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Infection and Immunity, May 2004, p. 2964-2975, Vol. 72, No. 5
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.5.2964-2975.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

LuxS Is Required for Persistent Pneumococcal Carriage and Expression of Virulence and Biosynthesis Genes

Elizabeth A. Joyce,1* Amita Kawale,1 Stefano Censini,2 Charles C. Kim,1 Antonello Covacci,2 and Stanley Falkow1

Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305,1 Immunobiological Research Institute of Siena, Chiron Vaccines, Siena, Italy2

Received 5 December 2003/ Returned for modification 16 January 2004/ Accepted 28 January 2004

Streptococcus pneumoniae causes several diseases, including otitis media, pneumonia, and meningitis. Although little is known about the regulation of or how individual pneumococcal factors contribute to these disease states, there is evidence suggesting that some factors are regulated by a cell-density-dependent mechanism (quorum sensing). Quorum sensing allows bacteria to couple transcription with changes in cell density; bacteria achieve this by sensing and responding to small diffusible signaling molecules. We investigated how the LuxS signaling system impacts the biology of S. pneumoniae. An analysis of the transcriptional profiles of a serotype 2 strain and an isogenic luxS deletion strain utilizing an S. pneumoniae-specific microarray indicated that LuxS regulates gene expression involved in discrete cellular processes, including pneumolysin expression. Contrary to the paradigm for quorum sensing, we observed pronounced effects on transcription in early log phase, where gene expression was repressed in the mutant. Assessing the mutant for its ability to infect and cause disease in animals revealed a profound defect in ability to persist in the nasopharyngeal tissues. Our analysis of an S. pneumoniae transcriptome revealed a function for LuxS in gene regulation that is not dependent upon high cell density and is likely involved in the maintenance of pneumococcal load in susceptible hosts.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305-5402. Phone: (650) 723-2671. Fax: (650) 723-1837. E-mail: ejoyce{at}stanford.edu.

Editor: A. D. O'Brien

Infection and Immunity, May 2004, p. 2964-2975, Vol. 72, No. 5
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.5.2964-2975.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



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