Undefined
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB64404 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11862305_1.fastq.gz | Fastqsanger.gz | |||
| ERR11862305_2.fastq.gz | Fastqsanger.gz | |||
| ERR11862306_1.fastq.gz | Fastqsanger.gz | |||
| ERR11862306_2.fastq.gz | Fastqsanger.gz | |||
| ERR11862307_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 94 |
Similar Datasets
Project description:Streptococcus pyogenes (Group A Streptococcus: GAS) is a major human pathogen that causes streptococcal pharyngitis, skin and soft-tissue infections, and life-threatening conditions such as streptococcal toxic shock syndrome (STSS). A large number of virulence-related genes are encoded on GAS genomes, which are involved in host-pathogen interaction, colonization, immune invasion, and long-term survival within hosts, causing the diverse symptoms. Here, we investigated the interaction between GAS-derived extracellular vesicles and host cells in order to reveal pathogenicity mechanisms induced by GAS infection.
2021-05-17 | PXD026040 | JPOST Repository
Project description:Group C Streptococcus dysgalactiae subsp. dysgalactiae (GCS) field strains causative of bovine mastitis and group C or group G Streptococcus dysgalactiae subsp. equisimilis (GCS/GGS) isolates from human infections were tested for the presence of virulence genes employing a microarray containing 220 virulence genes of S. pyogenes (GAS).
2011-05-05 | E-MEXP-3168 | biostudies-arrayexpress
Project description:Microarray was performed on RNA extracted from mid-logarithmic phase in vitro grown non-M1 Streptococcus pyogenes isolates, with either intact or mutant covRS operons. These isolates were compared with corresponding M1 covRS intact and mutant forms to link the expression prolfiles of these non-M1 isolates with invasive pathogenesis.
2010-08-27 | GSE23825 | GEO
Project description:Expression of the extensive arsenal of virulence factors by Streptococcus pyogenes are controlled by many regulators, of which covR/S is one of the best characterized and can influence ~15% of the genome. Animal models have established that mutants of CovR/S arise spontaneously in vivo resulting in highly invasive organisms. We analyzed a pharyngeal and a blood isolate of S. pyogenes recovered from the same individual 13 days apart. The two isolates varied in many phenotypic properties including speB production, which were reflected in transcriptome analyses. Pulsed field gel electrophoresis, multilocus sequence typing, and partial sequencing of some key genes failed to show any differences except for an 11-base insert in the covS gene in the blood isolate. These results showing that pharyngeal and blood isolates from a single individual which differ by a simple insertion, provide evidence for the model that regulatory gene mutations allow S. pyogenes to invade different niches in the body. A chip study using total RNA recovered from two separate wild-type cultures of group A Streptococcus, Streptococcus pyogenes UH322 and UH328. Each chip measures the expression level of 1865 genes replicated twice from 7 fully sequenced strains of Streptococcus pyogenes (M1_GAS NC_002737; MGAS10394 NC_006086; MGAS315 NC_004070; MGAS5005 NC_007297; MGAS6180 NC_007296; MGAS8232 NC_003485; SSI-1 NC_004606 with fourteen 24-mer probe pairs (PM/MM) per gene, with three-fold technical redundancy.
2010-05-01 | E-GEOD-21316 | biostudies-arrayexpress
Project description:Streptococcus dysgalactiae subspecies equisimilis (SDSE) is a Gram-positive bacterial pathogen that infects humans and is closely related to group A streptococcus (GAS). Compared to GAS, far less is known about SDSE pathobiology. Increased rates of invasive SDSE infections have recently been reported in many countries. One SDSE emm type, stG62647, is known to cause severe diseases, including necrotizing soft-tissue infections, endocarditis, and osteoarticular infections. To increase our understanding of the molecular pathogenesis of stG62647 SDSE isolates causing human infections, we sequenced to closure the genomes of 120 stG62647 SDSE isolates. The genomes varied in size from 2.1 to 2.24 megabase pairs. Consistent with previous data, the great majority of stG62647 isolates had IS1548 integrated into the silB gene, thereby inactivating it. Regions of difference in gene content, including putative mobile genetic elements, were the largest source of genomic diversity. All 120 stG62647 isolates were assayed for virulence using a well-established mouse model of necrotizing myositis. An unexpectedly wide range of virulence was identified (20% to 95%), as assessed by near-mortality data. To explore the molecular mechanisms underlying virulence differences, we analyzed RNAseq transcriptome profiles for 38 stG62647 isolates (comprising the 19 least and most virulent) grown in vitro. Genetic polymorphisms were identified from whole-genome sequence data. Collectively, the results suggest that these SDSE isolates use multiple genetic pathways to achieve an altered virulence phenotype. Our study integrates genomic, mouse virulence, and RNAseq data to advance our understanding of SDSE pathobiology and its molecular pathogenesis.
2024-07-20 | GSE272047 | GEO
Project description:CsrRS is a two component regulator which is known to regulate 10-18 % of the genome of the closely related Streptococcus pyogenes. We aimed to look for transcriptional differences between pairs of naturally occurring Streptococcus equi strains where one possessed a SNP in csrRS whereas the other did not. Such SNPs have not been identified in isolates from acute disease but have been identified in persistent isolates.
2018-10-01 | E-MTAB-5872 | biostudies-arrayexpress
Project description:Streptococcus pyogenes (group A streptococci; GAS) is the main causative pathogen of monomicrobial necrotizing soft tissue infections (NSTIs). To resist immuno-clearance, GAS adapt their genetic information and/or phenotype to the surrounding environment. Hyper-virulent streptococcal pyrogenic exotoxin B (SpeB) negative variants caused by covRS mutations are enriched during infection. A key driving force for this process is the bacterial Sda1 DNase. Here, we identify another strategy resulting in SpeB-negative variants, namely reversible abrogation of SpeB secretion triggered by neutrophil effector molecules. Analysis of NSTI patient tissue biopsies revealed that tissue inflammation, neutrophil influx, and degranulation positively correlate with increasing frequency of SpeB-negative GAS clones. Using single colony proteomics, we show that GAS isolated directly from tissue express but do not secrete SpeB. Once the tissue pressure is lifted, GAS regain SpeB secreting function. Neutrophils were identified as the main immune cells responsible for the observed phenotype. Subsequent analyses identified hydrogen peroxide and hypochlorous acid as reactive agents driving this phenotypic GAS adaptation to the tissue environment. SpeB-negative GAS show improved survival within neutrophils and induce increased degranulation. Our findings provide new information about GAS fitness and heterogeneity in the soft tissue milieu and provide new potential targets for therapeutic intervention in NSTIs.
2023-10-24 | PXD040160 | Pride
Project description:The human pathogen Streptococcus pyogenes, or group A streptococcus, is responsible for mild infections to life-threatening diseases. We previously have performed the transcription start site profiling of a Streptococcus pyogenes emm1 strain, strain S119, an invasive strain isolated from a blood culture. Here, we perform strand-specific RNA-seq experiments to complete this characterization and analyze the global coverage and the differential expression in growth medium complemented or not with 15 mM MgCl2. In addition we compare these results to those obtained with a related strain, strain S126, corresponding to a colonization sample, that differs from S119 by only one mutation in the two-component regulator of virulence CovRS.
2018-11-30 | E-MTAB-7101 | biostudies-arrayexpress
Project description:Origin of LA-MRSA CC398 bloodstream infections and skin and soft tissue infections, Denmark
| PRJEB19505 | ENA