Escherichia coli
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA909480 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22573184_1.fastq.gz | Fastqsanger.gz | |||
| SRR22573184_2.fastq.gz | Fastqsanger.gz | |||
| SRR22573185_1.fastq.gz | Fastqsanger.gz | |||
| SRR22573185_2.fastq.gz | Fastqsanger.gz | |||
| SRR22573186_1.fastq.gz | Fastqsanger.gz |
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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 (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.
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Project description:SVA Salmonella sequences, OH-EJP Discover
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Project description:A dynamic network approach was conducted to investigate the differential Caco-2 response to two STEC isolates - EH41, isolated from a HUS patient in Australia, and Ec472/01, isolated from bovine feces in Brazil - along in vitro enterocyte-bacteria interaction. The genomic analysis was based on temporal gene co-expression analysis (GCN) data in order to gain a better understanding on the molecular mechanisms underlying the capacity to cause HUS. The GCN topological analyses for Caco-2/EH41 group revealed loss of the scale-free status after one hour of interaction, persistence of this condition along the second hour and establishment of a new gene hierarchy thereafter. These events resemble the gene network mechanism of health-disease transition. The new established network represents an adaptive cell response to the pathogen and not the return to a “normal” state. Conversely, the networks for Caco-2/Ec472 group showed a slow and progressive loss of the scale-free status without its restoration at the end of the time interval here studied. These results contribute for a better understanding of the molecular mechanism involved in STEC pathogenicity associated to HUS.
2019-07-15 | GSE104489 | GEO
Project description:A dynamic network approach was conducted to investigate the differential Caco-2 response to two STEC isolates - EH41, isolated from a HUS patient in Australia, and Ec472/01, isolated from bovine feces in Brazil - along in vitro enterocyte-bacteria interaction. The genomic analysis was based on temporal gene co-expression analysis (GCN) data in order to gain a better understanding on the molecular mechanisms underlying the capacity to cause HUS. The GCN topological analyses for Caco-2/EH41 group revealed loss of the scale-free status after one hour of interaction, persistence of this condition along the second hour and establishment of a new gene hierarchy thereafter. These events resemble the gene network mechanism of health-disease transition. The new established network represents an adaptive cell response to the pathogen and not the return to a “normal” state. Conversely, the networks for Caco-2/Ec472 group showed a slow and progressive loss of the scale-free status without its restoration at the end of the time interval here studied. These results contribute for a better understanding of the molecular mechanism involved in STEC pathogenicity associated to HUS.
2019-07-15 | GSE104488 | GEO