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The Streptococcus sanguinis competence regulon is not required for infective endocarditis virulence in a rabbit model.

Callahan JE, Munro CL, Kitten T - PLoS ONE (2011)

Bottom Line: Strains deleted for the comCDE or comX master regulatory genes were created.These results suggest that the com regulon is not required for S. sanguinis infective endocarditis virulence in this model.We propose that the different roles of the S. sanguinis, S. pneumoniae, and S. mutans com regulons in virulence can be understood in relation to the pathogenic mechanisms employed by each species.

View Article: PubMed Central - PubMed

Affiliation: VCU Philips Institute of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, Virginia, United States of America.

ABSTRACT
Streptococcus sanguinis is an important component of dental plaque and a leading cause of infective endocarditis. Genetic competence in S. sanguinis requires a quorum sensing system encoded by the early comCDE genes, as well as late genes controlled by the alternative sigma factor, ComX. Previous studies of Streptococcus pneumoniae and Streptococcus mutans have identified functions for the >100-gene com regulon in addition to DNA uptake, including virulence. We investigated this possibility in S. sanguinis. Strains deleted for the comCDE or comX master regulatory genes were created. Using a rabbit endocarditis model in conjunction with a variety of virulence assays, we determined that both mutants possessed infectivity equivalent to that of a virulent control strain, and that measures of disease were similar in rabbits infected with each strain. These results suggest that the com regulon is not required for S. sanguinis infective endocarditis virulence in this model. We propose that the different roles of the S. sanguinis, S. pneumoniae, and S. mutans com regulons in virulence can be understood in relation to the pathogenic mechanisms employed by each species.

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Examination of com mutants by competitive index analysis in a rabbit model of endocarditis.Each symbol represents data from a single rabbit. (A) CI values from rabbits inoculated with 108 CFU. Median CI values from the combined results of two experiments are indicated in parentheses and by horizontal bars. The CI value for each rabbit was calculated as the ratio of mutant/JFP36 in the vegetation homogenate divided by the mutant/JFP36 ratio in the inoculum. Neither median value was significantly different from 1.0. (B) Recovery of competing strains from infected vegetations at multiple inoculum levels. Each pair of connected circles indicates recovery of JFP36 (filled circles) and JFP49 (open circles) from the same rabbit. Data for the 108 inoculum are from experiments depicted in panel A. Dashed line, limit of detection.
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pone-0026403-g001: Examination of com mutants by competitive index analysis in a rabbit model of endocarditis.Each symbol represents data from a single rabbit. (A) CI values from rabbits inoculated with 108 CFU. Median CI values from the combined results of two experiments are indicated in parentheses and by horizontal bars. The CI value for each rabbit was calculated as the ratio of mutant/JFP36 in the vegetation homogenate divided by the mutant/JFP36 ratio in the inoculum. Neither median value was significantly different from 1.0. (B) Recovery of competing strains from infected vegetations at multiple inoculum levels. Each pair of connected circles indicates recovery of JFP36 (filled circles) and JFP49 (open circles) from the same rabbit. Data for the 108 inoculum are from experiments depicted in panel A. Dashed line, limit of detection.

Mentions: Once we had confirmed that our com regulatory mutants had the expected phenotypes, we wanted to determine if the com regulon contributes to IE virulence in S. sanguinis. We began by testing the comCDE and comX mutants by competitive index (CI) assays in our standard rabbit endocarditis model [8]–[11], [22]. Rabbits catheterized to induce sterile vegetations were co-inoculated with ∼108 CFU of one of the mutants and JFP36—an Emr derivative of SK36 that we have shown to be indistinguishable in multiple traits, including growth rate, genetic competence, and virulence for IE [22]. CI values for each rabbit are presented Fig. 1A. Median CI values for both mutants were slightly greater than 1.0, although neither difference was statistically significant (P = 0.063 for the comCDE mutant and 0.56 for the comX mutant). The results suggested that neither comCDE nor comX was required for IE virulence in our standard assay.


