Related Experiment Videos
Role of monocytes in experimental Staphylococcus aureus endocarditis
M H Veltrop1, M J Bancsi, R M Bertina
1Department of Infectious Diseases, Leiden University Medical Center, Leiden, The Netherlands. mhamveltrop@LUMC.NL
Infection and Immunity
|July 19, 2000
Summary
Staphylococcus aureus induces tissue factor activity in monocytes during bacterial endocarditis. Monocytes play a protective role, but high bacterial loads can impair this function, impacting vegetation formation and clotting.
Area of Science:
- Microbiology
- Hematology
- Pathogenesis
Background:
- Bacterial endocarditis (BE) pathogenesis involves the clotting system and tissue factor (TF).
- Staphylococcus aureus is a common cause of BE.
- TF is crucial for coagulation pathway activation in vegetations.
Purpose of the Study:
- To investigate if Staphylococcus aureus induces TF activity (TFA) on fibrin-adherent monocytes in vitro.
- To assess the effect of S. aureus infection on vegetational TFA in vivo in rabbits.
- To evaluate the role of monocytes in S. aureus endocarditis.
Main Methods:
- In vitro study using fibrin-adherent monocytes and S. aureus.
- In vivo study in rabbits with catheter-induced vegetations.
- Assessment of TF activity, bacterial load, monocyte damage, and vegetation characteristics.
Main Results:
- S. aureus induced TFA on fibrin-adherent monocytes, with optimal activity at a 1:1 bacterium/monocyte ratio.
- In vivo, S. aureus increased vegetation weight but not TFA, likely due to high bacterium/monocyte ratios and monocyte damage.
- Monocytopenia in rabbits led to rapid death and absence of vegetations, indicating a protective role for monocytes.
Conclusions:
- S. aureus induces TFA in fibrin-adherent monocytes, similar to other bacteria.
- Monocytes exhibit a protective effect in S. aureus endocarditis.
- The bacterium/monocyte ratio and monocyte damage influence TFA and disease outcome.