Staphylococcus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA648411 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| SRR12333100_1.fastq.gz | Fastqsanger.gz | |||
| SRR12333100_2.fastq.gz | Fastqsanger.gz | |||
| SRR12333101_1.fastq.gz | Fastqsanger.gz | |||
| SRR12333101_2.fastq.gz | Fastqsanger.gz |
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Project description:Staphylococcus aureus (S. aureus) is a known pathogen able to infect humans and animals. Human S. aureus isolates are often associated with carriage of Sa3int prophages combined with loss of beta-hemolysin production due to gene disruption, whereas animal isolates are positive for beta-hemolysin associated with absence of Sa3int prophages. Sa3int prophages are known to contribute to staphylococcal fitness and virulence in human host by providing human-specific virulence factors encoded on the prophage genome. Strain-specific differences in regard to phage transfer, lysogenization and induction are attributable to yet unknown staphylococcal factors specifically influencing prophage gene expression. In this work we used tagRNA-sequencing approach to specifically search for these unknown host factors and differences in prophage gene expression. For this purpose, we established a workflow revealing the first direct comparison for differential gene expression analysis on two distinct single-lysogenic S. aureus isolates. Further, global gene expression patterns were investigated in two S. aureus isolates upon mitomycin C treatment and compared to uninduced conditions. This provides new insights into the tightly linked host-phage interaction network.
2022-10-03 | GSE214523 | GEO
Project description:The present work comprises the study of wound pathogenic bacteria as part of a community. It considers the interactions of two different S. aureus isolates with B. thuringiensis and K. oxytoca; all of them isolated from the same chronic wound of a patient with epidermolysis bullosa. Particular focus has been given on the interactions of S. aureus with other microbes due to its high prevalence among chronic wounds. During cultivation, no species performed as dominant or inhibited the growth of one another. Mass spectrometry was used to explore the inherent relationships between the staphylococcal strains and the coexisting bacteria exproteomes. The analysis showed an important reduction in the amount of staphylococcal cytoplasmic proteins when co-cultured with K. oxytoca and B. thuringiensis, this decrement did not occur with klebsiella and bacillus proteins. Interestingly, K. oxytoca and B. thuringiensis seemed to have a more evident response towards the presence of S. aureus in the culture, while the opposite was not observed with the staphylococcal isolates. Genomic analysis revealed isolate t13595 hypermutable characteristics, placing the interactions between staphylococcal isolates in the context of a chronic wound. Overall, the nature of the exoproteome variations among cultures suggests that adaptive mechanisms differ in all strains.
2018-10-17 | PXD005596 | Pride
Project description:The purpose of this study was to compare the global, growth phase-dependent transcriptional profiles of two isolates of Staphylococcus aureus. One isolate is a prototypic laboratory strain named RN6390, and has been used frequently as a model organism for study of staphylococcal physiology and virulence. However, recent studies indicate that RN6390 is not, in general, genotypically or phenotypically representative of clinical isolates of Staphyloccos aureus. Therefore, there is no current comprehensive picture of gene expression patterns in a virulent, clinical isolate of Staphyloccous aureus. For these reasons, we compare the transcriptional profile of RN6390 to that of a virulent clinical isolate, UAMS-1. Also included in this study is profiling of two UAMS-1 regulatory mutants, UAMS-155, and UAMS-929. These strains possess mutations in the accessory gene regulator (agr) and staphylococcal accessory regulator (sarA) genes, respectively. These two genes are well described global regulatory molecules that are reported to play important roles in controlling virulence factor production and biofilm formation in Staphylococcus aureus. However, most study of these two molecules has been limited to laboratory strains such as RN6390. For these reasons, this study also includes transcriptional profiling of UAMS agr and sarA mutants. Keywords: Comparative, growth phase-dependent transcriptional profiling of bacterial strains and isogenic regulatory mutants
2006-10-03 | GSE5466 | GEO
Project description:Staphylococcus aureus is a Gram-positive human pathogen causing a variety of human diseases in both hospital and community settings. This bacterium is so closely associated with prophages that it is rare to find S. aureus isolates without prophages. Two phages are known to be important for staphylococcal virulence: the beta-hemolysin (hlb) converting phage and the Panton-Valentine Leukocidin (PVL) converting phage. The hlb-converting phage is found in more than 90% of clinical isolates of S. aureus. This phage produces exotoxins and immune modulatory molecules, which inhibit human innate immune responses. The PVL-converting phage produces the two-component exotoxin PVL, which can kill human leucocytes. This phage is wide-spread among community-associated methicillin resistant S. aureus (CA-MRSA). It also shows strong association with soft tissue infections and necrotizing pneumonia. Several lines of evidence suggest that staphylococcal prophages increase bacterial virulence not only by providing virulence factors but also by altering bacterial gene expression: 1) Transposon insertion into prophage regulatory genes, but not into the genes of virulence factors, reduced S. aureus killing of Caenorhabditis elegans.; 2) Although the toxins and immune modulatory molecules encoded by the hlb- converting phages do not function in the murine system, deletion of ϕNM3, the hlb-converting phage in S. aureus Newman, reduced staphylococcal virulence in the murine abscess formation model. 3) In a preliminary microarray experiment, prophages in S. aureus Newman altered the expression of more than 300 genes. In this research proposal, using microarray and high-throughput quantitative RT-PCR (qRT-PCR) technologies, we will identify the effects of the two important staphylococcal phages on the gene expression of S. aureus in both in vitro and in vivo conditions. This project is intended to be completed within one year. All the data – microarray, qRT-PCR and all the primer sequences- will be made available to public 6 month after completion. Data from this project will help us to understand the role of prophages in the S. aureus pathogenesis and can lead to development of a strategy to interfere with the pathogenesis process.
