Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1271746 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33822793_1.fastq.gz | Fastqsanger.gz | |||
| SRR33822793_2.fastq.gz | Fastqsanger.gz | |||
| SRR33822794_1.fastq.gz | Fastqsanger.gz | |||
| SRR33822794_2.fastq.gz | Fastqsanger.gz |
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Project description:The opportunistic pathogen Staphylococcus aureus is carried asymptomatically by about one-third of the human population. Body sites known to be colonized by S. aureus are the skin, nasopharynx and gut. In particular, the mechanisms that allow S. aureus to pass the gut epithelial barrier and to invade the bloodstream are poorly understood. Therefore, our present study was aimed at investigating possible differences between gut-colonizing and bacteremia isolates of S. aureus. To this end, 74 gut-colonizing isolates from healthy individuals and 144 blood-culture isolates were characterized by whole-genome sequencing. Subsequently, the cellular and extracellular proteomes of six representative isolates were examined by mass spectrometry. Lastly, the virulence potential of these isolates was evaluated using infection models based on human gut epithelial cells, blood cells, and a small animal infection model. Intriguingly, our results show that gut-colonizing and bacteremia isolates with the same sequence type (ST1 or ST5) are very similar at the genomic and proteomic levels. Nonetheless, they display differences in virulence, but gut-colonizing isolates may be more virulent than bacteremia isolates and vice versa. Importantly, we show that the main decisive factor preventing infection of gut epithelial cells in vitro is the presence of a tight barrier. Based on our present observations, we propose that the integrity of the gut epithelial layer, rather than the pathogenic potential of a gut-colonizing S. aureus strain, is the main decisive factor that determines whether this colonizer will become an invasive pathogen.
2023-03-11 | PXD030971 | Pride
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: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.
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Project description:Staphylococcus aureus is the most common cause of hospital-acquired infection. In healthy hosts outside of the health care setting, S.aureus is a frequent colonizer of the human nose but rarely causes severe invasive infection such as bacteremia, endocarditis, or osteomyelitis. To identify genes associated with community-acquired invasive isolates, regions of genomic variability, and the S.aureus population structure, we compared 61 community-acquired invasive isolates of S.aureus and 100 nasal carriage isolates from healthy donors using a microarray spotted with PCR products representing every gene from the seven S.aureus sequencing projects. The core genes common to all strains were identified, and 10 dominant lineages of S.aureus were clearly discriminated. Each lineage carried a unique combination of hundreds of core variable (CV) genes scattered throughout the chromosome, suggesting a common ancestor but early evolutionary divergence. Many CV genes are regulators of virulence genes or known or predicted to be expressed on the bacterial surface and to interact with the host during nasal colonization and infection. Within each lineage, isolates showed substantial variation in the carriage of mobile genetic elements and their associated virulence and resistance genes, indicating frequent horizontal transfer. However, we were unable to identify any association between lineage or gene and invasive isolates. We suggest that the S.aureus gene combinations necessary for invasive disease may also be necessary for nasal colonization and that community-acquired invasive disease is strongly dependent on host factors. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-33
2007-01-30 | E-BUGS-33 | biostudies-arrayexpress
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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.
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Project description:Staphylococcus aureus is a major human pathogen and resistant to numerous clinically used antibiotics. The first antibiotic developed for S. aureus infections was the nonribosomal petide secondary metabolite penicillin. We discovered cryptic nonribosomal peptide secondary metabolites, the aureusimines, made by S. aureus itself that are not antibiotics, but function as small molecule regulators of virulence factor expression. Using established rules and codes for nonribosomal peptide assembly we predicted these nonribosomal peptides, and used these predictions to identify them from S. aureus culture broths. Functional studies using global microarray and mouse bacteremia models established that the aureusimines control virulence factor expression and are necessary for productive infections. This is the first report of the aureusimines and has important implications for the treatment of drug resistant S. aureus. Targeting aureusimine synthesis may provide novel anti-infectives. Commerically available S. aureus GeneChips (Affymetrix) were used to compare biological replicates of early and late exponential phase wild type (Newman) and aureusimine defective (ausA) organisms.
2010-07-30 | E-GEOD-21373 | biostudies-arrayexpress
Project description:Panton-valentine leukocidin (PVL) has been linked to worldwide emergence of community-associated methicillin resistant Staphylococcus aureus (CA-MRSA) -- its role in virulence in unclear. Here we show that PVL had no effect on global gene expression of prominent CA-MRSA strains nor did it affect bacterial clearance from lungs, spleen and kidneys in a highly discriminatory rabbit bacteremia model. These findings negate a large body of epidemiological research that implicated PVL in CA-MRSA virulence. Keywords: mutant vs wild type in 2 different growth phases grown in 2 different medias
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Project description:Staphylococcus aureus is a pulmonary pathogen associated with substantial human morbidity and mortality. As vaccines targeting virulence determinants have failed to be protective in humans, other factors are likely involved in pathogenesis. Here we analysed transcriptomic responses of human clinical isolates of S. aureus from initial and chronic infections. We observed upregulated collagenase and proline transporter gene expression in chronic infection isolates. Metabolomics of bronchiolar lavage fluid, fibroblast infection, growth assays and analysis of bacterial mutant strains showed that airway fibroblasts produce collagen during S. aureus infection. Host-adapted bacteria upregulate collagenase, which degrades collagen and releases proline. S. aureus then imports proline, which fuels oxidative metabolism via the tricarboxylic acid cycle. Proline metabolism provides host-adapted S. aureus with a metabolic benefit enabling out-competition of non-adapted strains. These data suggest that clinical settings characterized by airway repair processes and fibrosis provide a milieu that promotes S. aureus adaptation and supports infection.
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