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Tissue factor is a major stimulus for vegetation formation in enterococcal endocarditis in rabbits
The Journal of Clinical Investigation
|June 1, 1984
Summary
Enterococcal endocarditis involves vegetation formation. Host cells expressing tissue factor, not bacteria, initiate local coagulation, driving fibrin deposition in vegetations.
Area of Science:
- Microbiology
- Cardiovascular Research
- Hematology
Background:
- Enterococcal endocarditis is a serious infection characterized by vegetation formation on heart valves.
- The mechanisms initiating local coagulation within these vegetations are not fully understood.
- Understanding these mechanisms is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the role of contact activation and tissue factor expression in the local initiation of coagulation during enterococcal endocarditis vegetation formation.
- To determine whether bacteria or host cells are responsible for initiating procoagulant activity.
Main Methods:
- A rabbit model of enterococcal endocarditis was utilized.
- Freshly excised aortic valves were assessed for contact activation and tissue factor expression using cell-based assays.
- Bacterial load and tissue factor activity were quantified in infected and control valves.
Main Results:
- Bacteria alone did not exhibit procoagulant activity.
- Excised valves did not spontaneously activate plasma contact factors.
- Infected valves, even early in infection (1-2 days) and in immune-compromised animals, demonstrated significant tissue factor activity.
- Tissue factor activity correlated with infection, not bacterial numbers within vegetations.
Conclusions:
- Host cell-derived tissue factor expression, triggered by infection, is the primary initiator of local coagulation in enterococcal endocarditis.
- This tissue factor activity is a key driver of fibrin deposition, contributing significantly to vegetation development.
- Targeting host tissue factor may be a viable therapeutic strategy for enterococcal endocarditis.
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