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Infection and Immunity, June 2008, p. 2551-2559, Vol. 76, No. 6
0019-9567/08/$08.00+0     doi:10.1128/IAI.00338-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Identification of Streptococcus sanguinis Genes Required for Biofilm Formation and Examination of Their Role in Endocarditis Virulence{triangledown}

Xiuchun Ge,1 Todd Kitten,1,2,3 Zhenming Chen,1,2,3,{dagger} Sehmi P. Lee,1,3,{ddagger} Cindy L. Munro,4 and Ping Xu1,2,3*

The Philips Institute of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, Virginia 23298-0566,1 Center for the Study of Biological Complexity, Virginia Commonwealth University, Richmond, Virginia 23284-2030,2 Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia 23298-0678,3 Department of Adult Health Nursing, Virginia Commonwealth University, Richmond, Virginia 23298-06784

Received 13 March 2008/ Accepted 26 March 2008

Streptococcus sanguinis is one of the pioneers in the bacterial colonization of teeth and is one of the most abundant species in the oral biofilm called dental plaque. S. sanguinis is also the most common viridans group streptococcal species implicated in infective endocarditis. To investigate the association of biofilm and endocarditis, we established a biofilm assay and examined biofilm formation with a signature-tagged mutagenesis library of S. sanguinis. Four genes that have not previously been associated with biofilm formation in any other bacterium, purB, purL, thrB, and pyrE, were putatively identified as contributing to in vitro biofilm formation in S. sanguinis. By examining 800 mutants for attenuation in the rabbit endocarditis model and for reduction in biofilm formation in vitro, we found some mutants that were both biofilm defective and attenuated for endocarditis. However, we also identified mutants with only reduced biofilm formation or with only attenuation in the endocarditis model. This result indicates that the ability to form biofilms in vitro is not associated with endocarditis virulence in vivo in S. sanguinis.

* Corresponding author. Mailing address: The Philips Institute of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, VA 23298-0566. Phone: (804) 827-6264. Fax: (804) 828-0150. E-mail: pxu{at}vcu.edu

{triangledown} Published ahead of print on 7 April 2008.

Editor: A. Camilli

{dagger} Present address: College of Biological & Environmental Engineering, Zhejiang University of Technology, Hangzhou, Zhejiang 310032, China.

{ddagger} Present address: Department of Biomedical Sciences, University of Maryland Dental School, Baltimore, MD 21201.

Infection and Immunity, June 2008, p. 2551-2559, Vol. 76, No. 6
0019-9567/08/$08.00+0     doi:10.1128/IAI.00338-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Turner, L. S., Kanamoto, T., Unoki, T., Munro, C. L., Wu, H., Kitten, T. (2009). Comprehensive Evaluation of Streptococcus sanguinis Cell Wall-Anchored Proteins in Early Infective Endocarditis. Infect. Immun. 77: 4966-4975 [Abstract] [Full Text]  
  • Nobbs, A. H., Lamont, R. J., Jenkinson, H. F. (2009). Streptococcus Adherence and Colonization. Microbiol. Mol. Biol. Rev. 73: 407-450 [Abstract] [Full Text]  
  • Senty Turner, L., Das, S., Kanamoto, T., Munro, C. L., Kitten, T. (2009). Development of genetic tools for in vivo virulence analysis of Streptococcus sanguinis. Microbiology 155: 2573-2582 [Abstract] [Full Text]  
  • Das, S., Kanamoto, T., Ge, X., Xu, P., Unoki, T., Munro, C. L., Kitten, T. (2009). Contribution of Lipoproteins and Lipoprotein Processing to Endocarditis Virulence in Streptococcus sanguinis. J. Bacteriol. 191: 4166-4179 [Abstract] [Full Text]  


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