Journal of Leukocyte Biology
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Published online before print September 11, 2006
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0406236

Received for publication April 3, 2006.
Revised July 17, 2006.
Accepted for publication July 18, 2006.

Article

Effect of nicotine on IL-18-initiated immune response in human monocytes

Hideo Kohka Takahashi *, Hiromi Iwagaki {dagger}, Ryosuke Hamano {dagger}, Tadashi Yoshino {ddagger}, Noriaki Tanaka {dagger}, and Masahiro Nishibori *@

Departments of *Pharmacology, {dagger}Gastroenterological Surgery, Transplant, and Surgical Oncology, and {ddagger}Pathology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan

@ To whom correspondence should be addressed. E-mail: mbori{at}md.okayama-u.ac.jp.


  Abstract

Nicotine is thought to inhibit the production of proinflammatory cytokines from macrophages through an anti-inflammatory pathway that is dependent on nicotinic acetylcholine receptor {alpha}7 subunit ({alpha}7-nAChR). IL-18, an important proinflammatory cytokine, is reported to induce the expression of adhesion molecules on monocytes, thus enhancing cell-to-cell interactions with T-cells and contributing to IL-18-initiated cytokine production. Accordingly, inhibition of IL-18 suppresses systemic inflammatory responses. In the present study, we found that nicotine inhibited the IL-18-enhanced expression of ICAM-1, B7.2, and CD40 on monocytes, and the production of IL-12, IFN-{gamma}, and TNF-{alpha} by PBMC. A nonselective and a selective {alpha}7-nAChR antagonist, mecamylamine, and {alpha}-bungarotoxin abolished the effects of nicotine, suggesting that this depends on {alpha}7-nAChR stimulation. It is reported that nicotine induces prostaglandinE2 (PGE2) production in PBMC through the up-regulation of cyclooxygenase (COX)-2 expression. PGE2 is known to activate the EP2/EP4-receptor, leading to an increase in cyclic adenosine monophosphate (cAMP) levels and protein kinase A (PKA) activity. Consistent with this, we found that COX-2 and PKA inhibitors prevented the effects of nicotine on adhesion molecule expression and cytokine production, indicating that the mechanism of action of nicotine may be via endogenous PGE2 production.

Key Words: prostaglandin E2




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