Ontology highlight
ABSTRACT:
PROVIDER: PRJNA735700 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| JAHMAA01.dat.gz | Other | |||
| JAHMAA01.fasta.gz | Fasta.gz | |||
| JAHMAA01.master.dat | Other | |||
| SRR14750046_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 22 |
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Project description:Changes in endothelial phenotype induced by E. coli-derived Shiga toxins (Stx) are believed to play a critical role in the pathogenesis of hemolytic uremic syndrome. Stx inactivate host ribosomes, but also alter gene expression at concentrations that minimally affect global protein synthesis. The effect of Stx on the gene expression profile of human microvascular endothelial cells was examined using the Affymetrix HG-U133A platform. Data were processed using 13 different methods and revealed 369 unique differentially expressed genes, 318 of which were up-regulated and 51 of which were down-regulated. These studies implicated activation of the CXCR4/CXCR7/SDF-1 chemokine pathway in Stx-mediated pathogenesis. Primary human dermal microvascular endothelial cells were treated with vehicle or Shiga toxin (10 fM, 24 h, n = 6) and changes in steady-state mRNA levels were determined by hybridization to Affymetrix HG-U133A arrays
2011-10-10 | E-GEOD-32710 | biostudies-arrayexpress
Project description:Shiga toxin type 2 (Stx2) is the main virulence factor produced by Stx-producing Escherichia coli (STEC) responsible for hemorrhagic colitis and the life-threatening sequela hemolytic uremic syndrome.
2022-11-21 | PXD038256 |
Project description:The Escherichia coli strain Nissle 1917 (EcN) is used as a probiotic for the treatment of certain gastrointestinal diseases in several European and non-European countries. In vitro studies showed EcN to efficiently inhibit the production of Shiga toxin (Stx) by Stx producing E. coli (STEC) such as Enterohemorrhagic E. coli (EHEC). The occurrence of the latest EHEC serotype (O104:H4) responsible for the great outbreak in 2011 in Germany was due to the infection of an enteroaggregative E. coli by a Stx 2-encoding lambdoid phage turning this E. coli into a lysogenic and subsequently into a Stx producing strain. Since EHEC infected persons are not recommended to be treated with antibiotics, EcN might be an alternative medication. However, because a harmless E. coli strain might be converted into a Stx-producer after becoming host to a stx encoding prophage, we tested EcN for stx-phage genome integration. Our experiments revealed the resistance of EcN towards not only stx-phages but also against the lambda phage. This resistance was not based on the lack of or by mutated phage receptors. Rather the expression of certain genes (superinfection exclusion B (sieB) and a phage repressor (pr) gene) of a defective prophage of EcN was involved in the complete resistance of EcN to infection by the stx- and lambda phage. Obviously, EcN cannot be turned into a Stx producer. Furthermore, we observed EcN to inactivate phages and thereby to protect E. coli K-12 strains against infection by stx- as well as lambda-phages. Inactivation of lambda-phages was due to binding of lambda-phages to LamB of EcN whereas inactivation of stx-phages was caused by a thermostable protein of EcN. These properties together with its ability to inhibit Stx production make EcN a good candidate for the prevention of illness caused by EHEC and probably for the treatment of already infected people.
2018-06-14 | GSE109932 | GEO
Project description:Changes in endothelial phenotype induced by E. coli-derived Shiga toxins (Stx) are believed to play a critical role in the pathogenesis of hemolytic uremic syndrome. Stx inactivate host ribosomes, but also alter gene expression at concentrations that minimally affect global protein synthesis. The effect of Stx on the gene expression profile of human microvascular endothelial cells was examined using the Affymetrix HG-U133A platform. Data were processed using 13 different methods and revealed 369 unique differentially expressed genes, 318 of which were up-regulated and 51 of which were down-regulated. These studies implicated activation of the CXCR4/CXCR7/SDF-1 chemokine pathway in Stx-mediated pathogenesis.
2011-10-11 | GSE32710 | GEO
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
Project description:Genome sequence collection of Shiga toxin (Stx)-encoding phage in Stx-producing Escherichia coli
| PRJDB14896 | ENA
Project description:Transcriptomes of 24 clinical strains of E. coli O157:H7 that differ phylogenetically and by Shiga toxin profiles were compared after 30 min co-incubation with epithelial cells.
2010-07-22 | GSE20397 | GEO
Project description:The human intestinal microbiota associated with rats produces in vivo a soluble(s) factor(s) that down-regulates the expression of genes encoding for the Shiga toxin II in E. coli O157:H7. The Shiga toxin II is one of the major virulence factors of E. coli enterohemorragic leading to the deadly hemolitic and uremic syndrome. Investigation of the effect of the human intestinal microbiota on the whole transcriptome of EHEC O157:H7 is of major importance to increase our understanding of the pathogen transcriptomic adaptation in response to the human microbiota. We analysed by microarray hybridization the gene expression pattern of EHEC O157:H7 grown in the caecal content of germ-free rats or rats associated with the human microbiota of a healthy human subject. By doing so, we increased our understanding of the regulatory activities of the human gut microbiota on E. coli O157:H7
2013-09-10 | GSE37095 | GEO
Project description:Intestinal tissue responses to protein synthesis inhibition by Shiga toxin are complex. Organoid models allow for an unprecedented examination of human tissue responses to a deadly Shiga toxin.
2020-02-01 | GSE144633 | GEO