IAI Accepts, published online ahead of print on 29 June 2009

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Infect. Immun. doi:10.1128/IAI.00228-09
Copyright (c) 2009, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The NanA neuraminidase of Streptococcus pneumoniae is involved in biofilm formation

Dane Parker, Grace Soong, Paul Planet, Jonathan Brower, Adam J Ratner, and Alice Prince^*

Department of Pediatrics and Pharmacology, College of Physicians and Surgeons, Columbia University, New York, New York, USA; Department of Pediatrics and Microbiology, College of Physicians and Surgeons, Columbia University, New York, New York, USA

^* To whom correspondence should be addressed. Email: asp7{at}columbia.edu.

Streptococcus pneumoniae remains a major cause of bacteremia, pneumonia and otitis media despite vaccines and effective antibiotics. The neuraminidase of S. pneumoniae, which catalyzes the release of terminal sialic acid residues from glycoconjugates, is involved in host colonization in animal models of infection and may provide a novel target to prevent pneumococcal infection. We demonstrate that the S. pneumoniae neuraminidase (NanA) cleaves sialic acid and show that it is involved in biofilm formation, suggesting an additional role in pathogenesis, and sharing this property with the neuraminidase of Pseudomonas aeruginosa even though we show the two enzymes are phylogenetically divergent. Using an in vitro model of biofilm formation incorporating human airway epithelial cells, we demonstrate that small molecule inhibitors of NanA block biofilm formation and may provide a novel target for preventative therapy. This work highlights the role played by the neuraminidase in pathogenesis and represents an important step in drug development to prevent colonization of the respiratory tract by this important pathogen.

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