Ontology highlight
ABSTRACT:
PROVIDER: PRJNA476595 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7358361_1.fastq.gz | Fastqsanger.gz | |||
| SRR7358361_2.fastq.gz | Fastqsanger.gz | |||
| SRR7358362_1.fastq.gz | Fastqsanger.gz | |||
| SRR7358362_2.fastq.gz | Fastqsanger.gz | |||
| SRR7358363_1.fastq.gz | Fastqsanger.gz |
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Project description:Campylobacter jejuni is the most prevalent cause of foodborne bacterial enteritis worldwide. This study aims at the characterisation of pathomechanisms and signalling in Campylobacter-induced diarrhoea in the human mucosa. During routine colonoscopy, biopsies were taken from patients suffering from campylobacteriosis. RNA-seq of colon biopsies was performed to describe Campylobacter jejuni-mediated effects. Mucosal mRNA profiles of acutely infected patients and healthy controls were generated by deep sequencing using Illumina HiSeq 2500. This data provide the basis for subsequent upstream regulator analysis.
2017-10-10 | GSE88710 | GEO
Project description:Objective: We previously showed that Campylobacter jejuni Cas9 was necessary for full virulence and efficient induction of human cell stress followed by cell death, but no virulence mechanism could be unravelled then. Therefore, we carried out global genome-wide transcriptomics, using RNA samples extracted from cells infected by a wild-type C. jejuni strain and the corresponding cas9 deletion strain. Methods: Caco-2 epithelial cells were infected with C. jejuni wild-type or cas9 deletion strains and RNA was extracted at 5 timepoints post-infection. Results: Wild-type C. jejuni induced cellular stress, DNA damage and cell death pathways in Caco-2 cells continuously from 30 min up to 4 hours after infection, eventually followed by visual cell death induction after 24 hours; the corresponding cas9 deletion strain did also induce cell stress pathways within the first two hours of infection but at later timepoints, stress pathway induction had dropped and after 4 hours of infection, expression of the corresponding stress genes had normalised to near-t=0 (uninfected) expression values; the cas9 deletion strain did not lead to visual cell death induction after 24 hours. Conclusions: Campylobacter jejuni Cas9 is necessary for full virulence of C. jejuni and is involved in the efficient induction of cellular stress pathways and eventually, cell death.
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Project description:Campylobacter jejuni is susceptible to killing through exposure to blue light (405 nm) due to its poor ability to detoxify reactive oxygen species. This analysis aimed to elucidate the transcriptomic response of Campylobacter jejuni exposed to 405 nm light through illumina sequencing. C. jejuni was grown and exposed to 405nm light. Samples were taken at 15 min (7 J cm-1) and 30 min (14 J cm-1) after exposure. The data generated were compared to the transcriptome pre-exposure to determine the changes associated with blue light exposure
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Project description:This study investigates the CsrA regulon of the food-borne pathogen Campylobacter jejuni. Direct RNA binding targets of CsrA in two strains of C. jejuni, NCTC11168 and 81-176, were determined using RIP-seq.
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Project description:Campylobacter jejuni is the prevalent cause of bacterial gastroenteritis in human worldwide. The ability to survive stomach acidity is a fundamental requirement for C. jejuni to colonize the host and cause disease. However, the mechanism of C. jejuni acid survival is still unknown. Herein, we demonstrated that C. jejuni is able to survive acidic conditions at pH 4 up to 8 min without a drop in viability. The acid stimulon of C. jejuni 81-176 revealed the up-regulation of many genes important for Campylobacter acid survival such as heat shock genes and genes involved in energy metabolism. On the other hand, the repression of ribosomal genes highlights the ability of C. jejuni to direct its machinery to survive stressful conditions. Prior acid exposure cross-protected C. jejuni against oxidative stress suggesting an overlap in C. jejuni’s responses to various stresses. Interestingly, the induced expression of virulence genes in C. jejuni upon acid exposure such as the Campylobacter invasion antigen (ciaB) indicates that acid stress plays a role in C. jejuni host pathogenesis. Acid exposure significantly enhanced C. jejuni pathogenesis in both eukaryotic cells and G. melonella. To the best of our knowledge, this is the first study characterizes the influence of acid stress on C. jejuni pathogenesis in an infection model. Altogether, this study uncovers the transcriptional profile of C. jejuni in response to acidic conditions as those encountered in the stomach. In addition, our results demonstrate that acid stress jump-starts C. jejuni for efficient gut colonization and host pathogenesis. Campylobacter jejuni is the prevalent cause of bacterial gastroenteritis in human worldwide. The ability to survive stomach acidity is a fundamental requirement for C. jejuni to colonize the host and cause disease. However, the mechanism of C. jejuni acid survival is still unknown. Herein, we demonstrated that C. jejuni is able to survive acidic conditions at pH 4 up to 8 min without a drop in viability. The acid stimulon of C. jejuni 81-176 revealed the up-regulation of many genes important for Campylobacter acid survival such as heat shock genes and genes involved in energy metabolism. On the other hand, the repression of ribosomal genes highlights the ability of C. jejuni to direct its machinery to survive stressful conditions. Prior acid exposure cross-protected C. jejuni against oxidative stress suggesting an overlap in C. jejuni’s responses to various stresses. Interestingly, the induced expression of virulence genes in C. jejuni upon acid exposure such as the Campylobacter invasion antigen (ciaB) indicates that acid stress plays a role in C. jejuni host pathogenesis. Acid exposure significantly enhanced C. jejuni pathogenesis in both eukaryotic cells and G. melonella. To the best of our knowledge, this is the first study characterizes the influence of acid stress on C. jejuni pathogenesis in an infection model. Altogether, this study uncovers the transcriptional profile of C. jejuni in response to acidic conditions as those encountered in the stomach. In addition, our results demonstrate that acid stress jump-starts C. jejuni for efficient gut colonization and host pathogenesis.
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Project description:Campylobacter jejuni is a human pathogen which causes campylobacteriosis, one of the most widespread zoonotic enteric diseases worldwide. Most cases of sporadic C. jejuni infection occur through the handling or consumption of undercooked chicken meat, or cross-contamination of other foods with raw poultry fluid. A common practice to combat Campylobacter infection is to treat chickens with chlorine which kills the microbe. This analysis aimed to elucidate the transcriptomic response of Campylobacter jejuni treated with hypochlorite through Illumina sequencing. C. jejuni was grown and treated with hypochlorite. Samples were taken 5, 20 and 45 min after treatment for RNAseq analysis.The data generated were compared to the transcriptome pre-exposure to determine C. jejuni's response to hypochlorite.
2023-10-01 | E-MTAB-11479 | biostudies-arrayexpress
Project description:We report the use of RNA-seq analysis for the determination of RPKM transcript levels in wildtype and fur perR mutant of Campylobacter jejuni NCTC 11168. This allows for comparison of gene expression levels. Campylobacter jejuni NCTC 11168 wildtype and fur perR mutant were grown to late log phase, RNA was purified and used for RNA-sequencing by Illumina HiSeq sequencing
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Project description:RNA-seq was used to study gene expression profiles and potential processing sites in Campylobacter jejuni NCTC11168 wildtype and RNase Y (rny, Cj1209) deletion.
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Project description:This study investigates the CsrA regulon of the food-borne pathogen Campylobacter jejuni. Direct RNA binding targets of CsrA in two strains of C. jejuni, NCTC11168 and 81-176, were determined using RIP-seq. Identification of CsrA binding sites in two C. jejuni strains using RIP-seq
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