Background: Montelukast is known as a cysteinyl leukotriene 1 receptor antagonist. However, the action of montelukast in terms of nuclear factor KB (NF-kappaB) activation and the production of proinflammatory molecules is unknown.
Objective: To demonstrate the potential anti-inflammatory effect of montelukast.
Methods: We examined whether montelukast inhibits the activation of NF-kappaB, a transcription factor that regulates the expression of proinflammatory molecules. The inhibitory effects of montelukast on tumor necrosis factor kappa (TNF-kappa)--induced NF-kappaB activation on THP-1 cells, a human monocytic leukemia cell line, were evaluated by flow cytometry, and those on lipopolysaccharide-induced interleukin 1beta (IL-1beta), IL-6, TNF-alpha, and monocyte chemoattractant protein 1 (MCP-1) production in peripheral blood mononuclear cells were evaluated by enzyme-linked immunosorbent assay.
Results: Flow cytometry demonstrated that montelukast inhibited NF-kappaB activation in THP-1 cells in a dose-related manner. Furthermore, 10(-5)M montelukast significantly inhibited lipopolysaccharide-induced IL-6, TNF-alpha, and MCP-1 production in the peripheral blood mononuclear cells of controls and patients with asthma. Lipopolysaccharide-induced IL-1beta production was not inhibited by montelukast.
Conclusions: These findings suggest that high doses of montelukast modulate the production of IL-6, TNF-alpha, and MCP-1 through the inhibition of NF-kappaB activation. However, the anti-inflammatory effect of montelukast at therapeutic doses in patients with asthma needs to be further investigated.
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