Beta-very low density lipoprotein pretreatment of endothelial monolayers increases monocyte adhesion.

Treatment of rabbit aortic endothelial cells or human umbilical vein cells for as little as 1 day with 25 micrograms/ml of beta-migrating very low density lipoprotein (beta-VLDL), but not low density lipoprotein (LDL), caused an increased binding of human peripheral blood monocytes to the endothelium. This increase was maximal by 24 hours but was not significant at 4 hours of pre-incubation with beta-VLDL. Neutrophil binding was not significantly stimulated by beta-VLDL treatment of endothelial cells, while endotoxin (LPS) treatment of endothelial cells stimulated both neutrophil and monocyte binding. Antibody to leukocyte function-associated-antigen-1 and to Mo2 inhibited binding to both beta-VLDL-stimulated and LPS-stimulated cells by 25%. The fact that both rabbit and human cells were stimulated by beta-VLDL to bind human monocytes suggests that some mechanisms regulating binding are conserved between species. These studies suggest that beta-VLDL acts like a chronic inflammatory mediator to cause a sustained increase in binding of monocytes to the endothelium.