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

Jill E. Callahan, Cindy Munro, Todd Kitten

Research output: Contribution to journalArticle

9 Citations (Scopus)

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.

Original languageEnglish (US)
Article numbere26403
JournalPLoS One
Volume6
Issue number10
DOIs
StatePublished - Oct 25 2011
Externally publishedYes

Fingerprint

Streptococcus sanguinis
Regulon
regulon
endocarditis
Endocarditis
Streptococcus
Mental Competency
Virulence
virulence
Genes
rabbits
Rabbits
Streptococcus mutans
Streptococcus pneumoniae
Strain control
Sigma Factor
Quorum Sensing
Dental Plaque
sigma factors
Regulator Genes

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

The streptococcus sanguinis competence regulon is not required for infective endocarditis virulence in a rabbit model. / Callahan, Jill E.; Munro, Cindy; Kitten, Todd.

In: PLoS One, Vol. 6, No. 10, e26403, 25.10.2011.

Research output: Contribution to journalArticle

@article{2a87dcf3bbd344f6a9807589bff4a336,
title = "The streptococcus sanguinis competence regulon is not required for infective endocarditis virulence in a rabbit model",
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.",
author = "Callahan, {Jill E.} and Cindy Munro and Todd Kitten",
year = "2011",
month = "10",
day = "25",
doi = "10.1371/journal.pone.0026403",
language = "English (US)",
volume = "6",
journal = "PLoS One",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "10",

}

TY - JOUR

T1 - The streptococcus sanguinis competence regulon is not required for infective endocarditis virulence in a rabbit model

AU - Callahan, Jill E.

AU - Munro, Cindy

AU - Kitten, Todd

PY - 2011/10/25

Y1 - 2011/10/25

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=80054793128&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80054793128&partnerID=8YFLogxK

U2 - 10.1371/journal.pone.0026403

DO - 10.1371/journal.pone.0026403

M3 - Article

C2 - 22039480

AN - SCOPUS:80054793128

VL - 6

JO - PLoS One

JF - PLoS One

SN - 1932-6203

IS - 10

M1 - e26403

ER -