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The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation.
Br J Pharmacol. 2007 Aug; 151(7):915-29.BJ

Abstract

The physiological regulation of the immune system encompasses comprehensive anti-inflammatory mechanisms that can be harnessed for the treatment of infectious and inflammatory disorders. Recent studies indicate that the vagal nerve, involved in control of heart rate, hormone secretion and gastrointestinal motility, is also an immunomodulator. In experimental models of inflammatory diseases, vagal nerve stimulation attenuates the production of proinflammatory cytokines and inhibits the inflammatory process. Acetylcholine, the principal neurotransmitter of the vagal nerve, controls immune cell functions via the alpha7 nicotinic acetylcholine receptor (alpha7nAChR). From a pharmacological perspective, nicotinic agonists are more efficient than acetylcholine at inhibiting the inflammatory signaling and the production of proinflammatory cytokines. This 'nicotinic anti-inflammatory pathway' may have clinical implications as treatment with nicotinic agonists can modulate the production of proinflammatory cytokines from immune cells. Nicotine has been tested in clinical trials as a treatment for inflammatory diseases such as ulcerative colitis, but the therapeutic potential of this mechanism is limited by the collateral toxicity of nicotine. Here, we review the recent advances that support the design of more specific receptor-selective nicotinic agonists that have anti-inflammatory effects while eluding its collateral toxicity.

Authors+Show Affiliations

Department of Gastroenterology, Academic Medical Center, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. w.j.dejonge@amc.nlNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

17502850

Citation

de Jonge, W J., and L Ulloa. "The Alpha7 Nicotinic Acetylcholine Receptor as a Pharmacological Target for Inflammation." British Journal of Pharmacology, vol. 151, no. 7, 2007, pp. 915-29.
de Jonge WJ, Ulloa L. The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation. Br J Pharmacol. 2007;151(7):915-29.
de Jonge, W. J., & Ulloa, L. (2007). The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation. British Journal of Pharmacology, 151(7), 915-29.
de Jonge WJ, Ulloa L. The Alpha7 Nicotinic Acetylcholine Receptor as a Pharmacological Target for Inflammation. Br J Pharmacol. 2007;151(7):915-29. PubMed PMID: 17502850.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The alpha7 nicotinic acetylcholine receptor as a pharmacological target for inflammation. AU - de Jonge,W J, AU - Ulloa,L, Y1 - 2007/05/14/ PY - 2007/5/16/pubmed PY - 2007/11/6/medline PY - 2007/5/16/entrez SP - 915 EP - 29 JF - British journal of pharmacology JO - Br J Pharmacol VL - 151 IS - 7 N2 - The physiological regulation of the immune system encompasses comprehensive anti-inflammatory mechanisms that can be harnessed for the treatment of infectious and inflammatory disorders. Recent studies indicate that the vagal nerve, involved in control of heart rate, hormone secretion and gastrointestinal motility, is also an immunomodulator. In experimental models of inflammatory diseases, vagal nerve stimulation attenuates the production of proinflammatory cytokines and inhibits the inflammatory process. Acetylcholine, the principal neurotransmitter of the vagal nerve, controls immune cell functions via the alpha7 nicotinic acetylcholine receptor (alpha7nAChR). From a pharmacological perspective, nicotinic agonists are more efficient than acetylcholine at inhibiting the inflammatory signaling and the production of proinflammatory cytokines. This 'nicotinic anti-inflammatory pathway' may have clinical implications as treatment with nicotinic agonists can modulate the production of proinflammatory cytokines from immune cells. Nicotine has been tested in clinical trials as a treatment for inflammatory diseases such as ulcerative colitis, but the therapeutic potential of this mechanism is limited by the collateral toxicity of nicotine. Here, we review the recent advances that support the design of more specific receptor-selective nicotinic agonists that have anti-inflammatory effects while eluding its collateral toxicity. SN - 0007-1188 UR - https://www.unboundmedicine.com/medline/citation/17502850/The_alpha7_nicotinic_acetylcholine_receptor_as_a_pharmacological_target_for_inflammation_ L2 - https://doi.org/10.1038/sj.bjp.0707264 DB - PRIME DP - Unbound Medicine ER -