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 RGDS 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.

Conclusion--Our findings demonstrate a new concept of how C. pneumoniae activates platelets and thereby may cause atherosclerosis and thrombotic vascular occlusion.