2011-02-28 | GSE26623 | GEO
Project description:Staphylococcus aureus is a Gram-positive human pathogen causing a variety of human diseases in both hospital and community settings. This bacterium is so closely associated with prophages that it is rare to find S. aureus isolates without prophages. Two phages are known to be important for staphylococcal virulence: the beta-hemolysin (hlb) converting phage and the Panton-Valentine Leukocidin (PVL) converting phage. The hlb-converting phage is found in more than 90% of clinical isolates of S. aureus. This phage produces exotoxins and immune modulatory molecules, which inhibit human innate immune responses. The PVL-converting phage produces the two-component exotoxin PVL, which can kill human leucocytes. This phage is wide-spread among community-associated methicillin resistant S. aureus (CA-MRSA). It also shows strong association with soft tissue infections and necrotizing pneumonia. Several lines of evidence suggest that staphylococcal prophages increase bacterial virulence not only by providing virulence factors but also by altering bacterial gene expression: 1) Transposon insertion into prophage regulatory genes, but not into the genes of virulence factors, reduced S. aureus killing of Caenorhabditis elegans.; 2) Although the toxins and immune modulatory molecules encoded by the hlb- converting phages do not function in the murine system, deletion of NM3, the hlb-converting phage in S. aureus Newman, reduced staphylococcal virulence in the murine abscess formation model. 3) In a preliminary microarray experiment, prophages in S. aureus Newman altered the expression of more than 300 genes. In this research proposal, using microarray and high-throughput quantitative RT-PCR (qRT-PCR) technologies, we will identify the effects of the two important staphylococcal phages on the gene expression of S. aureus in both in vitro and in vivo conditions. This project is intended to be completed within one year. All the data – microarray, qRT-PCR and all the primer sequences- will be made available to public 6 month after completion. Data from this project will help us to understand the role of prophages in the S. aureus pathogenesis and can lead to development of a strategy to interfere with the pathogenesis process. Staphylococcus aureus subsp.aureus strain Newman (reference) and Staphylococcus aureus subsp.aureus strain Newman yhcR knockout(query) were grown in TSA broth.Samples were grown under aerobic and anaerobic conditions and RNA samples harvested at mid log, stationary, and log phases.Samples were hybridized on aminosilane coated slides with 70-mer oligos.
