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

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 invo...

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Published inJournal of Pharmacological Sciences Vol. 102; no. 1; pp. 143 - 146
Main Authors Takahashi, Hideo Kohka, Iwagaki, Hiromi, Hamano, Ryosuke, Yoshino, Tadashi, Tanaka, Noriaki, Nishibori, Masahiro
Format Journal Article
LanguageEnglish
Published Elsevier B.V 2006
The Japanese Pharmacological Society
Elsevier
Subjects
interleukin-18
prostaglandin E2
α7 nicotinic acetylcholine receptor
prostaglandin E2
interleukin-18
α7 nicotinic acetylcholine receptor
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Summary: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.
ISSN:1347-8613
1347-8648
DOI:10.1254/jphs.SC0060074