The Streptococcus sanguinis competence regulon is not required for infective endocarditis virulence in a rabbit model.

Callahan JE, Munro CL, Kitten T - PLoS ONE (2011)

Examination of com mutants by competitive index analysis in a rabbit model of endocarditis.Each symbol represents data from a single rabbit. (A) CI values from rabbits inoculated with 108 CFU. Median CI values from the combined results of two experiments are indicated in parentheses and by horizontal bars. The CI value for each rabbit was calculated as the ratio of mutant/JFP36 in the vegetation homogenate divided by the mutant/JFP36 ratio in the inoculum. Neither median value was significantly different from 1.0. (B) Recovery of competing strains from infected vegetations at multiple inoculum levels. Each pair of connected circles indicates recovery of JFP36 (filled circles) and JFP49 (open circles) from the same rabbit. Data for the 108 inoculum are from experiments depicted in panel A. Dashed line, limit of detection.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3198404&req=5

pone-0026403-g001: Examination of com mutants by competitive index analysis in a rabbit model of endocarditis.Each symbol represents data from a single rabbit. (A) CI values from rabbits inoculated with 108 CFU. Median CI values from the combined results of two experiments are indicated in parentheses and by horizontal bars. The CI value for each rabbit was calculated as the ratio of mutant/JFP36 in the vegetation homogenate divided by the mutant/JFP36 ratio in the inoculum. Neither median value was significantly different from 1.0. (B) Recovery of competing strains from infected vegetations at multiple inoculum levels. Each pair of connected circles indicates recovery of JFP36 (filled circles) and JFP49 (open circles) from the same rabbit. Data for the 108 inoculum are from experiments depicted in panel A. Dashed line, limit of detection.
Mentions: Once we had confirmed that our com regulatory mutants had the expected phenotypes, we wanted to determine if the com regulon contributes to IE virulence in S. sanguinis. We began by testing the comCDE and comX mutants by competitive index (CI) assays in our standard rabbit endocarditis model [8]–[11], [22]. Rabbits catheterized to induce sterile vegetations were co-inoculated with ∼108 CFU of one of the mutants and JFP36—an Emr derivative of SK36 that we have shown to be indistinguishable in multiple traits, including growth rate, genetic competence, and virulence for IE [22]. CI values for each rabbit are presented Fig. 1A. Median CI values for both mutants were slightly greater than 1.0, although neither difference was statistically significant (P = 0.063 for the comCDE mutant and 0.56 for the comX mutant). The results suggested that neither comCDE nor comX was required for IE virulence in our standard assay.

Bottom Line: Strains deleted for the comCDE or comX master regulatory genes were created.These results suggest that the com regulon is not required for S. sanguinis infective endocarditis virulence in this model.We propose that the different roles of the S. sanguinis, S. pneumoniae, and S. mutans com regulons in virulence can be understood in relation to the pathogenic mechanisms employed by each species.

View Article: PubMed Central - PubMed

Affiliation: VCU Philips Institute of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, Virginia, United States of America.

ABSTRACT
Streptococcus sanguinis is an important component of dental plaque and a leading cause of infective endocarditis. Genetic competence in S. sanguinis requires a quorum sensing system encoded by the early comCDE genes, as well as late genes controlled by the alternative sigma factor, ComX. Previous studies of Streptococcus pneumoniae and Streptococcus mutans have identified functions for the >100-gene com regulon in addition to DNA uptake, including virulence. We investigated this possibility in S. sanguinis. Strains deleted for the comCDE or comX master regulatory genes were created. Using a rabbit endocarditis model in conjunction with a variety of virulence assays, we determined that both mutants possessed infectivity equivalent to that of a virulent control strain, and that measures of disease were similar in rabbits infected with each strain. These results suggest that the com regulon is not required for S. sanguinis infective endocarditis virulence in this model. We propose that the different roles of the S. sanguinis, S. pneumoniae, and S. mutans com regulons in virulence can be understood in relation to the pathogenic mechanisms employed by each species.

Show MeSH
Related in: MedlinePlus