“…The anti-inflammatory effect of colchicine is induced by inhibition of the synthesis of tumor necrosis factor (TNF) by macrophages and down-regulation of surface expression of TNF-receptor on macrophages and endothelial cells, thus it interferes with the priming effect of TNF on neutrophils before their activation by monosodium urate crystals (Li et al, 1996;Ding et al, 1990), inhibition of leukotriene B4 synthesis, a powerful chemotactic agent (Serhen et al, 1984;Reibman et al, 1986). Colchicine reduces adhesion of neutrophils to endothelium inhibiting polymorphonuclear leucocyte (PMN) function (Firdham et al, 1981), E-selectin-mediated endothelial (Asako et al, 1992) and l-selectinmediated neutrophilic adhesiveness (Cronstein & Weissman, 1993;Cronstein et al, 1995). It has been reported that colchicine blocks the cyclooxygenase-2 (COX-2) activity, prostaglandin E 2 and thromboxane A 2 synthesis of mononuclear phagocytes with subsequent reduction of swelling and pain in gout and Familial Mediterranean Fever (FMF) (Pouliot et al, 1998).…”