Host response to systemic bacterial challenge (sepsis) with E. coli strains CFT073 and F11 at 6 and 12 hours post inoculum
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ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE79665 | GEO | 2016/03/29
SECONDARY ACCESSION(S): PRJNA316620
REPOSITORIES: GEO
Similar Datasets
Project description:Host response to systemic bacterial challenge (sepsis) with E. coli strains CFT073 and F11 at 6 and 12 hours post inoculum 48 hpf embryos were manually dechorianated, briefly anesthetized with 0.77 mM ethyl 3-aminobenzoate methanesulfonate salt (tricaine) (Sigma-Aldrich), and embedded in 0.8% low melt agarose (MO BIO Laboratories) without tricaine. After the agarose solidified, embryos were immersed in E3 media lacking methylene blue. Prior to injection, 1 ml of bacterial culture was pelleted, washed with 1 ml sterile PBS, and re-suspended in PBS to obtain ~1X109 CFU/ml. PBS. One nl of this bacterial suspension containing ~1000 CFU was microinjected into the bloodstream via the circulation valley using an Olympus SZ61 or SZX10 stereomicroscope together with a YOU-1 micromanipulator (Narishige), a Narishige IM-200 microinjector, and a JUN-AIR model 3-compressor. For each experiment, the average CFU per injection was determined by adding 10 1-nl drops to 1 ml of 0.7% NaCl, which was then serial diluted and plated on Luria-Bertani (LB) agar plates. Mock-infected controls were inoculated with 1 nl sterile PBS. Following injection, embryos were removed from agar and placed individually into wells of a 48-well plate (Nunc) containing E3 medium and incubated at 28.5°C. Experiments were performed in biological quadruplicate.
2016-03-29 | E-GEOD-79665 | biostudies-arrayexpress
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:Host response to systemic bacterial challenge (sepsis) with E. coli strains CFT073 and F11 at 6 and 12 hours post inoculum
| PRJNA316620 | ENA
Project description:In response to viral pathogens, the host upregulates antiviral genes that suppress translation of viral mRNAs. However, induction of such antiviral responses may not be exclusive to viruses as the pathways lie at the intersection of broad inflammatory networks that can also be induced by bacterial pathogens. Using a model of Gram-negative sepsis, we show that propagation of kidney damage initiated by a bacterial origin ultimately involves antiviral responses that result in host translation shutdown. We determined that activation of the Eif2ak2-Eif2α axis is the key mediator of translation initiation block in late phase sepsis. Reversal of this axis mitigated kidney injury. Furthermore, temporal profiling of the kidney translatome revealed that multiple genes involved in formation of the initiation complex were translationally altered during bacterial sepsis. Collectively, our findings implicate that translation shutdown is indifferent to the specific initiating pathogen and is an important determinant of tissue injury in sepsis.
2018-10-06 | GSE120877 | GEO
Project description:In response to viral pathogens, the host upregulates antiviral genes that suppress translation of viral mRNAs. However, induction of such antiviral responses may not be exclusive to viruses as the pathways lie at the intersection of broad inflammatory networks that can also be induced by bacterial pathogens. Using a model of Gram-negative sepsis, we show that propagation of kidney damage initiated by a bacterial origin ultimately involves antiviral responses that result in host translation shutdown. We determined that activation of the Eif2ak2-Eif2α axis is the key mediator of translation initiation block in late phase sepsis. Reversal of this axis mitigated kidney injury. Furthermore, temporal profiling of the kidney translatome revealed that multiple genes involved in formation of the initiation complex were translationally altered during bacterial sepsis. Collectively, our findings implicate that translation shutdown is indifferent to the specific initiating pathogen and is an important determinant of tissue injury in sepsis.
2018-11-16 | GSE122274 | 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. 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:Genome wide binding sites of NsrR in uropathogenic E.coli CFT073
| PRJNA286884 | ENA
Project description:Escherichia coli CFT073 isolate:PU_38 Genome sequencing
| PRJNA387644 | ENA
Project description:Escherichia coli CFT073 isolate:199310 Genome sequencing
| PRJNA624646 | ENA
Project description:Expression data from Total RNA extracted from murine spleen. Sepsis was induced in C57Bl/6J mice by cecal ligation and puncture (CLP), followed 6 hours later by an intravenous injection of Mesenchymal Stem Cell (MSC) or saline. Twenty-eight hours after CLP, plasma, bronchoalveolar lavage (BAL) fluid and tissues were collected for analyses. Total RNA was extracted using Trizol (as per manufactures' instruction) followed by clean-up procedure using Qiagen RNA easy Prep (as per manufactures instructions) In the following study we hypothesized that mesenchymal stem cells (MSCs), which have documented immunomodulatory properties, would reduce sepsis-associated inflammation and organ injury in a clinically relevant model of sepsis. To identify the molecular changes associated with decreased inflammation in CLP-injured mice treated with MSCs, we analyzed the gene expression profiles from spleens collected at 28 hours from 4 animals per group: sham/saline, CLP/saline, and CLP/MSCs.
2010-11-22 | E-GEOD-24357 | biostudies-arrayexpress