Kitten Lab Research

Currently Funded Research:

• (2011-2012) NIH-NIAID 1R56AI085195 Kitten (PI) Endocarditis virulence in Streptococcus sanguinis.
• (2011-2012) Presidential Research Incentive Program  Kitten (PI) Examination of the role of Mn-dependent superoxide dismutase in SsaB-mediated oxygen tolerance and endocarditis virulence.
• (2008-2013)  NIH-NIDCR R01DE18138  Xu (PI) Regulation of fitness and virulence in oral streptococci. 

Research Interests:

We are interested in examining oral bacteria using genetic, genomic, post-genomic, and molecular biological approaches. We are particularly interested in examining Streptococcus sanguinis in the two different environments in which it is most often found—the mouth and infected heart valves. In the first case, we are interested in identifying factors affecting the fitness of this bacterium in the mouth and its ability to serve as a beneficial member of the normal flora by competing with oral pathogens. In the second case, we are interested in determining how S. sanguinis causes the serious cardiac infection known as infective endocarditis. We have recently identified a protein produced by S. sanguinis that is absolutely required for infective endocarditis causation but has no demonstrable importance in the mouth. We are investigating this protein as a promising target for preventing harmful infections such as infective endocarditis without eliminating beneficial oral colonization. These projects have been facilitated by the sequencing of the genome of S. sanguinis. 

Recent Publications:        Perform a PubMed search

Kitten, T., Munro, C. L., Zollar, N. Q., Lee, S. P., and Patel, R. D. (2012) Oral streptococcal bacteremia in hospitalized patients: taxonomic identification and clinical characterization. J Clin Microbiol. in press.

Xu, P, Ge, X, Chen, L, Dou, Y, Wang, X, Patel, J. R., Trinh, M., Evans, K., Stone, V., Kitten T., Bonchev, D., and Buck, G. A. 2011. Genome-wide essential gene identification in Streptococcus sanguinis. Sci. Rep. 1: DOI: 10.1038/srep00125.

Callahan, J. E., Munro C.L., and Kitten, T. 2011. The Streptococcus sanguinis competence regulon is not required for infective endocarditis virulence in a rabbit model. PLoS ONE 6:e26403.

Rodriguez, A. M., Callahan, J. E., Fawcett, P. Ge, X., Xu, P., and Kitten, T. 2011. Physiological and molecular characterization of genetic competence in Streptococcus sanguinis. Mol Oral Microbiol. 26: 99-116.

Kitten, T., Turner, L. S., and Xu, P. 2011. Biological implications of the Streptococcus sanguinis genome, p. 43-61. In P. E. Kolenbrander (ed.), Oral Microbial Communities: Genomic Inquiry and Interspecies Communication. ASM Press, Washington, D.C.

Jones D.J., Munro C.L., Grap M.J., Kitten T., and Edmond M. 2010. Oral care and bacteremia risk in mechanically ventilated adults. Heart Lung: 39:S57-65.

Ge, X., Kitten, T., Munro, C. L., Conrad, D. H., and Xu, P. 2010. Pooled protein immunization for identification of cell surface antigens in Streptococcus sanguinis. PLoS ONE 5:e11666.

Turner, L. S., Kanamoto, T., Unoki, T., Munro, C. L., Wu, H., and Kitten, T. 2009. A comprehensive evaluation of Streptococcus sanguinis cell wall-anchored proteins in early infective endocarditis. Infect. Immun. 77: 4966-4975.

Turner, L. S., Das, S., Kanamoto, T., Munro, C. L., and Kitten, T. 2009. Development of genetic tools for in vivo virulence analysis of Streptococcus sanguinis. Microbiology 155: 2573-2582.

Das, S., Kanamoto, T., Ge, X., Xu, P., Unoki, T., Munro, C. L., and Kitten, T. 2009. Contribution of lipoproteins and lipoprotein processing to endocarditis virulence in Streptococcus sanguinis. J. Bacteriol 191:4166-4179.

Tang, G., Kitten, T., Munro, C. L., Wellman, G. C., and Mintz, K. P. 2008. EmaA, a potential virulence determinant of Aggregatibacter (Actinobacillus) actinomycetemcomitans in infective endocarditis. Infect Immun 76:2316-2324.

Ge, X., Kitten, T., Chen, Z., Lee, S. P., Munro, C. L., and Xu, P. 2008. Identification of Streptococcus sanguinis genes required for biofilm formation and examination of their role in endocarditis virulence. Infect Immun 76:2551-2559.

Xu, P., J. M. Alves, T. Kitten, A. Brown, Z. Chen, L. S. Ozaki, P. Manque, X. Ge, M. G. Serrano, D. Puiu, S. Hendricks, Y. Wang, M. D. Chaplin, D. Akan, S. Paik, D. L. Peterson, F. L. Macrina, and G. A. Buck. 2007. Genome of the opportunistic pathogen Streptococcus sanguinis. J Bacteriol 189:3166-3175.

Paik, S., Senty, L., Das, S., Noe, J. C., Munro, C. L., & Kitten, T. 2005. Identification of virulence determinants for endocarditis in Streptococcus sanguinis by signature-tagged mutagenesis. Infect Immun 73:6064-74.

Das, S., Noe, J. C., Paik, S., & Kitten, T. 2005. An improved arbitrary primed PCR method for rapid characterization of transposon insertion sites. J Microbiol Methods 63: 89-94.

Paik, S. Brown, A. Munro, C. L. Cornelissen, C. N. & Kitten, T. 2003. The sloABCR Operon of Streptococcus mutans Encodes a Mn and Fe Transport System Required for Endocarditis Virulence and its Mn-Dependent Repressor. J. Bacteriol. 185: 5967-5975.

Califano, J.V., Arimoto, T., & Kitten, T. 2003. The genetic relatedness of Porphyromonas gingivalis clinical and laboratory strains assessed by analysis of insertion sequence (IS) element distribution. J. Periodont. Res. 38: 411-416.

Kitten, T., Munro, C. L., Wang, A., & Macrina, F. L. 2002. Vaccination with FimA from Streptococcus parasanguis protects rats from endocarditis caused by other viridans streptococci. Infect. Immun. 70:422-425.

Kitten, T., Munro, C. L., Michalek, S. M., & Macrina, F. L. 2000. Genetic characterization of a Streptococcus mutans LraI family operon and role in virulence. Infect. Immun. 68:4441-4451.

Califano, J. V., Kitten, T., Lewis, J. P., Macrina, F. L., Fleischmann, R. D., Frasier, C. M., Duncan, M. J., & Dewhirst, F. E. 2000. Characterization of the Porphyromonas gingivalis Insertion Sequence-Like Element, ISPg5. Infect. Immun. 68:5247-5253.

Training Opportunities:
Opportunities for research rotations often arise, dependent upon the availability of space and resources. The most successful laboratory experiences usually involve extended or recurring commitments.