Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA650301 | ENA |
REPOSITORIES: ENA
Similar Datasets
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:Purpose: In this work, we evaluated the role of two indicative species, Citrobacter werkmanii (CW) and Escherichia albertii (EA), in the virulence of two DEC pathotypes, Shiga toxin-producing (STEC) and enteroaggregative (EAEC) Escherichia coli. Methods: To determine the effect of supernatant obtained from CW and EA cultures in STEC strain 86-24 and EAEC strain 042 gene expression, a RNA-seq analysis was performed. T84 cells were infected with DEC strains in the presence or absence of supernatant from EA and IL-8 secretion was evaluated. The effect of supernatant from EA on the growth and adherence of STEC and EAEC to T84 cells was also evaluated. Finally, we studied the participation of long polar fimbriae (Lpf) in STEC and plasmid-encoded toxin (Pet) in EAEC during DEC infection in the presence of supernatant from EA. Results: RNA-seq analysis revealed that several virulence factors in STEC and EAEC were up-regulated in the presence of supernatants from CW and EA. Interestingly, an increase in the secretion of IL-8 was observed in T84 cells infected with STEC or EAEC in the presence of a supernatant from EA. Similar results were observed with the supernatants obtained from clinical strains of E. albertii. Supernatant from EA had no effect on the growth of STEC and EAEC, or on the ability of these DEC strains to adhere to intestinal epithelial cells. Finally, we found that Pet toxin in EAEC was up-regulated in the presence of a supernatant from EA. In STEC, using mutant strains for Lpf fimbriae, our data suggested that these fimbriae might be participating in the increase of IL-8 induced by STEC on intestinal epithelial cells in the presence of a supernatant from EA. Conclusion:Supernatant obtained from an indicative species of DEC-positive diarrhea could modulate gene expression in STEC and EAEC, and IL-8 secretion induced by these bacteria. These data provide new insights into the effect of gut microbiota species in the pathogenicity of STEC and EAEC.
2022-07-22 | GSE197797 | GEO
Project description:Shiga toxin-producing Escherichia coli phylogenetics
| PRJNA624229 | ENA
Project description:Shiga toxin-producing Escherichia coli genome sequencing
| PRJNA383591 | ENA
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:Shiga toxin-producing Escherichia coli (STEC) is a major foodborne pathogen associated with raw produce such as sprouts, where it encounters fluctuating nutrient, temperature, and oxidative stress. This study elucidated the global transcriptional adaptations of E. coli O157:H7 EDL933 during colonization and persistence on alfalfa sprouts under simulated commercial sprouting and refrigerated storage. RNA sequencing was used to compare STEC grown in tryptic soy broth (D0), colonizing fresh sprouts for 5 days (D5), and held during sprout refrigeration for additional 3 days (D8). Among 5,002 expressed genes, 782 and 826 were differentially expressed (DEGs; |log2FC| ≥ 2, adjusted p < 0.05) at D5 vs. D0, and D8 vs. D0, respectively, whereas 11 genes only differed in the D8 vs. D5 comparison, indicating that the STEC transcriptome was largely stabilized by the time sprouts reach maturity, with refrigeration inducing minimal further shifts. Transition of STEC from nutrient rich broth to sprout tissues induced a profound metabolic reprograming, characterized by the up-regulation of de novo amino acid biosynthesis (e.g., hisA–H, leuABCD, and ilv operons), to compensate for nitrogen limitation within sprout tissues. STEC further adapted to sprout environment by inducing high-affinity uptake systems for potassium (kdpA/B/C/F), phosphorus (pstSCAB), and sulfur (tauABCD), alongside enterobactin-mediated iron acquisition. To survive sprout microenvironment, STEC elevated the transcription of acid resistance (gadA/C, cadA/B), oxidative stress defense (sodA, katE/G), and envelope protection (degP, pspA–D, baeS) genes. Although initial colonization at D5 involved the induction of flagellar components, the transition to a sessile biofilm-associated lifestyle at D8 was marked by the repression of motility genes and the strong induction of curli fimbriae (csg) and colanic acid (wca) loci. Functional enrichment at D5 and D8, compared to D0, indicated coordinated stress regulation and translation. The major transcriptional trends observed in RNA seq were confirmed using RT-qPCR. Collectively, these findings highlight a multi tiered molecular adaptation strategy, enabling STEC adaptation and persistence in sprout environment, thus, providing insights that could be translated into STEC risk mitigation during sprout production
2026-05-01 | GSE329149 | GEO
Project description:Genomic characterization of Escherichia coli, including Shiga-toxin producing E.coli (STEC), in river water
| PRJDB38360 | ENA
Project description:Shiga-toxin producing Enterotoxigenic Escherichia coli
| PRJEB25657 | ENA
Project description:Shiga-toxin producing Escherichia coli isolate of a STEC long-term carrier
| PRJNA1076112 | ENA