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Infection and Immunity, January 2003, p. 211-217, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.211-217.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Cleavage of Antigen-Bound Immunoglobulin G by SpeB Contributes to Streptococcal Persistence in Opsonizing Blood

Anna Eriksson1,2* and Mari Norgren1

Department of Biomedical Laboratory of Science,1 Department of Clinical Bacteriology, Umeå University, S-901 85 Umeå, Sweden2

Received 4 March 2002/ Returned for modification 10 June 2002/ Accepted 23 September 2002

Group A streptococci (GAS) express a superantigen, SpeB, having cysteine protease activity. SpeB exhibits several properties that might contribute to virulence, the most recently discovered being the ability to cleave immunoglobulin G (IgG) in a manner similar to that of papain. In the present study, we confirmed this latter finding and found that the irreversible inhibition of SpeB protease activity completely abolishes IgG cleavage. SpeB cleavage of IgG was not species restricted since SpeB cleaved both human, rabbit, and mouse IgG. In order to investigate the nature of the SpeB cleavage of IgG, antibodies were immobilized prior to exposure to SpeB, either by unspecific binding of the Fc to GAS surface proteins or by antigen-specific binding. Analysis of the IgG molecules by SDS-PAGE showed that SpeB could cleave antigen-bound antibodies, while the IgG bound to IgG-binding proteins was protected from cleavage. In a phagocytosis assay using whole blood, the M49 GAS strain NZ131 showed a significantly higher survival than its isogenic speB mutant. Furthermore, the addition of extracellular supernatant derived from an overnight culture of native NZ131 increased the survival of its isogenic speB derivative. This indicates that SpeB's ability to cleave off the Fc part of antigen-bound IgG contributes to GAS escape from opsonophagocytosis while not interfering with the formation of a host-like coat by unspecific IgG binding.

* Corresponding author. Mailing address: Department of Clinical Bacteriology, Umeå University, S-901 85 Umeå, Sweden. Phone: 46 90 785 23 47. Fax: 46 90 785 22 45. E-mail: anna.eriksoon{at}climi.umu.se.

Editor: E. I. Tuomanen

Infection and Immunity, January 2003, p. 211-217, Vol. 71, No. 1
0019-9567/03/$08.00+0     DOI: 10.1128/IAI.71.1.211-217.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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