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

Research output: Contribution to journalArticle

16 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)143-146
Number of pages4
JournalJournal of Pharmacological Sciences
Volume102
Issue number1
DOIs
Publication statusPublished - Sep 29 2006

Keywords

  • Interleukin-18
  • Prostaglandin E
  • α7 nicotinic acetylcholine receptor

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology

Fingerprint Dive into the research topics of 'α7 nicotinic acetylcholine receptor stimulation inhibits lipopolysaccharide-induced interleukin-18 and -12 production in monocytes'. Together they form a unique fingerprint.

  • Cite this