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Streptococcus pyogenes strain:5448

ABSTRACT: Genome-wide Discovery of Novel M1T1 Group A Streptococcal Determinants Important for Fitness and Virulence During Soft-Tissue Infection

PROVIDER: PRJNA391181 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5800860.fastq.gz	Fastqsanger.gz
	SRR5800861.fastq.gz	Fastqsanger.gz
	SRR5800862.fastq.gz	Fastqsanger.gz
	SRR5800853.fastq.gz	Fastqsanger.gz
	SRR5800863.fastq.gz	Fastqsanger.gz

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Comparison of gene expression in the GAS M1T1 strain 5448, wild-type vs pepO mutant

Project description:Manuscript title: The endopeptidase PepO regulates the SpeB cysteine protease and is essential for the virulence of invasive M1T1 Streptococcus pyogenes. The study investigates the effect of pepO mutation on global gene expression in GAS M1T1 strain 5448.

2018-01-05 | GSE108748 | GEO

Streptococcus pyogenes strain:M1T1 5448

Project description:Tn-seq analysis of M1T1 5448 Group A Streptococcus (GAS) genetic fitness under Metal Stress Conditions

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Proteome analysis of extracellular vesicles released from Streptococcus pyogenes

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

Streptococcus pyogenes strain:5448

Project description:RofA Regulon of M1T1 Group A Streptococcus pyogenes 5448

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Streptococcus pyogenes strain:5448

Project description:M1T1 Group A Streptococcus Transcriptome in glucose versus fructose

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Streptococcus pyogenes strain:5448

Project description:Impact of the ScfCDE L-tryptophan transporter on M1T1 Group A Streptococcus pyogenes 5448 transcriptome.

| PRJNA1037583 | ENA

Transcriptomic comparison of serotype M1 S. pyogenes

Project description:S. pyogenes strains were compared with the intact covRS form of the globally disseminated M1T1 clone to track transcriptomic changes engendered during the emergence of the M1T1 clone. The mutant covRS form of the M1T1 clone was included as a transcriptomic outlier and to provide a context for the magnitude of transcriptional shifts detected within the isolate set examined.

2012-08-21 | GSE35568 | GEO

Microarray analysis for Streptococcus pyogenes M1-CdhA (-) mutant

Project description:A total of 163 genes were found to be differentially expressed; 38 genes of them were up regulated and 125 genes were down regulated. Most notably the functional categories that were affected include Virulence genes (18 genes 11% of the total significantly differentiated genes), carbohydrate metabolism and cell envelop realted genes ( 31, 19.1% of the total), and aminoacid transport genes (21genes, 12.9%). Among the virulence-related genes, the most notable one were those belong to the production of capsule, the M protein, exotoxin, NAD glycohydrolase and Streptolysin S. Some of the capsule related genes were down regulated by more than 64 fold. These results indicate that CdhA (group A Streptococcal Cell division controlling and Chain-forming cell wall hydrolase) plays an important role in the regulation of virulence.

2010-10-01 | GSE15546 | GEO

Streptococcus pyogenes strain:strain 5448

Project description:Transcriptomic profiling of Streptococcus pyogenes M1T1 strain in a mouse model of necrotizing fasciitis

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Neutrophil-derived reactive agents induce a transient SpeB negative phenotype in Streptococcus pyogenes

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

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