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Chlamydia pneumoniae binds to platelets and triggers P-selectin expression and aggregation: a causal role in
Hanna Kälvegren1, Meytham Majeed, Torbjörn Bengtsson
1Division of Medical Microbiology, Department of Molecular and Clinical Medicine, Faculty of Health Sciences, Linköping University, Sweden. hanjo@imk.liu.se
Insights
Chlamydia pneumoniae directly activates human platelets, promoting aggregation and P-selectin expression. This finding reveals a novel mechanism linking this infection to atherosclerosis and thrombotic vascular occlusion.
Area of Science:
- Cardiovascular Research
- Infectious Disease Immunology
- Hematology
Background:
- Growing evidence links Chlamydia pneumoniae to atherosclerotic cardiovascular disease.
- Platelets are crucial in cardiovascular diseases but not previously linked to infectious atherosclerosis.
- The role of Chlamydia pneumoniae in platelet activation remains unclear.
Purpose of the Study:
- To investigate the interaction between Chlamydia pneumoniae and human platelets.
- To elucidate a potential novel mechanism in atherosclerosis pathogenesis involving C. pneumoniae and platelets.
Main Methods:
- Platelet aggregation and secretion assessed using lumiaggregometry.
- Platelet binding and P-selectin expression analyzed via flow cytometry.
- Glycoprotein IIb/IIIa inhibition and polymyxin B exposure used to probe mechanisms.
Main Results:
- Chlamydia pneumoniae adheres to platelets, triggering P-selectin expression within 1 minute.
- Significant platelet aggregation and ATP secretion observed after 20 minutes.
- Chlamydial lipopolysaccharide plays an active role; other bacteria showed minimal effects.
Conclusions:
- Chlamydia pneumoniae activates platelets, suggesting a new pathway for atherosclerosis development.
- This interaction may contribute to thrombotic vascular occlusion in infected individuals.
Objective:
Evidence linking Chlamydia pneumoniae to atherosclerotic cardiovascular disease is expanding. Platelets are considered to play an essential role in cardiovascular diseases; however, so far platelets have not been associated with an infectious cause of atherosclerosis. This study aims to clarify the interaction between C pneumoniae and platelets and possibly present a novel mechanism in the pathogenesis of atherosclerosis.
Methods And Results:
The effects of C pneumoniae on platelet aggregation and secretion were assessed with lumiaggregometry, and the ability of C pneumoniae to bind to platelets and stimulate expression of P-selectin was analyzed with flow cytometry. We found that C pneumoniae, at a chlamydia:platelet ratio of 1:15, adheres to platelets and triggers P-selectin expression after 1 minute and causes an extensive aggregation and ATP secretion after 20 minutes of incubation. Inhibition of glycoprotein IIb/IIIa with Arg-Gly-Asp-Ser or abciximab markedly reduced C pneumoniae-induced platelet aggregation. Exposure of C pneumoniae to polymyxin B, but not elevated temperature, abolished the stimulatory effects on platelet activation, suggesting that chlamydial lipopolysaccharide has an active role. In contrast, other tested bacteria had no or only moderate effects on platelet functions.
Conclusions:
Our findings demonstrate a new concept of how C pneumoniae activates platelets and thereby may cause atherosclerosis and thrombotic vascular occlusion.