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Infection and Immunity, July 2009, p. 2824-2831, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00986-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Role of Teichoic Acid Choline Moieties in the Virulence of Streptococcus pneumoniae{triangledown}

Florian Gehre,1 Radek Spisek,2,3 Arun S. Kharat,1,4 Phillip Matthews,3 Anjli Kukreja,3 Robert M. Anthony,5 Madhav V. Dhodapkar,3,6 Waldemar Vollmer,7 and Alexander Tomasz1*

Laboratory of Microbiology, The Rockefeller University, New York, New York,1 Second Medical Faculty and University Hospital Moto, Department of Immunology, Prague, Czech Republic,2 Laboratory of Tumor Immunology and Immunotherapy, The Rockefeller University, New York, New York,3 Department of Biotechnology, Marathwada University, Aurungabad, India,4 Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, New York,5 Section of Hematology, Yale University, New Haven, Connecticut,6 Institute for Cell and Molecular Biosciences, University of Newcastle upon Tyne, Newcastle upon Tyne, United Kingdom7

Received 7 August 2008/ Returned for modification 16 September 2008/ Accepted 24 April 2009

In recent reports it was shown that genetically modified choline-free strains of Streptococcus pneumoniae (D39Cho–licA64 and D39ChiplicB31) expressing the type II capsular polysaccharide were virtually avirulent in the murine sepsis model, in sharp contrast to the isogenic and highly virulent strains D39Cho– and D39Chip, which have retained the choline residues at their surface. We now demonstrate that this choline-associated virulence is independent of Toll-like receptor 2 recognition. Also, despite the lack of virulence, choline-free strains of S. pneumoniae were able to activate splenic dendritic cells, induce secretion of proinflammatory cytokines, and produce specific protective immunity against subsequent challenge. However, after this transient engagement of the immune system the choline-free bacteria were rapidly cleared from the blood, while the isogenic virulent strain D39Cho– continued to grow, accompanied by prolonged expression of cytokines, eventually killing the experimental animals. The critical contribution of choline residues to the virulence potential of pneumococci appears to be the role that these amino alcohol residues play in a pneumococcal immune evasion strategy, the mechanism of which is unknown at the present time.

* Corresponding author. Mailing address: Laboratory of Microbiology, The Rockefeller University, 1230 York Avenue, New York, NY 10065. Phone: (212) 327-8278. Fax: (212) 327-8688. E-mail: tomasz{at}rockefeller.edu

{triangledown} Published ahead of print on 11 May 2009.

Editor: A. Camilli

Infection and Immunity, July 2009, p. 2824-2831, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00986-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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