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Accumulating evidence has shown a strong association between the metabolic syndrome(MS) and a chronic inflammatory state predisposing to atherosclerosis. We investigated leukocyte, platelet, and endothelial activation markers and cellular interactions in 33 patients with the MS and 25 healthy controls. Using flow cytometry, we measured:(1) P-selectin expression in platelets;(2) platelet microparticles identified by CD31 expression;(3) endothelial microparticles(EMPs) identified by expression of CD31(EMP31), CD62E(EMP62E), and CD51(EMP51);(4) conjugates of leukocytes with platelet microparticles/ platelets and with EMPs identified by CD54(EMP54); and(5) CD11b expression in leukocytes. Patients with the MS had markedly elevated EMP31, although EMP62E levels were normal, suggesting that EMP31 levels were increased because of endothelial cell apoptosis, rather than activation. EMP51, EMP54-lymphocyte conjugates, platelet expression of P-selectin, CD11b expression in leukocytes, and platelet-lymphocyte conjugates were also increased in patients with the MS. Platelet-leukocyte conjugates correlated with leukocyte activation, suggesting that platelet binding to leukocytes regulates leukocyte activation in vivo. In conclusion, our data demonstrate endothelial cell microparticle release, platelet and leukocyte activation, and increased binding of EMPs and platelets to leukocytes in patients with the MS.
Accumulating evidence has shown a strong association between the metabolic syndrome (MS) and a chronic inflammatory state predisposing to atherosclerosis. We investigated leukocyte, platelet, and endothelial activation markers and cellular interactions in 33 patients with the MS and 25 healthy controls. , (2) platelet microparticles identified by CD31 expression; (3) endothelial microparticles (EMPs) identified by expression of CD31 (EMP31), CD62E (EMP62E), and CD51 (4) conjugates of leukocytes with platelet microparticles / platelets and with EMPs identified by CD54 (EMP54); and (5) CD11b expression in leukocytes. Patients with the MS had markedly elevated EMP31, although EMP62E levels were normal, suggesting that EMP31 levels were increased because of endothelial cell apoptosis, rather than activation. EMP51, EMP54-lymphocyte conjugates, platelet expression of P-selectin, CD11b expression in leukocytes, and platelet T-lymphocyte conjugates were also increased in patients with the MS. Platelet-leukocyte conjugates correlated with leukocyte activation, suggesting that platelet binding to leukocytes regulates leukocyte activation in vivo. In conclusion, our data demonstrate endothelial cell microparticle release, platelet and leukocyte activation, and increased binding of EMPs and platelets to leukocytes in patients with the MS.