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

• Main Authors: Hideo Kohka Takahashi, Hiromi Iwagaki, Ryosuke Hamano, Tadashi Yoshino, Noriaki Tanaka, Masahiro Nishibori
• Format: Article
• Language: English
• Published: Elsevier 2006-01-01
• Series: Journal of Pharmacological Sciences
• Online Access: http://www.sciencedirect.com/science/article/pii/S1347861319344275

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. Keywords:: α7 nicotinic acetylcholine receptor, prostaglandin E2, interleukin-18