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Infection and Immunity, November 1998, p. 5399-5405, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Impact of M49, Mrp, Enn, and C5a Peptidase Proteins on Colonization of the Mouse Oral Mucosa by Streptococcus pyogenes

Yinduo Ji,1 Norbert Schnitzler,2 Eric DeMaster,1 and Patrick Cleary1,*

Department of Microbiology, University of Minnesota, Minneapolis, Minnesota,1 and Institute of Medical Microbiology and National Reference Laboratory for Streptococci, University Hospital, Aachen, Germany2

Received 29 June 1998/Accepted 27 August 1998

Resistance to phagocytosis is a hallmark of virulent Streptococcus pyogenes (group A streptococcus). Surface-bound C5a peptidase reduces recruitment of phagocytes to the site of infection, and hyaluronic acid capsules and/or the M protein limit the uptake of streptococci. In this study the relative impact of M and M-like proteins and the C5a peptidase on the virulence of a serotype M49 strain was assessed. The capacities of isogenic strains with an insertion mutation in emm49; with a deletion mutation in scpA49 (C5a peptidase gene); and with a deletion that removes all three M-like genes, mrp49, emm49, and enn49, to colonize mice and resist phagocytosis were compared. Experiments confirmed results obtained in an earlier study, which showed that the M49 protein was not required for in vitro resistance to phagocytosis, and also showed that the M protein was not required for colonization of mice. Failure to produce all three M-like proteins, M49, Mrp, and Enn49, significantly reduced the ability of these streptococci to resist phagocytosis in vitro but did not significantly alter the persistence of streptococci on the oral mucosa. In vitro experiments indicate that M+ streptococci are phagocytized by polymorphonuclear leukocytes that have been activated with phorbol-12-myristate 13-acetate or recombinant human C5a. This observation may explain the finding that expression of M49 protein is not essential for short-term colonization of the mouse oral mucosa.

* Corresponding author. Mailing address: Box 196 FUMC, Department of Microbiology, University of Minnesota, Minneapolis, MN 55455. Phone: (612) 624-6190. Fax: (612) 626-0623. E-mail: cleary{at}lenti.med.umn.edu.

Infection and Immunity, November 1998, p. 5399-5405, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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