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Infection and Immunity, December 2002, p. 6646-6651, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6646-6651.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

EndoS and SpeB from Streptococcus pyogenes Inhibit Immunoglobulin-Mediated Opsonophagocytosis

Mattias Collin,1,{dagger} Mikael D. Svensson,2 Anders G. Sjöholm,2 Jens C. Jensenius,3 Ulf Sjöbring,2 and Arne Olsén1*

Department of Cell and Molecular Biology, Lund University, S-221 84 Lund,1 Institute of Laboratory Medicine, University Hospital of Lund, S-221 85 Lund, Sweden,2 Department of Medical Microbiology and Immunology, University of Aarhus, DK-8000 Aarhus, Denmark3

Received 20 May 2002/ Returned for modification 14 August 2002/ Accepted 26 August 2002

The human pathogen Streptococcus pyogenes primarily infects the upper respiratory tract and skin, but occasionally it disseminates and causes severe invasive disease with high mortality. This study revealed that the activity of extracellular EndoS, which hydrolyzes the functionally important N-linked oligosaccharides on opsonizing immunoglobulin G (IgG), contributes to increased survival of S. pyogenes in human blood ex vivo. The inability to kill the bacteria is due to reduced binding of IgG to Fc receptors and impaired classical pathway-mediated activation of complement. In addition, the activity of extracellular SpeB, which cleaves IgG into Fc and Fab fragments, also increases bacterial survival. This suggests that S. pyogenes expresses two enzymes, EndoS and SpeB, which modulate IgG by different mechanisms in order to evade the adaptive immune system.


* Corresponding author. Present address: Department of Clinical Immunology, Göteborg University, Guldhedsgatan 10A, S-413 46 Göteborg, Sweden. Phone: 46 31 342-4895. Fax: 46 31 342-4621. E-mail: arne.olsen{at}immuno.gu.se.

Editor: J. T. Barbieri

{dagger} Present address: Laboratory of Bacterial Pathogenesis and Immunology, The Rockefeller University, New York, NY 10021.


Infection and Immunity, December 2002, p. 6646-6651, Vol. 70, No. 12
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.12.6646-6651.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.




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