Bacteriophage content of M49 strains of<i>Streptococcus pyogenes</i>

Suvorov, Alexander; Polyakova, Ekaterina M.; McShan, W. Michael; Ferretti, Joseph J.

doi:10.1111/j.1574-6968.2009.01538.x

Cited by 5 publications

(4 citation statements)

References 21 publications

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“…Groups of mice were i.n. immunized with the M1 strain 90–226 three times and challenged with M1 (highly invasive), M49 (noninvasive) [21] or M28 streptococci (associated with puerperal sepsis and neonatal infections and the common cause of other invasive infections and pharyngitis in many countries) [22]. 24 hr after challenge viable bacteria associated with NALT were determined.…”

Section: Resultsmentioning

confidence: 99%

Sortase A Induces Th17-Mediated and Antibody-Independent Immunity to Heterologous Serotypes of Group A Streptococci

Fan

Wang

et al. 2014

PLoS ONE

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Group A streptococci (GAS) are associated with a variety of mucosal and invasive human infections. Recurrent infections by highly heterologous serotypes indicate that cross-serotype immunity is critical for prevention of GAS infections; however, mechanisms underlying serotype-independent protection are poorly understood. Here we report that intranasal vaccination of mice with Sortase A (SrtA), a conserved cell wall bound protein, reduced colonization of nasal-associated lymphoid tissue (NALT) by heterologous serotypes of GAS. Vaccination significantly increased CD4+ IL-17A+ cells in NALT and depletion of IL-17A by neutralizing antibody prevented GAS clearance from NALT which was dependent on immunization with SrtA. Vaccination also induced high levels of SrtA-specific antibodies; however, immunized, B cell-deficient mice cleared streptococcal challenges as efficiently as wild type mice, indicating that the cross-serotype protection is Th17-biased and antibody-independent. Furthermore, efficient GAS clearance from NALT was associated with a rapid neutrophil influx into NALT of immunized mice. These results suggest that serotype independent immune protection against GAS mucosal infection can be achieved by intranasal vaccination with SrtA and enhanced neutrophil function is critical for anti-GAS defense and might be a target for prevention of GAS infections.

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Section: Resultsmentioning

confidence: 99%

Sortase A Induces Th17-Mediated and Antibody-Independent Immunity to Heterologous Serotypes of Group A Streptococci

Fan

Wang

et al. 2014

PLoS ONE

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“…M serotypes associated with SpyCI carriage currently include M1, M2, M4, M5, M6, M18, M25, M28, M31, M37, M49, M53, M59, M78, and M123 (Scott et al, 2008, 2012; Suvorov et al, 2009). Currently, it is not known whether SpyCI infect only a subset of S. pyogenes serotypes, perhaps defined by surface targets for phage attachment, or whether most serotypes may serve as SpyCI hosts and the current sample size is simply too small.…”

Section: Spycim1 and The Host Mutator Phenotypementioning

confidence: 99%

Chromosomal islands of Streptococcus pyogenes and related streptococci: molecular switches for survival and virulence

Nguyen

McShan

2014

Front. Cell. Infect. Microbiol.

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Streptococcus pyogenes is a significant pathogen of humans, annually causing over 700,000,000 infections and 500,000 deaths. Virulence in S. pyogenes is closely linked to mobile genetic elements like phages and chromosomal islands (CI). S. pyogenes phage-like chromosomal islands (SpyCI) confer a complex mutator phenotype on their host. SpyCI integrate into the 5′ end of DNA mismatch repair (MMR) gene mutL, which also disrupts downstream operon genes lmrP, ruvA, and tag. During early logarithmic growth, SpyCI excise from the bacterial chromosome and replicate as episomes, relieving the mutator phenotype. As growth slows and the cells enter stationary phase, SpyCI reintegrate into the chromosome, again silencing the MMR operon. This system creates a unique growth-dependent and reversible mutator phenotype. Additional CI using the identical attachment site in mutL have been identified in related species, including Streptococcus dysgalactiae subsp. equisimilis, Streptococcus anginosus, Streptococcus intermedius, Streptococcus parauberis, and Streptococcus canis. These CI have small genomes, which range from 13 to 20 kB, conserved integrase and DNA replication genes, and no identifiable genes encoding capsid proteins. SpyCI may employ a helper phage for packaging and dissemination in a fashion similar to the Staphylococcus aureus pathogenicity islands (SaPI). Outside of the core replication and integration genes, SpyCI and related CI show considerable diversity with the presence of many indels that may contribute to the host cell phenotype or fitness. SpyCI are a subset of a larger family of streptococcal CI who potentially regulate the expression of other host genes. The biological and phylogenetic analysis of streptococcal chromosomal islands provides important clues as to how these chromosomal islands help S. pyogenes and other streptococcal species persist in human populations in spite of antibiotic therapy and immune challenges.

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“…All isolates sequenced thus far are polylysogenized, with as many as eight bacteriophages in the chromosome, which can constitute as much as 10% of the genome (20). These lambda-like viruses belong to the family Siphoviridae and often encode important virulence factors, including superantigens, hyaluronidases, and secreted nucleases (8,25,41,50). Although some of the bacteriophage-encoded virulence genes were previously shown to be expressed during the course of infection, relatively little is known about the molecular factors that control their expression (54).…”

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confidence: 99%

Identification of Rgg Binding Sites in the Streptococcus pyogenes Chromosome

Anbalagan

et al. 2011

J Bacteriol

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Streptococcus pyogenes Rgg is a regulatory protein that controls the transcription of 588 genes in strain NZ131 during the post-exponential phase of growth, including the virulence-associated genes encoding the extracellular SpeB protease, pullulanase A (PulA), and two extracellular nucleases (SdaB and Spd-3). Rgg binds to DNA proximally to the speB promoter (PspeB) to activate transcription; however, it is not known if Rgg binds to the promoters of other genes to influence expression, or if the perturbation of other global regulons accounts for the genome-wide changes in expression associated with the mutant. To address this issue, chromatin immunoprecipitation followed by DNA microarray analysis (ChIP-chip) was used to identify the DNA binding sites of Rgg. Rgg bound to 65 sites in the chromosome. Thirty-five were within noncoding DNA, and 43% of these were adjacent to genes previously identified as regulated by Rgg. Electrophoretic mobility shift assays were used to assess the binding of Rgg to a subset of sites bound in vivo, including the noncoding DNA upstream of speB, the genes encoding PulA, Spd-3, and a transcriptional regulator (SPY49_1113), and prophage-associated genes encoding a putative integrase (SPY49_0746) and a surface antigen (SPY49_0396). Rgg bound to all target DNAs in vitro, consistent with the in vivo results. Finally, analyses with a transcriptional reporter system showed that the DNA bound by Rgg contained an active promoter that was regulated by Rgg. Overall, the results indicate that Rgg binds specifically to multiple sites in the chromosome, including prophage DNA, to influence gene expression.

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Bacteriophage content of M49 strains ofStreptococcus pyogenes

Cited by 5 publications

References 21 publications

Sortase A Induces Th17-Mediated and Antibody-Independent Immunity to Heterologous Serotypes of Group A Streptococci

Sortase A Induces Th17-Mediated and Antibody-Independent Immunity to Heterologous Serotypes of Group A Streptococci

Chromosomal islands of Streptococcus pyogenes and related streptococci: molecular switches for survival and virulence

Identification of Rgg Binding Sites in the Streptococcus pyogenes Chromosome

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