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Atherosclerosis is an inflammatory disease with fundamental primitive events including endothelial dysfunction and platelet aggregation [1]. Human neutrophil peptides (HNP) are the most abundant cationic proteins in neutrophils and are released into the extracellular milieu upon activation [2]. HNP have previously been detected in atherosclerotic lesions, and are in high concentrations in blood of patients with acute coronary syndrome [2]. We have previously demonstrated that HNP can induce foam cell formation, platelet aggregation and leukocyte recruitment through the LRP8 signaling pathway [3], but there is no direct interaction between HNP and LRP8.

0593. Reelin mediates the human neutrophil peptide-induced endothelial dysfunction and platelet aggregation