2011-12-31 | E-GEOD-26585 | biostudies-arrayexpress
Project description:Staphylococcus aureus is a Gram-positive human pathogen causing a variety of human diseases in both hospital and community settings. This bacterium is so closely associated with prophages that it is rare to find S. aureus isolates without prophages. Two phages are known to be important for staphylococcal virulence: the beta-hemolysin (hlb) converting phage and the Panton-Valentine Leukocidin (PVL) converting phage. The hlb-converting phage is found in more than 90% of clinical isolates of S. aureus. This phage produces exotoxins and immune modulatory molecules, which inhibit human innate immune responses. The PVL-converting phage produces the two-component exotoxin PVL, which can kill human leucocytes. This phage is wide-spread among community-associated methicillin resistant S. aureus (CA-MRSA). It also shows strong association with soft tissue infections and necrotizing pneumonia. Several lines of evidence suggest that staphylococcal prophages increase bacterial virulence not only by providing virulence factors but also by altering bacterial gene expression: 1) Transposon insertion into prophage regulatory genes, but not into the genes of virulence factors, reduced S. aureus killing of Caenorhabditis elegans.; 2) Although the toxins and immune modulatory molecules encoded by the hlb- converting phages do not function in the murine system, deletion of phiNM3, the hlb-converting phage in S. aureus Newman, reduced staphylococcal virulence in the murine abscess formation model. 3) In a preliminary microarray experiment, prophages in S. aureus Newman altered the expression of more than 300 genes. In this research proposal, using microarray and high-throughput quantitative RT-PCR (qRT-PCR) technologies, we will identify the effects of the two important staphylococcal phages on the gene expression of S. aureus in both in vitro and in vivo conditions. This project is intended to be completed within one year. All the data – microarray, qRT-PCR and all the primer sequences- will be made available to public 6 month after completion. Data from this project will help us to understand the role of prophages in the S. aureus pathogenesis and can lead to development of a strategy to interfere with the pathogenesis process.
2011-12-31 | GSE26756 | GEO
Project description:Staphylococcus aureus is a Gram-positive human pathogen causing a variety of human diseases in both hospital and community settings. This bacterium is so closely associated with prophages that it is rare to find S. aureus isolates without prophages. Two phages are known to be important for staphylococcal virulence: the beta-hemolysin (hlb) converting phage and the Panton-Valentine Leukocidin (PVL) converting phage. The hlb-converting phage is found in more than 90% of clinical isolates of S. aureus. This phage produces exotoxins and immune modulatory molecules, which inhibit human innate immune responses. The PVL-converting phage produces the two-component exotoxin PVL, which can kill human leucocytes. This phage is wide-spread among community-associated methicillin resistant S. aureus (CA-MRSA). It also shows strong association with soft tissue infections and necrotizing pneumonia. Several lines of evidence suggest that staphylococcal prophages increase bacterial virulence not only by providing virulence factors but also by altering bacterial gene expression: 1) Transposon insertion into prophage regulatory genes, but not into the genes of virulence factors, reduced S. aureus killing of Caenorhabditis elegans.; 2) Although the toxins and immune modulatory molecules encoded by the hlb- converting phages do not function in the murine system, deletion of NM3, the hlb-converting phage in S. aureus Newman, reduced staphylococcal virulence in the murine abscess formation model. 3) In a preliminary microarray experiment, prophages in S. aureus Newman altered the expression of more than 300 genes. In this research proposal, using microarray and high-throughput quantitative RT-PCR (qRT-PCR) technologies, we will identify the effects of the two important staphylococcal phages on the gene expression of S. aureus in both in vitro and in vivo conditions. This project is intended to be completed within one year. All the data – microarray, qRT-PCR and all the primer sequences- will be made available to public 6 month after completion. Data from this project will help us to understand the role of prophages in the S. aureus pathogenesis and can lead to development of a strategy to interfere with the pathogenesis process.
2011-12-31 | GSE26585 | GEO
Project description:Staphylococcus aureus is a Gram-positive human pathogen causing a variety of human diseases in both hospital and community settings. This bacterium is so closely associated with prophages that it is rare to find S. aureus isolates without prophages. Two phages are known to be important for staphylococcal virulence: the beta-hemolysin (hlb) converting phage and the Panton-Valentine Leukocidin (PVL) converting phage. The hlb-converting phage is found in more than 90% of clinical isolates of S. aureus. This phage produces exotoxins and immune modulatory molecules, which inhibit human innate immune responses. The PVL-converting phage produces the two-component exotoxin PVL, which can kill human leucocytes. This phage is wide-spread among community-associated methicillin resistant S. aureus (CA-MRSA). It also shows strong association with soft tissue infections and necrotizing pneumonia. Several lines of evidence suggest that staphylococcal prophages increase bacterial virulence not only by providing virulence factors but also by altering bacterial gene expression: 1) Transposon insertion into prophage regulatory genes, but not into the genes of virulence factors, reduced S. aureus killing of Caenorhabditis elegans.; 2) Although the toxins and immune modulatory molecules encoded by the hlb- converting phages do not function in the murine system, deletion of ϕNM3, the hlb-converting phage in S. aureus Newman, reduced staphylococcal virulence in the murine abscess formation model. 3) In a preliminary microarray experiment, prophages in S. aureus Newman altered the expression of more than 300 genes. In this research proposal, using microarray and high-throughput quantitative RT-PCR (qRT-PCR) technologies, we will identify the effects of the two important staphylococcal phages on the gene expression of S. aureus in both in vitro and in vivo conditions. This project is intended to be completed within one year. All the data – microarray, qRT-PCR and all the primer sequences- will be made available to public 6 month after completion. Data from this project will help us to understand the role of prophages in the S. aureus pathogenesis and can lead to development of a strategy to interfere with the pathogenesis process. Following strains were grown in TSA broth: Staphylococcus aureus USA300 (reference) Staphylococcus aureus USA300 with deletion of ϕSa2usa (Query) Staphylococcus aureus USA300 with deletion of ϕSa3usa (Query) Staphylococcus aureus USA300 Prophage-free mutant (Query) Staphylococcus aureus USA300 Prophage-free mutant lysogenized with ϕSa2mw (Query) Staphylococcus aureus USA300 Prophage-free mutant lysogenized with ϕSa3usa (Query) strain: Staphylococcus aureus USA300 Prophage-free mutant lysogenized with both ϕSa2mw and ϕSa3usa (Query) RNA samples were harvested at early log, midlog and stationary phase.Samples were hybridized on aminosilane coated slides with 70-mer oligos.
