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

Hideo Kohka Takahashi, Hiromi Iwagaki, Ryosuke Hamano, Tadashi Yoshino, Noriaki Tanaka, Masahiro Nishibori
2006 Journal of Pharmacological Sciences  
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 E 2 (PGE 2 ) production in monocytes through the up-regulation of cyclooxygenase (COX)-2 expression. PGE 2 is known to
more » ... E 2 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 PGE 2 production.
doi:10.1254/jphs.sc0060074 pmid:16960420 fatcat:nemmnyrwgraodajgsdosejzxmm