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Serotype- and strain- dependent contribution of the sensor kinase CovS of the CovRS two-component system to Streptococcus pyogenes pathogenesis.

Sugareva V, Arlt R, Fiedler T, Riani C, Podbielski A, Kreikemeyer B - BMC Microbiol. (2010)

Bottom Line: However, a serotype- and even strain-dependent contribution on survival in whole human blood and biofilm formation was noted, respectively.These data provide new information on the action of the CovS sensor kinase and revealed that its activity on capsule expression and keratinocyte adherence is uniform across serotypes, whereas the influence on biofilm formation and blood survival is serotype or even strain dependent.This adds the CovRS system to a growing list of serotype-specific acting regulatory loci in S. pyogenes.

View Article: PubMed Central - HTML - PubMed

Affiliation: University of Rostock, Medical Faculty, Institute of Medical Microbiology, Virology and Hygiene, Department of Med, Microbiology and Hospital Hygiene, Schillingallee 70, 18055 Rostock, Germany.

ABSTRACT

Background: The Streptococcus pyogenes (group A streptococci, GAS) two-component signal transduction system CovRS has been described to be important for pathogenesis of this exclusively human bacterial species. If this system acts uniquely in all serotypes is currently unclear. Presence of serotype- or strain-dependent regulatory circuits and polarity is an emerging scheme in Streptococcus pyogenes pathogenesis. Thus, the contribution of the sensor kinase (CovS) of the global regulatory two-component signal transduction system CovRS on pathogenesis of several M serotypes was investigated.

Results: CovS mutation uniformly repressed capsule expression and hampered keratinocyte adherence in all tested serotypes. However, a serotype- and even strain-dependent contribution on survival in whole human blood and biofilm formation was noted, respectively.

Conclusions: These data provide new information on the action of the CovS sensor kinase and revealed that its activity on capsule expression and keratinocyte adherence is uniform across serotypes, whereas the influence on biofilm formation and blood survival is serotype or even strain dependent. This adds the CovRS system to a growing list of serotype-specific acting regulatory loci in S. pyogenes.

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Biofilm production of serotype M18 GAS and M18::covS mutant strains. The GAS strains were grown on a polystyrene well surface or plastic coverslips, coated with human collagen type I, for 72 h in static culture. A. Safranin assay. B. Scanning electron microscopy. Different magnifications are presented as follows: 200×, 2000×, 5000× (from lower to upper panel, respectively). The P-value of differences as determined by two-tailed paired Student's t test is shown above the columns in panel A.
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Figure 2: Biofilm production of serotype M18 GAS and M18::covS mutant strains. The GAS strains were grown on a polystyrene well surface or plastic coverslips, coated with human collagen type I, for 72 h in static culture. A. Safranin assay. B. Scanning electron microscopy. Different magnifications are presented as follows: 200×, 2000×, 5000× (from lower to upper panel, respectively). The P-value of differences as determined by two-tailed paired Student's t test is shown above the columns in panel A.

Mentions: As shown in Fig. 2A the inactivation of CovS sensor kinase expression in the M18 serotype led to biofilm defective mutants. This observation was further confirmed by SEM analysis (Fig. 2B). A similar phenotype of biofilm defectiveness was observed for the other CovS mutant GAS serotype strains irrespective of using none-coated or fibronectin-coated polystyrene surfaces (Fig. 3). Inactivation of CovS expression in the M49 serotype background resulted in a biofilm-negative phenotype (Fig. 3A). Even when human fibronectin was used as a matrix protein surface coating, the CovS M49 mutant strain was still defective in biofilm production. Likewise, the M2::covS, M2_583::covS and M18_588::covS mutant strains were attenuated in their biofilm-forming capacity in contrast to the corresponding parental strains (Fig. 3B and 3C).


Serotype- and strain- dependent contribution of the sensor kinase CovS of the CovRS two-component system to Streptococcus pyogenes pathogenesis.

Sugareva V, Arlt R, Fiedler T, Riani C, Podbielski A, Kreikemeyer B - BMC Microbiol. (2010)

Biofilm production of serotype M18 GAS and M18::covS mutant strains. The GAS strains were grown on a polystyrene well surface or plastic coverslips, coated with human collagen type I, for 72 h in static culture. A. Safranin assay. B. Scanning electron microscopy. Different magnifications are presented as follows: 200×, 2000×, 5000× (from lower to upper panel, respectively). The P-value of differences as determined by two-tailed paired Student's t test is shown above the columns in panel A.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2823723&req=5

Figure 2: Biofilm production of serotype M18 GAS and M18::covS mutant strains. The GAS strains were grown on a polystyrene well surface or plastic coverslips, coated with human collagen type I, for 72 h in static culture. A. Safranin assay. B. Scanning electron microscopy. Different magnifications are presented as follows: 200×, 2000×, 5000× (from lower to upper panel, respectively). The P-value of differences as determined by two-tailed paired Student's t test is shown above the columns in panel A.
Mentions: As shown in Fig. 2A the inactivation of CovS sensor kinase expression in the M18 serotype led to biofilm defective mutants. This observation was further confirmed by SEM analysis (Fig. 2B). A similar phenotype of biofilm defectiveness was observed for the other CovS mutant GAS serotype strains irrespective of using none-coated or fibronectin-coated polystyrene surfaces (Fig. 3). Inactivation of CovS expression in the M49 serotype background resulted in a biofilm-negative phenotype (Fig. 3A). Even when human fibronectin was used as a matrix protein surface coating, the CovS M49 mutant strain was still defective in biofilm production. Likewise, the M2::covS, M2_583::covS and M18_588::covS mutant strains were attenuated in their biofilm-forming capacity in contrast to the corresponding parental strains (Fig. 3B and 3C).

Bottom Line: However, a serotype- and even strain-dependent contribution on survival in whole human blood and biofilm formation was noted, respectively.These data provide new information on the action of the CovS sensor kinase and revealed that its activity on capsule expression and keratinocyte adherence is uniform across serotypes, whereas the influence on biofilm formation and blood survival is serotype or even strain dependent.This adds the CovRS system to a growing list of serotype-specific acting regulatory loci in S. pyogenes.

View Article: PubMed Central - HTML - PubMed

Affiliation: University of Rostock, Medical Faculty, Institute of Medical Microbiology, Virology and Hygiene, Department of Med, Microbiology and Hospital Hygiene, Schillingallee 70, 18055 Rostock, Germany.

ABSTRACT

Background: The Streptococcus pyogenes (group A streptococci, GAS) two-component signal transduction system CovRS has been described to be important for pathogenesis of this exclusively human bacterial species. If this system acts uniquely in all serotypes is currently unclear. Presence of serotype- or strain-dependent regulatory circuits and polarity is an emerging scheme in Streptococcus pyogenes pathogenesis. Thus, the contribution of the sensor kinase (CovS) of the global regulatory two-component signal transduction system CovRS on pathogenesis of several M serotypes was investigated.

Results: CovS mutation uniformly repressed capsule expression and hampered keratinocyte adherence in all tested serotypes. However, a serotype- and even strain-dependent contribution on survival in whole human blood and biofilm formation was noted, respectively.

Conclusions: These data provide new information on the action of the CovS sensor kinase and revealed that its activity on capsule expression and keratinocyte adherence is uniform across serotypes, whereas the influence on biofilm formation and blood survival is serotype or even strain dependent. This adds the CovRS system to a growing list of serotype-specific acting regulatory loci in S. pyogenes.

Show MeSH
Related in: MedlinePlus