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Development and Assessment of Intracellular Infection Models for Staphylococcus aureus
Published on: January 17, 2025
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Staphylococcus aureus-induced complement activation promotes tissue factor-mediated coagulation
E W Skjeflo1,2, D Christiansen1, H Fure1
1Research Laboratory, Nordland Hospital, Bodø, Norway.
Journal of Thrombosis and Haemostasis : JTH
|February 14, 2018
Summary
Staphylococcus aureus infection triggers blood coagulation via complement system activation, specifically C5a-induced tissue factor production. Inhibiting complement component C5 significantly reduced this effect, highlighting complement
Area of Science:
- Immunology
- Hematology
- Microbiology
Background:
- Extensive cross-talk exists between the complement system, Toll-like receptors (TLRs), and hemostasis.
- Consumptive coagulopathy, marked by increased tissue factor (TF) expression, is a hallmark of sepsis.
- Staphylococcus aureus bacteremia involves complex interactions between these systems.
Purpose of the Study:
- To investigate the roles of complement, TLRs, and TF in Staphylococcus aureus-induced coagulation.
- To elucidate the mechanisms of thromboinflammation in a human whole-blood model.
Main Methods:
- Human whole blood was incubated with S. aureus strains (Cowan, Wood, Newman).
- Specific inhibitors were used: compstatin (C3), eculizumab (C5), peptide inhibitors (C5aR1, FXII), and neutralizing antibodies (CD14, TLR2, TF), eritoran (TLR4).
- Measurements included complement activation (ELISA), coagulation markers (PTF1+2 ELISA), and TF expression/activity (qPCR, flow cytometry, ELISA).
Main Results:
- S. aureus induced significant C5a generation, complement activation, TF production, and coagulation.
- Inhibition of C5 cleavage was most effective in reducing coagulation markers and TF activity.
- Complement inhibition's effect was dependent on C5a receptor 1 (C5aR1) and potentiated by CD14 or TLR2 inhibition.
Conclusions:
- Staphylococcus aureus-induced coagulation in human whole blood is primarily driven by C5a-mediated TF upregulation.
- The complement system is a key mediator in S. aureus-induced coagulation.
- Combined inhibition strategies targeting complement and TF show potential for managing thromboinflammation.
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