EFFECT OF NI IONS ON EXPRESSION OF INTERCELLULAR-ADHESION MOLECULE-1 BY ENDOTHELIAL-CELLS

Previous studies have shown that Ni-based alloys implanted into soft t issues cause an infiltration of inflammatory cells around the implant. This phenomenon is potentially important to dental alloys which are a djacent to oral tissues. To help define the mechanisms by which Ni cau ses an infiltration of inflammatory cells, we exposed endothelial cell s in vitro to Ni ions and measured the expression of intercellular adh esion molecule 1 (ICAM-1). ICAM-1 is known to be involved in the recru itment of inflammatory cells from the bloodstream. We also exposed mac rophages to Ni ions to test the hypothesis that Ni might alter cytokin e secretion and subsequently cause expression of ICAM-1 on endothelial cells. The results showed that Ni ions could promote the expression o f ICAM-1 on endothelial cells, but only at concentrations which were h igh enough (850 mu mol/L for 24 h) to suppress cell metabolic activity . Although we had previous evidence that Ni could cause macrophages to secrete cytokines such as interleukin 1 beta, Ni-exposed macrophage s upernatants did not induce expression of ICAM-1 on endothelial cells a t concentrations subtoxic to the macrophages (85 mu mol/L). At subtoxi c concentrations, Ni ions were able to suppress ICAM-1 expression on e ndothelial cells which were stimulated with Lipopolysaccharide. Thus, Ni ions either promoted or suppressed the expression of ICAM-1 dependi ng on their concentration. This dual action of Ni ions may be importan t in vivo where a gradient of concentrations of released ions is Likel y to exist around the implanted biomaterial. Further studies are neces sary to determine the effect of time of exposure and the molecular mec hanisms of increased ICAM-1 expression. (C) 1997 John Wiley & Sons, In c.