Escherichia coli CFT073
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA286883 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR2061822.fastq.gz | Fastqsanger.gz | |||
| SRR2061823.fastq.gz | Fastqsanger.gz | |||
| SRR2061824.fastq.gz | Fastqsanger.gz | |||
| SRR2061825.fastq.gz | Fastqsanger.gz | |||
| SRR2061826.fastq.gz | Fastqsanger.gz |
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Project description:While in transit within and between hosts, uropathogenic E. coli (UPEC) encounter multiple stresses, including substantial levels of nitric oxide and reactive nitrogen intermediates. Strains of UPEC become conditioned to high concentrations of acidified sodium nitrite (ASN), a model system used to generate nitrosative stress. We used microarrays to define the expression profile of UPEC that have been conditioned for growth in ASN.
2009-03-21 | GSE15319 | GEO
Project description:The experiment design involves RNA-seq of Hfq bound RNA co-immunoprecipitation in the uropathogenic Escherichia coli (UPEC) strain UTI89.
2016-05-31 | E-MTAB-3498 | biostudies-arrayexpress
Project description:We previously determined that loss of respiratory quinol oxidase cytochrome bd disrupts biofilm formation in uropathogenic Escherichia coli (UPEC). In this study, we extracted and interrogated the outer membrane and extracellular matrix of colony biofilms formed by UPEC isolate UTI89 and an isogenic mutant lacking cytochrome bd (∆cydAB).
2021-04-01 | PXD023998 | Pride
Project description:Escherichia coli release Extracellular Vesicles (EVs) which carry diverse molecular cargo. Pathogenic E.coli EVs contain virulence factors which assist during infection in the host in different mechanisms.The RNA cargo of E.coli EVs has not been assessed in their effect in the host. We used microarray data to asses and compare the global response of bladder cells to EV-RNA from pathogenic E.coli (Uropathogenic UPEC 536) and non-pathogenic E. coli (probiotic Nissle 1917)
2020-07-08 | GSE148711 | GEO
Project description:The features of Mycoplasma in human organ such lung and urinary tract are enigmatic. Here, the role of M. hominis in regard to biofilm formation of uropathogenic Escherichia coli (UPEC) strain CFT073 was investigated. Although M. hominis were inferred to not impact on UPEC bacterial fitness including growth and productions of signaling molecules as autoinducer-2 (AI-2) and indole, we found that the presence of M. hominis dramatically decreased biofilm formation of UPEC CFT073 as well as slightly repressed attachment and cytotoxicity of that. Importantly, this activity was observed on UPEC strain specifically, not enterohemorrhagic E. coli (EHEC) strain that exists on intestine. Whole-transcriptome profiling and quantitative real-time polymerase chain reaction (qRT-PCR) analysis revealed PhoPQ system and anti-termination protein (encoded by ybcQ) participates on the reduction of biofilm formation by M. hominis (corroborated by qRT-PCR). Furthermore, collaborating with previous report that toxin-antitoxin (TA) system involved in biofilm formation, M. hominis increased on the transcriptions of toxin genes including hha (toxin gene in Hha-TomB TA system) and pasT (toxin part in PasT-PasI TA system). Hence, we propose that one possible role of M. hominis is to influence bacterial biofilm formation in urinary tract. Only fourteen genes were induced (2.5-fold) by the presence of M. hominis in Uropathogenic Escherichia coli (UPEC) biofilm cells. Among upregulated genes, ybcQ (encodes anti-termination protein Q homolog) and phoP/phoQ (encode DNA-binding response regulators in two-component regulatory system), were induced by the presence of M. hominis. Two-condition experiment, UPEC CFT073 alone vs. UPEC CFT073 with Mycoplasma hominis PG21 (10^5 ccu/ml). For preparing the total RNA, UPEC CFT073 cells were grown at 37°C in biofilm cells on glass wool with or without M. hominis for 24 h.
