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Pathogen activators of plasminogen.
I M Verhamme1, P R Panizzi2, P E Bock1
1Department of Pathology, Microbiology, and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA.
Journal of Thrombosis and Haemostasis : JTH
|July 8, 2015
Summary
Group A streptococci use streptokinase to activate human plasminogen, forming plasmin on their surface. This process, involving M-like proteins and fibrinogen, aids bacterial spread and infection.
Area of Science:
- Microbiology
- Biochemistry
- Molecular Biology
Background:
- Group A streptococci (GAS) possess virulence factors, including secreted streptokinase (SK) variants.
- GAS pathogenicity is linked to plasminogen (Pg) activation and plasmin (Pm) surface localization, facilitating bacterial dissemination.
- GAS effectively manipulates the host's proteolytic system for its benefit.
Purpose of the Study:
- To elucidate the mechanisms by which GAS activate host plasminogen.
- To understand the role of streptokinase allelic variants in this activation process.
- To define the combined in vivo mechanisms of SK variants and PAM proteins.
Main Methods:
- Discussion of molecular mechanisms, including conformational activation of plasminogen zymogen (Pg*) and subsequent activation by catalytic complexes (S•KPg* and SK•Pm).
- Analysis of bacterial surface coating by plasmin via direct and indirect pathways involving PAM and fibrin(ogen).
- Optimization of transgenic mouse models with human plasminogen to study SK variants in vivo.
Main Results:
- A unified mechanism for GAS usurpation of the host proteolytic system has been substantially delineated.
- Plasmin coats GAS through interactions with PAM protein and fibrin(ogen).
- Ongoing development of mouse models to investigate in vivo mechanisms.
Conclusions:
- GAS employ sophisticated strategies involving streptokinase and plasminogen activation for pathogenicity.
- Understanding these mechanisms is crucial for developing targeted therapies against GAS infections.
- Further in vivo studies are needed to fully characterize the interplay of virulence factors.
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