Objective To observe whether homocysteine can directly alter the expressions of CD11b, CD18, CD14 and Lselectin on neutrophils, monocytes, and lymphocytes in whole blood from healthy human subjectsMethods Leukocyte surface adhesive molecule expressions were analyzed by immunofluorescence flow cytometry Results Homocysteine at the lowest concentration (20μmol/L) significantly increased surface adhesive molecule expressions of CD11b and CD18 on each cell type and CD14 on monocytes and neutrophils in whole blood These effects were increased at homocysteine concentrations of 200 and 400μmol/L, but at concentrations 1 mmol/L, CD11b/CD18 and CD14 expressions on all types of leukocytes were decreased Lselectin expression was slightly decreased on all cell types in whole blood by homocysteineConclusion Homocysteine alters leukocyte expressions of CD11b/CD18, CD14 and Lselectin on leukocytes, which may be involved into homocysteineinduced leukocyte adhesion and migration

OBJECTIVETo determine whether homocysteine induced endothelial damage through monocyte-endothelial interaction and to characterize both cell types in vitro.

METHODSRadiomethods were performed on monocyte adhesion to/through endothelium and endothelial damage experiments.

RESULTSHomocysteine-treated endothelial cells increased monocyte adhesion and transmigration. Homocysteine-treated monocytes induced endothelial detachment, but this effect was blocked by catalase. These effects were increased with higher concentrations of homocysteine. Monocyte surface glycoprotein antibodies CD11b/CD18 and CD14 inhibited these processes.

CONCLUSIONSHomocysteine alters monocyte-endothelial interaction in vitro, eventually bringing about endothelial damage through release of H(2)O(2). These phenomena are mediated through monocyte surface glycoproteins CD11b/CD18 and CD14. Upregulation of these processes in vivo may contribute to acceleration of atherosclerosis in patients with elevated plasma homocysteine levels.

Arteriosclerosis ; etiology ; Cell Adhesion ; drug effects ; Cell Communication ; drug effects ; Cell Movement ; drug effects ; Dose-Response Relationship, Drug ; Endothelium, Vascular ; cytology ; drug effects ; Homocysteine ; pharmacology ; Humans ; Monocytes ; drug effects ; physiology