Rainer H. Straub MD
, 
and Peter Härle MD
Laboratory of Neuroendocrinoimmunology, Department of Internal Medicine I, University Hospital Regensburg, FJS-Allee 11, 93042 Regensburg, Germany
Available online 5 January 2005.
This article is not included in your organization's subscription. However, you may be able to
access this article under your organization's agreement with Elsevier.
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 β-to-
adrenergic signaling in the progressing course of the inflammatory disease (β-to- 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.