2011-02-28 | E-GEOD-26623 | biostudies-arrayexpress
Project description:Background: S. aureus is one of the main pathogen involved in ruminant mastitis worldwide. The severity of staphylococcal infection is highly variable and ranges from subclinical to gangrenous mastitis. Such variability implies host as well as staphylococcal factors. This work is an in-depth characterization of S. aureus mastitis isolates to identify factors involved in mastitis severity. Methods and findings: We combined three “omic” approaches to comprehensively compare two clonally related S. aureus strains that were isolated from and shown to reproducibly induce severe (strain O11) and milder (strain O46) mastitis in ewes. The genomes of O11 and O46 were sequenced (Illumina technology) to determine their respective gene content and comparative transcriptomic and proteomic analyses were carried out on both strains grown in conditions mimicking mastitis context. High differences were highlighted in mobile genetic elements, iron acquisition and metabolism, transcriptional regulation and exoprotein production. In particular, O11 overproduced exoproteins, including toxins and proteases when compared to O46. This was confirmed in 4 other S. aureus strains isolated from subclinical or clinical mastitis cases. Dose-dependant production of some staphylococcal factors seem to play a role in hypervirulence of strains isolated from severe mastitis. Mobile genetic elements, transcriptional regulators, exoproteins or strain ability to deal with iron starvation constitute good targets for further research to better define the underlying mechanisms of mastitis severity. Conclusions: Differences observed in mastitis severity likely result from the ability of the strains to adapt and to express virulence factors in the mastitis context rather than from deep variations in gene content. Expression of S. aureus O46 from subclinical mastitis and O11 from a lethal gangrenous mastitis were compared at two different times
2011-11-11 | E-GEOD-25084 | biostudies-arrayexpress
Project description:Background: S. aureus is one of the main pathogen involved in ruminant mastitis worldwide. The severity of staphylococcal infection is highly variable and ranges from subclinical to gangrenous mastitis. Such variability implies host as well as staphylococcal factors. This work is an in-depth characterization of S. aureus mastitis isolates to identify factors involved in mastitis severity. Methods and findings: We combined three “omic” approaches to comprehensively compare two clonally related S. aureus strains that were isolated from and shown to reproducibly induce severe (strain O11) and milder (strain O46) mastitis in ewes. The genomes of O11 and O46 were sequenced (Illumina technology) to determine their respective gene content and comparative transcriptomic and proteomic analyses were carried out on both strains grown in conditions mimicking mastitis context. High differences were highlighted in mobile genetic elements, iron acquisition and metabolism, transcriptional regulation and exoprotein production. In particular, O11 overproduced exoproteins, including toxins and proteases when compared to O46. This was confirmed in 4 other S. aureus strains isolated from subclinical or clinical mastitis cases. Dose-dependant production of some staphylococcal factors seem to play a role in hypervirulence of strains isolated from severe mastitis. Mobile genetic elements, transcriptional regulators, exoproteins or strain ability to deal with iron starvation constitute good targets for further research to better define the underlying mechanisms of mastitis severity. Conclusions: Differences observed in mastitis severity likely result from the ability of the strains to adapt and to express virulence factors in the mastitis context rather than from deep variations in gene content.
2011-11-11 | GSE25084 | GEO