Ontology highlight
ABSTRACT:
PROVIDER: PRJNA513326 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8404401_1.fastq.gz | Fastqsanger.gz | |||
| SRR8404401_2.fastq.gz | Fastqsanger.gz | |||
| SRR8404402_1.fastq.gz | Fastqsanger.gz | |||
| SRR8404402_2.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:Rickettsia conorii is the etiologic agent of Mediterranean spotted fever, a re-emerging disease with significant mortality. This obligate, gram-negative intracellular pathogen is transmitted via tick bites, resulting in disseminated vascular endothelial cell infection with vascular leakage. In the infected human, Rickettsia conorii infects endothelial cells, stimulating expression of cytokines and pro-coagulant factors. However, the integrated proteomic response of human endothelial cells to R. conorii infection is not known. In this study, we performed quantitative proteomic profiling of R conorii –infected primary HUVECs vs those stimulated with LPS alone.
2015-11-17 | PXD002650 | Pride
Project description:Rickettsia conorii, the causative agent of the MSF is transmitted to humans by the bite of infected ticks Rhipicephalus sanguineus. The skin thus constitutes an important barrier for the entry and propagation of R. conorii. Given this, analysis of the survival strategies used by the bacterium within infected skin is critical for our understanding of rickettsiosis. Here, we report the first genome-wide analysis of R. conorii gene expression from infected human skin biopsies. Our data showed that R. conorii exhibit a striking transcript signature that was remarkably conserved across patients, regardless of genotype. The expression profiles obtained using custom Agilent microarrays were validated by quantitative RT-PCR. Within eschars, approximately 15% (n = 211) of the total predicted R. conorii ORFs appeared differentially expressed. These genes are mostly down-regulated and encode proteins essential for bacterial replication. Some of the strategies displayed by rickettsiae to overcome the host defense barriers, thus avoiding killing, were also pointed out. The observed up-regulation of rickettsial genes associated with DNA repair is likely to correspond to a DNA-damaging agent enriched environment generated by the host cells to eradicate the pathogens. Survival of R. conorii within eschars also involves adaptation to osmotic stress, changes in cell surface proteins and up-regulation of some virulence factors. Interestingly, in contrast to down-regulated transcripts, we noticed that up-regulated ones rather exhibit a small nucleotide size, most of them being exclusive for the spotted fever group rickettsiae. On the overall, this work provides some insights on how R. conorii counteracts the host cell attack at the site of inoculation which corresponds to the front line of human host defense against rickettsia diffusion and that resembles to battlefield. 9 R.conorii clinical isolates from eschars co-hybridized with reference strain R.conorii Strain Malish 7
2008-11-06 | E-GEOD-12130 | biostudies-arrayexpress
Project description:Rickettsia conorii, the causative agent of the MSF is transmitted to humans by the bite of infected ticks Rhipicephalus sanguineus. The skin thus constitutes an important barrier for the entry and propagation of R. conorii. Given this, analysis of the survival strategies used by the bacterium within infected skin is critical for our understanding of rickettsiosis. Here, we report the first genome-wide analysis of R. conorii gene expression from infected human skin biopsies. Our data showed that R. conorii exhibit a striking transcript signature that was remarkably conserved across patients, regardless of genotype. The expression profiles obtained using custom Agilent microarrays were validated by quantitative RT-PCR. Within eschars, approximately 15% (n = 211) of the total predicted R. conorii ORFs appeared differentially expressed. These genes are mostly down-regulated and encode proteins essential for bacterial replication. Some of the strategies displayed by rickettsiae to overcome the host defense barriers, thus avoiding killing, were also pointed out. The observed up-regulation of rickettsial genes associated with DNA repair is likely to correspond to a DNA-damaging agent enriched environment generated by the host cells to eradicate the pathogens. Survival of R. conorii within eschars also involves adaptation to osmotic stress, changes in cell surface proteins and up-regulation of some virulence factors. Interestingly, in contrast to down-regulated transcripts, we noticed that up-regulated ones rather exhibit a small nucleotide size, most of them being exclusive for the spotted fever group rickettsiae. On the overall, this work provides some insights on how R. conorii counteracts the host cell attack at the site of inoculation which corresponds to the front line of human host defense against rickettsia diffusion and that resembles to battlefield.
