%0 Journal Article %A Juan J. Moreno %T Antiflammin-2 Prevents HL-60 Adhesion to Endothelial Cells and Prostanoid Production Induced by Lipopolysaccharides %D 2001 %J Journal of Pharmacology and Experimental Therapeutics %P 884-889 %V 296 %N 3 %X We studied the effect of antiflammin-2 (AF-2) on adhesion molecule expression by HL-60 cells and endothelial (ECV304) cells stimulated by lipopolysaccharides (LPSs), and on leukocyte-endothelial cell interaction in an in vitro coculture system. The action of AF-2 on prostanoid production in these experimental conditions was also tested. LPS increased the adhesion molecule expression, such as lymphocyte function-associated antigen-1 and membrane attack complex-1 on HL-60 cells and E-selectin and intercellular adhesion molecule-1 on ECV304 cells. The LPS-stimulated adhesion molecule expression on HL-60/ECV304 coculture system was higher than on HL-60 or ECV304 cultures. LPS also induced HL-60 adhesion to ECV304 monolayer and thromboxane B2 and prostaglandin E2(PGE2) production in HL-60 culture and PGE2 in ECV304 culture. Prostanoid production by HL-60/ECV304 cocultures was higher than by simple cultures. AF-2 inhibited the enhancement of adhesion molecule expression induced by LPSs, especially E-selectin. Thus, AF-2 significantly reduced the HL-60 adhesion to endothelial cells stimulated by LPSs. AF-2 also inhibited prostanoid synthesis by ECV304 cells or HL-60/ECV304 coculture challenged by LPSs. In conclusion, AF-2 reduced HL-60 adhesion to endothelial cells, suggesting that it reduces inflammation by blocking leukocyte trafficking and the subsequent eicosanoid production. The American Society for Pharmacology and Experimental Therapeutics %U https://jpet.aspetjournals.org/content/jpet/296/3/884.full.pdf