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Selective distribution of a high-affinity plasminogen-binding site among group A streptococci associated with
M D Svensson1, U Sjöbring, D E Bessen
1Department of Laboratory Medicine, Lund University, Lund, Sweden.
Abstract:
Group A streptococci can be classified according to their tendency to cause either impetigo, pharyngitis, or both types of infection. Genotypic markers for tissue site preference lie within emm genes, which encode fibrillar surface proteins that play a key role in virulence. emm gene products (M and M-like proteins) display an extensive array of binding activities for tissue and plasma proteins of the human host. In a previous study, a high-affinity binding site for human plasmin(ogen) was mapped to the emm53 gene product. In this report, a structurally similar plasminogen-binding domain is found to be widely and selectively distributed among group A streptococci harboring the emm gene marker for the skin as the preferred tissue site for infection. The findings are highly suggestive of a central role for bacterial modulation of host plasmin(ogen) during localized infection at the epidermis.
Insights
Group A Streptococcus skin infections are linked to specific emm genes. These genes produce proteins that bind to human plasminogen, suggesting a key role in skin infections.
Area of Science:
- Microbiology
- Molecular Biology
- Infectious Diseases
Background:
- Group A Streptococcus (GAS) causes impetigo and pharyngitis.
- emm genes encode surface proteins crucial for GAS virulence.
- emm gene products bind human tissue and plasma proteins.
Purpose of the Study:
- To investigate the role of plasminogen-binding domains in GAS tissue tropism.
- To identify genetic markers associated with skin-predominant GAS infections.
Main Methods:
- Analysis of emm gene sequences and protein domains.
- Comparison of GAS strains with different infection profiles (skin vs. throat).
Main Results:
- A plasminogen-binding domain, similar to that in emm53, is prevalent in GAS strains causing skin infections.
- This domain is selectively distributed among emm-genotyped GAS isolates.
Conclusions:
- Bacterial modulation of host plasminogen is critical for epidermal infections caused by GAS.
- The identified plasminogen-binding domain is a potential virulence factor for skin infections.