2008-11-07 | GSE12130 | GEO
Project description:We have previously reported that Rickettsia conorii and Rickettsia montanensis have distinct intracellular fates within THP-1 macrophages, suggesting that the ability to proliferate within macrophages may be a distinguishable factor between pathogenic and non-pathogenic Spotted fever group (SFG) members. To start unraveling the molecular mechanisms underlying the capacity (or not) of SFG Rickettsia to establish their replicative niche in macrophages, we have herein profiled the host proteomic alterations resulted by the infection of THP-1 macrophages with R. conorii and R. montanensis using a high throughput quantitative proteomics approach (SWATH-MS). Our results revealed that these two members of SFG Rickettsia with distinct pathogenicity attributes for humans, trigger differential proteomic signatures in macrophage-like cells. Although infection by both rickettsial species resulted in a lower abundance of enzymes of glycolysis and pentose phosphate pathway, the pathogenic R. conorii specifically induced the accumulation of several enzymes of the tricarboxylic acid cycle, oxidative phosphorylation, fatty acid -oxidation and glutaminolysis, as well as of several inner and outer membrane mitochondrial transporters. These results suggest a profound metabolic rewriting of macrophages by R. conorii towards a metabolic signature of an M2-like (anti-inflammatory) activation program. Moreover, our results revealed that several subunits forming the proteasome and immunoproteasome are found in lower abundance upon infection with both rickettsial species, which may help bacteria to escape immune surveillance. Remarkably, R. conorii-infection specifically induced the accumulation of several host proteins implicated in protein processing and quality control in ER, suggesting that this pathogenic Rickettsia may be able to compensate the accumulation of misfolded proteins by increasing the ER protein folding capacity and subsequently restore host cell homeostasis. This work reveals novel aspects of macrophage-Rickettsia interactions, expanding our knowledge of how pathogenic rickettsiae explore host cells to their advantage.
2019-02-16 | PXD010330 | Pride
Project description:Rickettsia conorii is the etiologic agent of Mediterranean spotted fever, a re-emerging disease with significant mortality. This obligate, gram-negative intracellular pathogen is transmitted via tick bites, resulting in disseminated vascular endothelial cell infection with vascular leakage. In the infected human, Rickettsia conorii infects endothelial cells, stimulating expression of cytokines and pro-coagulant factors. However, the integrated proteomic response of human endothelial cells to R. conorii infection is not known. In this study, we performed quantitative proteomic profiling of R conorii â??infected primary HUVECs vs those stimulated with LPS alone.
2017-04-01 | MSV000080856 | MassIVE
Project description:Rickettsia conorii are obligate intracellular bacteria responsible for the Mediterranean spotted fever. Their adaptation to highly divergent environments ranging from the arthropod vector to the human beings is essential to survival and virulence. Through a combination of total RNA purification and random prokaryotic cDNA amplification, we successfully analyzed transcription profiles by microarrays starting from 100 ng of R. conorii RNA. Real-time quantitative PCR results performed on unpurified total RNA was consistent with microarray measurements. Here, from the selected targets spotted on our microarray, we showed that in R. conorii, nutrient stress is accompanied by over-expression of the virB operon. Regulation of these genes could be mediated by the stringent response through ppGpp, consistent with the observed up-regulation of spoT and gmk. Exposure of R. conorii to a nutrient stress paradoxically reduced the expression of both GroEL and its transcriptional regulator RpoH. This shows that the over-expression of this chaperonin is a part of the natural life of intracellular growing rickettsiae. Our findings also evidenced that, unexpectedly, many atypical sequences, including small-size split genes, ORFans genes and highly conserved intergenic regions contains expressed sequences that are differentially regulated. The notable deficiency of transcriptional regulators within R. conorii genome does not reflect its incapability to undergo transcriptional changes but rather the existence of an alternative adaptation strategy. Keywords: Global transcriptional analysis
2006-07-06 | GSE5201 | GEO
Project description:Rickettsia conorii subsp. raoultii Genome sequencing and assembly
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Project description:Rickettsia conorii subsp. heilongjiangensis strain:B8 Genome sequencing
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