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α-hemolysin of Staphylococcus aureus impairs thrombus formation
Kristin Jahn1, Stefan Handtke2, Raghavendra Palankar2
1Department of Molecular Genetics and Infection Biology, Interfaculty Institute for Genetics and Functional Genomics, Center for Functional Genomics of Microbes, University of Greifswald, Greifswald, Germany.
Journal of Thrombosis and Haemostasis : JTH
|March 18, 2022
Summary
Staphylococcus aureus alpha-hemolysin impairs platelet function and thrombus stability, unlike other toxins. This finding is crucial for treating bacterial bloodstream infections and conditions like endocarditis.
Area of Science:
- Microbiology
- Immunology
- Hematology
Background:
- Pathogen toxins critically influence virulence and can disrupt host immune cell functions, notably platelets.
- Understanding how toxins affect platelets is vital for improving treatments for bacterial bloodstream infections.
Purpose of the Study:
- To investigate the impact of Staphylococcus aureus toxins (alpha-hemolysin, LukAB, LukDE, LukSF) on human platelets.
- To compare these effects with Streptococcus pneumoniae's pneumolysin.
- To assess the influence of these toxins on platelet activation, function, and thrombus formation.
Main Methods:
- Flow cytometry, aggregometry, platelet viability assays, fluorescence microscopy, and intracellular calcium release measurements were employed.
- Platelet activation markers (CD62P, αIIbβ3 integrin) and calcium flux were analyzed.
- Thrombus formation was evaluated in whole blood assays.
Main Results:
- Staphylococcus aureus alpha-hemolysin (Hla) initially activates platelets but ultimately alters their phenotype and impairs thrombus formation.
- Other S. aureus leukocidins (LukAB, LukED, LukSF) and pneumolysin did not significantly affect platelet activation or viability.
- Low concentrations of Hla abrogated thrombus formation in whole blood, indicating impaired stability in S. aureus infections.
- Intravenous immune globulins did not neutralize Hla-induced platelet damage.
Conclusions:
- Staphylococcus aureus alpha-hemolysin significantly impacts platelet function and thrombus stability.
- These findings have potential clinical implications for managing S. aureus-induced endocarditis by targeting Hla to prevent septic embolization.
- Inhibiting Hla's effect on platelets may reduce the risk of micro-embolization in systemic infections.
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