathogen is essential for delineating the pathogenesis of disease caused by EHEC infection and may offer novel approaches to prevent and treat EHEC infections.
2009-06-26 | GSE14069 | GEO