 | |  | |  | |  | |  | |  | |  | |  |
| IJCEM Copyright © 2008-All rights reserved. Published by e-Century Publishing Corporation, Madison, WI 53711 |
Int J Clin Exp Med 1(3),203-212;2008
Review Article
Cholinergic Modulation of Inflammation
Valentin A. Pavlov
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030
Received May 16, 2008; accepted May 22, 2008; available online June 10, 2008
Abstract: Recent studies have demonstrated that cytokine levels and inflammation can be regulated by specifically augmenting
cholinergic signaling via the efferent vagus nerve and the 7 subunit-containing nicotinic acetylcholine receptor7nAChR).
Cholinergic modalities, acting through vagus nerve- and/or 7nAChR-mediated mechanisms have been shown to suppress
excessive inflammation in several experimental models of disease, including endotoxemic shock, sepsis, ischemia-reperfusion injury,
hemorrhagic shock, colitis, postoperative ileus and pancreatitis. These studies have advanced the current understanding of the
mechanisms regulating inflammation. They have also provided a rationale for exploring new possibilities to treat excessive, disease-
underlying inflammation by applying selective cholinergic modalities in preclinical and clinical settings. An overview of this research is
presented here. (IJCEM805003).
Key Words: Inflammation; inflammatory diseases, cytokines, vagus nerve, alpha-7nAChR, cholinergic anti-inflammatory pathway
Full Text PDF
Address all correspondence to: Valentin A. Pavlov, PhD, Laboratory of Biomedical Science, The Feinstein Institute for Medical
Research, 350 Community Drive, Manhasset, NY 11030, Tel: (516) 562-2316, Fax: (516) 562-2356, E-mail: vpavlov@nshs.edu
Review Article
Cholinergic Modulation of Inflammation
Valentin A. Pavlov
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030
Received May 16, 2008; accepted May 22, 2008; available online June 10, 2008
Abstract: Recent studies have demonstrated that cytokine levels and inflammation can be regulated by specifically augmenting
cholinergic signaling via the efferent vagus nerve and the 7 subunit-containing nicotinic acetylcholine receptor7nAChR).
Cholinergic modalities, acting through vagus nerve- and/or 7nAChR-mediated mechanisms have been shown to suppress
excessive inflammation in several experimental models of disease, including endotoxemic shock, sepsis, ischemia-reperfusion injury,
hemorrhagic shock, colitis, postoperative ileus and pancreatitis. These studies have advanced the current understanding of the
mechanisms regulating inflammation. They have also provided a rationale for exploring new possibilities to treat excessive, disease-
underlying inflammation by applying selective cholinergic modalities in preclinical and clinical settings. An overview of this research is
presented here. (IJCEM805003).
Key Words: Inflammation; inflammatory diseases, cytokines, vagus nerve, alpha-7nAChR, cholinergic anti-inflammatory pathway
Full Text PDF
Address all correspondence to: Valentin A. Pavlov, PhD, Laboratory of Biomedical Science, The Feinstein Institute for Medical
Research, 350 Community Drive, Manhasset, NY 11030, Tel: (516) 562-2316, Fax: (516) 562-2356, E-mail: vpavlov@nshs.edu
