High-density lipoproteins inhibit fibrinogen binding on adenosine diphosphate-activated monocytes

High levels of fibrinogen and tow levels of high-density lipoprotein (HDL) cholesterol were reported to be risk factors for coronary heart disease. CD 11b/CD18, a fibrinogen-binding protein, is expressed on the surface of mono cytes, which play a crucial role in the formation of atherosclerotic lesion s. In the present study, we investigate the effects of antibodies against C D11b and CD18, as well as HDL3 and low-density lipoprotein (LDL) cholestero l on fibrinogen binding on monocytes. We find that binding of fibrinogen on monocytes activated with adenosine diphosphate (ADP) was reduced to 66.0 /- 8.3% (mean ie SD) in the presence of anti-CD11b antibodies (12.5 mu g/ml ; P less than or equal to 0.02) and to 54.5 4.9% in the presence of anti-CD 18 antibodies (20 mu g/ml; P less than or equal to 0.01), respectively. Fib rinogen binding on Cytochalasin-B-activated monocytes was reduced to 79.8 /- 6.0% in the presence of anti-CD18 (20 mu g/ml; P less than or equal to 0 .05). Incubation of ADP-activated monocytes with HDL3 (0.5 g/l) led to a lo wering of fibrinogen binding to 65.0 +/- 6.6% (P less than or equal to 0.05 ). No effect of HDL3 on fibrinogen binding was seen on Cytochalasin-B-activ ated monocytes. A slight, non-significant stimulatory effect of LDL on fibr inogen binding on ADP-activated but not on Cytochalasin-B-activated monocyt es was additionally observed. Neither incubation with HDL3 or with LDL had a significant influence on ADP-activated cellular binding of anti-CD11b or anti-CD18 antibodies. The inhibition of fibrinogen binding on monocytes in the presence of HDL3 is a major new finding of this study. Since inhibition of fibrinogen binding in the presence of HDL might impair both monocyte re cruitment to the arterial wall and foam cells formation, our findings sugge sts a novel mechanism by which HDL may prevent development of arteriosclero sis. Blood Coagul Fibrinolysis 11:505-509 (C) 2000 Lippincott Williams & Wi lkins.