Restoring the Balance of the Autonomic Nervous System as an Innovative Approach to the Treatment of Rheumatoid Arthritis

Koopman, Frieda A. and Stoof, Susanne P. and Straub, Rainer H. and van Maanen, Marjolein A. and Vervoordeldonk, Margriet J. and Tak, Paul P. (2011) Restoring the Balance of the Autonomic Nervous System as an Innovative Approach to the Treatment of Rheumatoid Arthritis. MOLECULAR MEDICINE, 17 (9-10). pp. 937-948. ISSN 1076-1551, 1528-3658

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Abstract

The immunomodulatory effect of the autonomic nervous system has raised considerable interest over the last decades. Studying the influence on the immune system and the role in inflammation of the sympathetic as well as the parasympathetic nervous system not only will increase our understanding of the mechanism of disease, but also could lead to the identification of potential new therapeutic targets for chronic immune-mediated inflammatory diseases, such as rheumatoid arthritis (RA). An imbalanced autonomic nervous system, with a reduced parasympathetic and increased sympathetic tone, has been a consistent finding in RA patients. Studies in animal models of arthritis have shown that influencing the sympathetic (via alpha- and beta-adrenergic receptors) and the parasympathetic (via the nicotinic acetylcholine receptor alpha 7nAChR or by electrically stimulating the vagus nerve) nervous system can have a beneficial effect on inflammation markers and arthritis. The immunosuppressive effect of the parasympathetic nervous system appears less ambiguous than the immunomodulatory effect of the sympathetic nervous system, where activation can lead to increased or decreased inflammation depending on timing, doses and kind of adrenergic agent used. In this review we will discuss the current knowledge of the role of both the sympathetic (SNS) and parasympathetic nervous system (PNS) in inflammation with a special focus on the role in RA. In addition, potential antirheumatic strategies that could be developed by targeting these autonomic pathways are discussed. (C) 2011 The Feinstein Institute for Medical Research, www.feinsteininstitute.org Online address: http://www.molmed.org doi: 10.2119/molmed.2011.00065

Item Type: Article
Uncontrolled Keywords: NICOTINIC ACETYLCHOLINE-RECEPTOR; COLLAGEN-INDUCED ARTHRITIS; CHOLINERGIC ANTIINFLAMMATORY PATHWAY; ADJUVANT-INDUCED ARTHRITIS; TUMOR-NECROSIS-FACTOR; ADHESION MOLECULE EXPRESSION; FIBROBLAST-LIKE SYNOVIOCYTES; ACUTE PSYCHOLOGICAL STRESS; TO-BRAIN COMMUNICATION; VAGUS NERVE;
Subjects: 600 Technology > 610 Medical sciences Medicine
Divisions: Medicine > Lehrstuhl für Innere Medizin I
Depositing User: Dr. Gernot Deinzer
Date Deposited: 02 Jun 2020 08:21
Last Modified: 02 Jun 2020 08:21
URI: https://pred.uni-regensburg.de/id/eprint/20225

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