This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by McKay, F. C.
Right arrow Articles by Walker, M. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McKay, F. C.
Right arrow Articles by Walker, M. J.

 Previous Article  |  Next Article 

Infection and Immunity, January 2004, p. 364-370, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.364-370.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Plasminogen Binding by Group A Streptococcal Isolates from a Region of Hyperendemicity for Streptococcal Skin Infection and a High Incidence of Invasive Infection

Fiona C. McKay,1 Jason D. McArthur,1,{dagger} Martina L. Sanderson-Smith,1 Sandra Gardam,1,{ddagger} Bart J. Currie,2,3 Kadaba S. Sriprakash,2,3,4 Peter K. Fagan,5,§ Rebecca J. Towers,2,3 Michael R. Batzloff,4 Gursharan S. Chhatwal,5 Marie Ranson,1 and Mark J. Walker1*

Department of Biological Sciences, University of Wollongong, Wollongong, New South Wales 2522,1 Menzies School of Health Research,2 Cooperative Research Centre for Aboriginal and Tropical Health, Darwin, Northern Territory 0810,3 and Queensland Institute of Medical Research, Herston, Queensland 4006, Australia,4 German National Centre for Biotechnology, Braunschweig 38124, Germany5

Received 15 May 2003/ Returned for modification 10 July 2003/ Accepted 9 September 2003

Reports of resurgence in invasive group A streptococcal (GAS) infections come mainly from affluent populations with infrequent exposure to GAS. In the Northern Territory (NT) of Australia, high incidence of invasive GAS disease is secondary to endemic skin infection, serotype M1 clones are rare in invasive infection, the diversity and level of exposure to GAS strains are high, and no particular strains dominate. Expression of a plasminogen-binding GAS M-like protein (PAM) has been associated with skin infection in isolates elsewhere (D. Bessen, C. M. Sotir, T. M. Readdy, and S. K. Hollingshead, J. Infect. Dis. 173:896-900, 1996), and subversion of the host plasminogen system by GAS is thought to contribute to invasion in animal models. Here, we describe the relationship between plasminogen-binding capacity of GAS isolates, PAM genotype, and invasive capacity in 29 GAS isolates belonging to 25 distinct strains from the NT. In the presence of fibrinogen and streptokinase, invasive isolates bound more plasminogen than isolates from uncomplicated infections (P <= 0.004). Only PAM-positive isolates bound substantial levels of plasminogen by a fibrinogen-streptokinase-independent pathway (direct binding). Despite considerable amino acid sequence variation within the A1 repeat region of PAM where the plasminogen-binding domain maps, the critical lysine residue was conserved.

* Corresponding author. Mailing address: Department of Biological Sciences, University of Wollongong, Wollongong, NSW 2522, Australia. Phone: 61-2-4221-3439. Fax: 61-2-4221-4135. E-mail: mwalker{at}uow.edu.au.

Editor: S. H. E. Kaufmann

{dagger} Present address: Queensland Institute of Medical Research, Queensland 4006, Australia.

{ddagger} Present address: Centenary Institute, Royal Prince Alfred Hospital Grounds, Camperdown, New South Wales 2050, Australia.

§ Present address: Menzies School of Health Research and Cooperative Research Centre for Aboriginal and Tropical Health, Darwin, Northern Territory 0810, Australia.

Infection and Immunity, January 2004, p. 364-370, Vol. 72, No. 1
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.1.364-370.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Cork, A. J., Jergic, S., Hammerschmidt, S., Kobe, B., Pancholi, V., Benesch, J. L. P., Robinson, C. V., Dixon, N. E., Aquilina, J. A., Walker, M. J. (2009). Defining the Structural Basis of Human Plasminogen Binding by Streptococcal Surface Enolase. J. Biol. Chem. 284: 17129-17137 [Abstract] [Full Text]  
  • McArthur, J. D., McKay, F. C., Ramachandran, V., Shyam, P., Cork, A. J., Sanderson-Smith, M. L., Cole, J. N., Ringdahl, U., Sjobring, U., Ranson, M., Walker, M. J. (2008). Allelic variants of streptokinase from Streptococcus pyogenes display functional differences in plasminogen activation. FASEB J. 22: 3146-3153 [Abstract] [Full Text]  
  • Sanderson-Smith, M. L., Dinkla, K., Cole, J. N., Cork, A. J., Maamary, P. G., McArthur, J. D., Chhatwal, G. S., Walker, M. J. (2008). M protein-mediated plasminogen binding is essential for the virulence of an invasive Streptococcus pyogenes isolate. FASEB J. 22: 2715-2722 [Abstract] [Full Text]  
  • Fu, Q., Figuera-Losada, M., Ploplis, V. A., Cnudde, S., Geiger, J. H., Prorok, M., Castellino, F. J. (2008). The Lack of Binding of VEK-30, an Internal Peptide from the Group A Streptococcal M-like Protein, PAM, to Murine Plasminogen Is due to Two Amino Acid Replacements in the Plasminogen Kringle-2 Domain. J. Biol. Chem. 283: 1580-1587 [Abstract] [Full Text]  
  • Sanderson-Smith, M. L., Dowton, M., Ranson, M., Walker, M. J. (2007). The Plasminogen-Binding Group A Streptococcal M Protein-Related Protein Prp Binds Plasminogen via Arginine and Histidine Residues. J. Bacteriol. 189: 1435-1440 [Abstract] [Full Text]  
  • Sanderson-Smith, M. L., Walker, M. J., Ranson, M. (2006). The Maintenance of High Affinity Plasminogen Binding by Group A Streptococcal Plasminogen-binding M-like Protein Is Mediated by Arginine and Histidine Residues within the a1 and a2 Repeat Domains. J. Biol. Chem. 281: 25965-25971 [Abstract] [Full Text]  
  • Sun, H. (2006). The interaction between pathogens and the host coagulation system.. Physiology 21: 281-288 [Abstract] [Full Text]  
  • Cole, J. N., McArthur, J. D., McKay, F. C., Sanderson-Smith, M. L., Cork, A. J., Ranson, M., Rohde, M., Itzek, A., Sun, H., Ginsburg, D., Kotb, M., Nizet, V., Chhatwal, G. S., Walker, M. J. (2006). Trigger for group A streptococcal M1T1 invasive disease. FASEB J. 20: 1745-1747 [Abstract] [Full Text]  
  • Sanderson-Smith, M., Batzloff, M., Sriprakash, K. S., Dowton, M., Ranson, M., Walker, M. J. (2006). Divergence in the Plasminogen-binding Group A Streptococcal M Protein Family: FUNCTIONAL CONSERVATION OF BINDING SITE AND POTENTIAL ROLE FOR IMMUNE SELECTION OF VARIANTS. J. Biol. Chem. 281: 3217-3226 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»