YciR, a specific 3′-phosphodiesterases, plays a role in the pathogenesis of Uropathogenic Escherichia coli CFT073
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ABSTRACT:
PROVIDER: PRJNA782451 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16999055_1.fastq.gz | Fastqsanger.gz | |||
| SRR16999055_2.fastq.gz | Fastqsanger.gz | |||
| SRR16999056_1.fastq.gz | Fastqsanger.gz | |||
| SRR16999056_2.fastq.gz | Fastqsanger.gz |
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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:Transcriptional profiles of uropathogenic Escherichia coli CFT073 exposed to cranberry-derived proanthocyanidins (PACs) were determined. Our results indicate that bacteria grown on media supplemented with PACs were iron-deprived. To our knowledge, this is the first time that PACs have been shown to induce a state of iron-limitation in this bacterium.
2010-12-02 | GSE25745 | GEO
Project description:We applied ChIP-seq to identify genome wide binding targets of NsrR in E.coli CFT073. NsrR is a nitric oxide sensitive regulator of transcription. Genome wide binding targets of NsrR have been identified in E.coli K12 using ChIP-chip. The genome of CFT073 is about 0.6Mb larger than that of K12. In this study, we identify the novel NsrR binding sites in CFT073.
2015-06-15 | GSE69829 | GEO
Project description:Transcriptional profiles of uropathogenic Escherichia coli CFT073 exposed to cranberry-derived proanthocyanidins (PACs) were determined. Our results indicate that bacteria grown on media supplemented with PACs were iron-deprived. To our knowledge, this is the first time that PACs have been shown to induce a state of iron-limitation in this bacterium. Cultures of E. coli CFT073 were streaked onto LB agar plates and incubated (37°C, 24 h). A single colony was inoculated into 150 mL of LB broth. Three inoculated flasks contained LB broth alone (controls), and three inoculated flasks were supplemented with cranberry PACs (100 µg/mL). After incubation (37°C, 5 h, 200 rpm to mid-log growth phase), bacteria were harvested for RNA extraction.
2010-12-02 | E-GEOD-25745 | biostudies-arrayexpress
Project description:Urinary tract infections (UTIs), with the characteristics of recurrence and resistance to antibiotics due to misuse, remain a common health and economic issue for patients. Uropathogenic Escherichia coli (UPEC), which is capable of evading the immune response by forming intracellular bacterial communities (IBCs) in the cytoplasm of bladder epithelial cells (BECs) after invasion, has been shown to be the prevailing cause of UTIs. Cyclic dimeric guanosine monophosphate (c-di-GMP) is a small molecule responsible for eliciting the innate immune response of the host only if it has not been degraded by some phosphodiesterases (PDEs), such as YciR. The relationship between YciR and c-di-GMP levels in UPEC is inconclusive. In this study, we investigated the gene expression profile of UPEC in BECs and identified yciR as an upregulated gene. Western blot revealed that YciR enhanced the virulence of UPEC by inhibiting the phosphorylation of NF-κB. The expression of yciR could be repressed by HupB in a directly binding manner. We identified YciR, a novel PDE, and defined its possible function in innate immune evasion. We also demonstrated that YciR is an HupB-dependent PDE that degrades c-di-GMP and that a low concentration of c-di-GMP might make NF-κB less phosphorylated, thereby reducing the host's pro-inflammatory response. This is the first time that YciR has been identified as a virulence factor in the pathogenesis of UPEC. These findings further increase our understanding of the pathogenesis of UPEC and provide a theoretical basis for further studies.
| S-EPMC9339999 | biostudies-literature
Project description:ppGpp signal plays critical role in pathogenesis of Acinetobacter baumannii 17978
| PRJNA726423 | ENA
Project description:We applied ChIP-seq to identify genome wide binding targets of NsrR in E.coli CFT073. NsrR is a nitric oxide sensitive regulator of transcription. Genome wide binding targets of NsrR have been identified in E.coli K12 using ChIP-chip. The genome of CFT073 is about 0.6Mb larger than that of K12. In this study, we identify the novel NsrR binding sites in CFT073. The nsrR gene was modified by the addition of DNA sequences encoding a C-terminal 3X-Flag tag, and the tagged gene was integrated into the chromosome. NsrR bound DNA was isolated by chromatin immunoprecipitation and it was sequenced using Miseq platform.
2015-06-15 | E-GEOD-69829 | biostudies-arrayexpress
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:Genome wide binding sites of NsrR in uropathogenic E.coli CFT073
| PRJNA286884 | ENA
Project description:Biocides are chemical compounds widely used in hospital settings for a variety of purposes, but mainly for disinfection. The chemical properties of a biocide, as well as the biocide concentration, influence which cellular targets are affected. Exposure of bacteria to residual concentrations of biocides could lead to development of increased resistance towards the biocide in use, as well as cross-resistance towards other antimicrobials, including antibiotics. The aim of this study was to examine whether biocides could induce any potentially relevant genes that could affect pathogen's drug resistance or fitness. By examining global gene expression of the uropathogenic Escherichia coli CFT073 after exposure to subinhibitory concentrations of five biocides (benzalkonium chloride - BAC, chlorhexidine - CHX, ethanol - EtOH, hydrogen peroxide - H2O2, triclosan - TSN), we found that each biocide changed expression of different groups of genes and that exposure to ethanol caused changes in expression of the largest number of genes among all biocides. In general, the five biocides tested in this study at subinhibitory concentrations did not increase the resistance potential of the pathogen to other antimicrobials. We could, however, identify clusters of genes that could possibly help the strain to grow in the presence of a biocide in the medium. A culture of E. coli CFT073 without any biocide treatment served as the control sample. That culture was grown under the exact same conditions as the five biocide-treated samples. Each sample was collected in three biological replicates at the mid-exponential phase of growth.
2016-03-01 | E-GEOD-72738 | biostudies-arrayexpress