Journal of Pharmacological Sciences (Jan 2006)

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

Journal volume & issue
Vol. 102, no. 1
pp. 143 – 146

Abstract

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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