α7 Nicotinic Acetylcholine Receptor Stimulation Inhibits Lipopolysaccharide-Induced Interleukin-18 and -12 Production in Monocytes

Abstract

Nicotine inhibited interleukin (IL)-18 and -12 production in lipopolysaccharide (LPS)-stimulated monocytes, and the action of nicotine was antagonized by a non-selective and a selective α7 nicotinic acetylcholine receptor (α7-nAChR) antagonist, suggesting that the stimulation of α7-nAChR may be involved in the action of nicotine. Nicotine is reported to induce prostaglandin E₂ (PGE₂) production in monocytes through the up-regulation of cyclooxygenase (COX)-2 expression. PGE₂ is known to increase cAMP levels and to activate protein kinase A (PKA). COX-2 and PKA inhibitors prevented the action of nicotine, indicating that the mechanism of action of nicotine may be via endogenous PGE₂ production.