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

doi:10.1254/jphs.SC0060074

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 journal › Article › peer-review

23 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 language	English
Pages (from-to)	143-146
Number of pages	4
Journal	Journal of Pharmacological Sciences
Volume	102
Issue number	1
DOIs	https://doi.org/10.1254/jphs.SC0060074
Publication status	Published - 2006

Keywords

Interleukin-18
Prostaglandin E
α7 nicotinic acetylcholine receptor

ASJC Scopus subject areas

Molecular Medicine
Pharmacology

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10.1254/jphs.SC0060074

Cite this

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title = "α7 nicotinic acetylcholine receptor stimulation inhibits lipopolysaccharide-induced interleukin-18 and -12 production in monocytes",

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.",

keywords = "Interleukin-18, Prostaglandin E, α7 nicotinic acetylcholine receptor",

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AU - Takahashi, Hideo Kohka

AU - Iwagaki, Hiromi

AU - Hamano, Ryosuke

AU - Yoshino, Tadashi

AU - Tanaka, Noriaki

AU - Nishibori, Masahiro

PY - 2006

Y1 - 2006

N2 - 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.

AB - 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.

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KW - Prostaglandin E

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α7 nicotinic acetylcholine receptor stimulation inhibits lipopolysaccharide-induced interleukin-18 and -12 production in monocytes

Abstract

Keywords

ASJC Scopus subject areas

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