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Journal of Bacteriology, February 2005, p. 1105-1113, Vol. 187, No. 3
0021-9193/05/$08.00+0     doi:10.1128/JB.187.3.1105-1113.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Regulation of Virulence by a Two-Component System in Group B Streptococcus{dagger}

Sheng-Mei Jiang,1,2 Michael J. Cieslewicz,1,2 Dennis L. Kasper,1,2,3 and Michael R. Wessels1,2,4*

Channing Laboratory, Brigham and Women's Hospital,1 Division of Infectious Diseases, Children's Hospital Boston,4 Department of Microbiology and Molecular Genetics,3 Harvard Medical School, Boston, Massachusetts2

Received 14 July 2004/ Accepted 2 November 2004

Group B Streptococcus (GBS) is frequently carried in the gastrointestinal or genitourinary tract as a commensal organism, yet it has the potential to cause life-threatening infection in newborn infants, pregnant women, and individuals with chronic illness. Regulation of virulence factor expression may affect whether GBS behaves as an asymptomatic colonizer or an invasive pathogen, but little is known about how such factors are controlled in GBS. We now report the characterization of a GBS locus that encodes a two-component regulatory system similar to CsrRS (or CovRS) in Streptococcus pyogenes. Inactivation of csrR, encoding the putative response regulator, in two unrelated wild-type strains of GBS resulted in a marked increase in production of beta-hemolysin/cytolysin and a striking decrease in production of CAMP factor, an unrelated cytolytic toxin. Quantitative RNA hybridization experiments revealed that these two phenotypes were associated with a marked increase and decrease in expression of the corresponding genes, cylE and cfb, respectively. The CsrR mutant strains also displayed increased expression of scpB encoding C5a peptidase. Similar, but less marked, changes in gene expression were observed in CsrS (putative sensor component) mutants, evidence that CsrR and CsrS constitute a functional two-component system. Experimental infection studies in mice demonstrated reduced virulence of both CsrR and CsrS mutant strains relative to the wild type. Together, these results indicate that CsrRS regulates expression of multiple GBS virulence determinants and is likely to play an important role in GBS pathogenesis.

* Corresponding author. Mailing address: Children's Hospital Boston, 300 Longwood Ave., Boston, MA 02115. Phone: (617) 919-2900. Fax: (617) 730-0254. E-mail: michael.wessels{at}childrens.harvard.edu.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

Journal of Bacteriology, February 2005, p. 1105-1113, Vol. 187, No. 3
0021-9193/05/$08.00+0     doi:10.1128/JB.187.3.1105-1113.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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