Journal of Leukocyte Biology
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Originally published online as doi:10.1189/jlb.0906544 on November 15, 2006

Published online before print November 15, 2006
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(Journal of Leukocyte Biology. 2007;81:599-606.)
© 2007 by Society for Leukocyte Biology

Nicotine and serotonin in immune regulation and inflammatory processes: a perspective

Isabelle Cloëz-Tayarani1 and Jean-Pierre Changeux

Unité de Recherche Associée, Centre National de la Recherche Scientifique, D2182 Récepteurs et Cognition, Institut Pasteur, Paris, France

1 Correspondence: Unité "Récepteurs et Cognition", Institut Pasteur, 25 rue du Docteur Roux, 75724 Paris Cedex 15, France. E-mail: icloez{at}pasteur.fr

Nicotine and serotonin modulate the innate and adaptive immune responses and the inflammatory states. Several nicotinic cholinergic and serotonergic receptor subtypes have been characterized in B and T lymphocytes, monocytes, macrophages, and dendritic cells. The use of knockout mice has allowed a better characterization of nicotinic receptors and their role in anti-inflammatory processes in these cells. Cytokines play a crucial role in controlling inflammatory reactions. Nicotine and serotonin have been reported to regulate cytokine release. Cholinergic mechanisms also play an important role in inflammation through endogenous acetylcholine. Nicotine mimics this effect by activating the cholinergic anti-inflammatory pathways. New concepts of reciprocal interactions between nicotine and serotonin are emerging. The role of nicotine as an anti-inflammatory agent has been established, whereas that of serotonin remains more controversial.

Key Words: immune cells • inflammation • cytokine • neuromodulator • 5-HT receptors • nicotinic cholinergic receptors




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