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The streptokinase-plasminogen system. I. Its effect on the pathogenicity of streptococci and other organisms for mice
Abstract:
Human plasminogen, plasma, or serum increased the pathogenicity of six streptokinase-positive streptococcal strains for mice. Combinations of commercial streptokinase and plasminogen or streptokinase and plasma did not usually increase mouse mortality to a greater degree than did plasminogen or plasma alone, suggesting that the maximal effective amount of streptokinase was produced by the organisms. The pathogenicity of Salmonella paratyphi (fibrinolysin variable) and a Group D streptococcus (streptokinase-negative) was not increased by plasminogen, plasma, or streptokinase, whereas a combination of streptokinase and plasminogen, or streptokinase and plasma did significantly increase mouse mortality resulting from these organisms. Combinations of certain concentrations of streptokinase and plasminogen increased the pathogenicity of a fibrinolysin-negative staphylococcal strain for mice to a greater extent than did either substance alone. The observed results provide evidence that streptokinase, by an interaction with plasminogen, contributes to the pathogenicity of streptokinase-positive streptococci.
Insights
Streptokinase enhances bacterial pathogenicity by interacting with plasminogen. This interaction increases the virulence of certain streptococcal and staphylococcal strains, impacting host susceptibility.
Area of Science:
- Microbiology
- Immunology
- Pathogenesis
Background:
- Bacterial pathogenicity is influenced by various factors, including enzymes that interact with host systems.
- Streptokinase, an enzyme produced by certain bacteria, is known to activate plasminogen, a key component of the fibrinolytic system.
Purpose of the Study:
- To investigate the role of streptokinase and plasminogen in the pathogenicity of different bacterial strains in a murine model.
- To determine if exogenous streptokinase and plasminogen enhance the virulence of bacteria that do not naturally produce high levels of streptokinase.
Main Methods:
- Administering various bacterial strains (Streptococcus, Salmonella paratyphi, Staphylococcus) to mice.
- Supplementing the bacterial challenge with human plasminogen, plasma, serum, or commercial streptokinase, individually or in combination.
- Assessing the impact on mouse mortality as a measure of pathogenicity.
Main Results:
- Human plasminogen, plasma, or serum increased the pathogenicity of streptokinase-positive streptococci.
- Combinations of streptokinase and plasminogen/plasma did not significantly increase mortality beyond that caused by plasminogen/plasma alone for streptokinase-positive strains.
- Exogenous streptokinase and plasminogen/plasma significantly increased mortality for Salmonella paratyphi and a streptokinase-negative Group D streptococcus.
- Combined streptokinase and plasminogen enhanced the pathogenicity of a fibrinolysin-negative staphylococcal strain more than either substance alone.
Conclusions:
- Streptokinase contributes to the pathogenicity of streptokinase-positive streptococci through interaction with plasminogen.
- The combination of streptokinase and plasminogen can enhance the virulence of bacteria that are otherwise less pathogenic or do not produce sufficient streptokinase.