2016-01-08 | E-GEOD-43376 | biostudies-arrayexpress
Project description:Uropathogenic Escherichia coli are a prevailing causation of urinary tract infections infections and characterized by recurrence and resistance to antibiotics due to their misuse, causing a large economic burden to individuals and countries. An early determinant of the pathogenicity of UPEC is its ability to form intracellular bacterial communities in the cytoplasm of bladder epithelial cells after its invasion for evading immune response. Cyclic dimeric guanosine monophosphate (c-di-GMP) is a recently high frequency discussed small molecule from bacterial to trigger the innate immune response form the host while YciR has been demonstrated that had an ability to degrade the level of c-di-GMP. There is no definite conclusion in the contribution of YciR and the level of c-di-GMP in the pathogenesis of UPEC. In this study, we used transcriptomic techniques approach to analyze the gene expression profiles of UPEC at the stage of bacterial survival in bladder epithelial cells and we screened yciR gene that may be associated with virulence that was upregulated in the transcriptome by differential gene analysis. In the absence of yciR, there is a Phosphorylation of NF-kappaB analyzed by Western Blot which results in decreased bacterial colonization in vitro and a reducing in mice bladder. In this study, we identified for the first time that YciR as a virulence factor in the pathogenesis of UPEC and discovered that UPEC manipulate YciR to facilitate colonization in vitro and vivo causing acute bladder infection. In addition, we also found that hupB regulated the expression of yciR to mediate the Phosphorylation of NF-kappaB These findings further increase the understanding of the pathogenesis of UPEC and provide a theoretical basis for further studies.
2021-11-24 | GSE189294 | GEO
Project description:The features of Mycoplasma in human organ such lung and urinary tract are enigmatic. Here, the role of M. hominis in regard to biofilm formation of uropathogenic Escherichia coli (UPEC) strain CFT073 was investigated. Although M. hominis were inferred to not impact on UPEC bacterial fitness including growth and productions of signaling molecules as autoinducer-2 (AI-2) and indole, we found that the presence of M. hominis dramatically decreased biofilm formation of UPEC CFT073 as well as slightly repressed attachment and cytotoxicity of that. Importantly, this activity was observed on UPEC strain specifically, not enterohemorrhagic E. coli (EHEC) strain that exists on intestine. Whole-transcriptome profiling and quantitative real-time polymerase chain reaction (qRT-PCR) analysis revealed PhoPQ system and anti-termination protein (encoded by ybcQ) participates on the reduction of biofilm formation by M. hominis (corroborated by qRT-PCR). Furthermore, collaborating with previous report that toxin-antitoxin (TA) system involved in biofilm formation, M. hominis increased on the transcriptions of toxin genes including hha (toxin gene in Hha-TomB TA system) and pasT (toxin part in PasT-PasI TA system). Hence, we propose that one possible role of M. hominis is to influence bacterial biofilm formation in urinary tract. Only fourteen genes were induced (2.5-fold) by the presence of M. hominis in Uropathogenic Escherichia coli (UPEC) biofilm cells. Among upregulated genes, ybcQ (encodes anti-termination protein Q homolog) and phoP/phoQ (encode DNA-binding response regulators in two-component regulatory system), were induced by the presence of M. hominis.
2016-01-08 | GSE43376 | GEO
Project description:Transcriptional analysis of UTI89 - uropathogenic E.coli (UPEC) strain grown in urine/Luria bertani medium culture in vitro as well as during three distinct phases of UPEC bladder infection: intracellular growth, filament formation and filament reversal. UTI89 was used to infect a bladder epithelial cell line cultured within a dynamic flow chamber system and harvested at particular stages of its pathogenecity cascade. Total RNA was processed and cy3 labeled for microarray analysis using Agilent custom Escherichia coli UTI89 arrays designed using E-Array.
2017-05-28 | E-MTAB-3611 | biostudies-arrayexpress
Project description:Conditioning of uropathogenic Escherichia coli to nitrosative stress
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