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Rheum Dis Clin North Am. 2005 Feb;31(1):43-59, viii.

Sympathetic neurotransmitters in joint inflammation.

Author information

1
Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University Hospital Regensburg, FJS-Allee 11, 93042 Regensburg, Germany. rainer.straub@klinik.uni-regensburg.de

Abstract

This article demonstrates the dual pro- and anti-inflammatory role of the sympathetic nervous system (SNS) in inflammatory joint disease (IJD) by way of distinct adrenoceptors. The dual role of the SNS depends on involved compartments, timing of distinct effector mechanisms during the inflammatory process, availability of respective adrenoceptors on target cells, and an intricate shift from beta-to-alpha adrenergic signaling in the progressing course of the inflammatory disease (beta-to-alpha adrenergic shift). Additional critical points for the dual role of the SNS in inflammation are the underlying change of immune effector mechanisms during the process of disease progression and the behavior of sympathetic nerve fibers in inflamed tissue (nerve fiber loss). This is accompanied by a relative lack of anti-inflammatory glucocorticoids in relation to inflammation. In quintessence, in early stages of IJD, the SNS plays a predominantly proinflammatory role, whereas in late stages of the disease the SNS most probably exerts anti-inflammatory effects. Because patients who have rheumatoid arthritis most often present in the chronic phase of the disease, support of anti-inflammatory sympathetic pathways can be a promising therapeutic option.

PMID:
15639055
DOI:
10.1016/j.rdc.2004.09.003
[Indexed for MEDLINE]
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