Escherichia coli O157
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB10137 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| BLZJ01.dat.gz | Other | |||
| BLZJ01.fasta.gz | Fasta.gz | |||
| BLZJ01.master.dat | Other | |||
| BLZK01.dat.gz | Other |
Items per page: 5 1 - 5 of 17 |
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Project description:Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a notorious foodborne pathogen capable of causing severe gastrointestinal infections in humans. The bovine rectoanal junction (RAJ) has been identified as a primary reservoir of STEC O157:H7, playing a critical role in its transmission to humans through contaminated food sources. Despite the relevance of this host-pathogen interaction, the molecular mechanisms behind the adaptation of STEC O157:H7 in the bovine RAJ and its subsequent infection of human colonic epithelial cells remain largely unexplored. This study aimed to unravel the intricate dynamics of STEC O157:H7 in two distinct host environments: bovine RAJ squamous epithelial (RSE) cells and human colonic epithelial cells. Comparative transcriptomics analysis was employed to investigate the differential gene expression profiles of STEC O157:H7 during its interaction with these cell types. The bacterial cells were cultured under controlled conditions to simulate the microenvironments of both bovine RAJ and human colonic epithelial cells. Using high-throughput RNA sequencing, we identified key bacterial genes and regulatory pathways that are significantly modulated in response to each specific host environment. Our findings reveal distinct expression patterns of virulence factors, adhesion proteins, and stress response genes in STEC O157:H7 grown in bovine RAJ cells as opposed to human colonic epithelial cells. Additionally, the comparative analysis highlights the potential role of certain genes in host adaptation and tissue-specific pathogenicity. Furthermore, this study sheds light on the potential factors contributing to the survival and persistence of STEC O157:H7 in the bovine reservoir and its ability to colonize and cause disease in humans.
2023-11-09 | GSE240423 | GEO
Project description:National Surveillance of STEC O157:H7 in England
| PRJNA248042 | ENA
Project description:Transcriptional profiling of E.coli O157:H7 cells comparing control untreated cells with PEG8000treated cells
2011-04-02 | GSE28312 | GEO
Project description:The effect of pooled immunoglobulins (IgG) on E. coli O157:H7 colonization and the course of disease in an EHEC mouse model was investigated showing an improved survival and decreased intestinal and renal pathology. Treatment was given after inoculation thereby corresponding to the clinical setting. In vitro studies identified E. coli serine protease EspP as the E. coli O157:H7 protein that IgG bound to, via the Fc fragment, in both murine and human IgG preparations, and blocked its enzymatic activity. EspP is a virulence factor previously shown to promote colonic cell injury and the uptake of Shiga toxin by intestinal cells. The results suggest that IgG in commercial preparations binds to EspP protecting the host from E. coli O157:H7 infection and could potentially be beneficial in patients.
2022-02-08 | PXD029563 | Pride
Project description:Cinnamaldehyde is a natural antimicrobial and has been found to be effective against many foodborne pathogens including Escherichia coli O157:H7. Although its antimicrobial effects have been well investigated, limited information is available on its effects at the molecular level. Sublethal treatment at 200 mg/l cinnamaldehyde inhibited growth of E. coli O157:H7 at 37oC and for ≤ 2 h caused cell elongation, but from 2 to 4 h growth resumed and cells reverted to normal length. To understand this transient behaviour, genome-wide transcriptional analysis of E. coli O157:H7 was performed at 2 and 4 h exposure to cinnamaldehyde. Drastically different gene expression profiles were obtained at 2 and 4 h. At 2 h exposure, cinnamaldehyde induced overexpression of many oxidative stress-related genes, reduced DNA replication, and synthesis of protein, O-antigen and fimbriae. At 4 h, many cinnamaldehyde-induced repressive effects on E. coli O157:H7 gene expressions were reversed and oxidatve stress genes were nolonger differentially expressed.
2012-09-08 | GSE40693 | GEO
Project description:We have used RNA sequencing to compare transcriptomes of 30 stx2a and eae positive STEC strains of non-O157 serogroups isolated from children < 5 years of age. The strains were from children with HUS (HUS group, n=15), and children with asymptomatic or mild disease (non-HUS group, n=15), either induced with mitomycin C or non-induced, to reveal potential differences in gene expression levels between groups. When the HUS and non-HUS group were compared for differential expression of protein-encoding gene families, 399 of 6119 gene families were differentially expressed (log2 fold change ≥ 1, FDR < 0.05) in the non-induced condition, whereas only one gene family was differentially expressed in the induced condition. Gene ontology and cluster analysis showed that several fimbrial operons, as well as a putative type VI secretion system (T6SS) were more highly expressed in the HUS group than in the non-HUS group, indicating a role of these in the virulence of STEC strains causing severe disease.
2018-07-16 | GSE112430 | GEO
Project description:Deletion of yhaO was found to signifcantly decrease type three secretion in EHEC O157:H7. Transcriptional profiles of Escherichia coli O157: H7 and the isogenic yhaO mutant were generated and compared.
2017-07-24 | GSE15261 | GEO
Project description:Deletion of yedL was found to signifcantly decrease type three secretion in EHEC O157:H7. Transcriptional profiles of Escherichia coli O157: H7 and the isogenic yedL mutant were generated and compared.
2017-07-24 | GSE15265 | GEO
Project description:There is increasing evidence to support a role for sigma factor 54 (RpoN) in the regulation of stress resistance factors and protein secretion systems important to bacterial transmission and pathogenesis. In enterohemorrhagic E. coli O157:H7, acid resistance and type III secretion are essential determinants of gastric passage and colonization. This study thus described the transcriptome of an rpoN null strain of E. coli O157:H7 (EcJR-8) to determine the influence of RpoN on virulence and stress resistance gene regulation, and further explored its contribution to glutamate-dependent acid resistance (GDAR). Inactivation of rpoN resulted in the growth phase-dependent, differential expression of 104 genes. This included type III secretion structural and regulatory genes encoded on the locus of enterocyte effacement (LEE), as well as GDAR genes gadA, gadBC and gadE. Upregulation of gad transcript levels in EcJR-8 during logarithmic growth correlated with increased GDAR and survival in a model stomach. Acid susceptibility was reconstituted in EcJR-8 complemented in trans with wild-type rpoN. Acid resistance in EcJR-8 was dependent on exogenous glutamate, gadE and rpoS, but was independent of hns. Results also suggest that GDAR may be controlled by RpoN at multiple regulatory levels. This study supports the hypothesis that RpoN is an important regulator of virulence and stress resistance factors in E. coli O157:H7, and is the first to examine the mechanism by which it represses GDAR.
2009-08-08 | GSE17467 | GEO