ABSTRACT
Over the past two decades it has become known that the effect of the central nervous system (CNS) on immune responses is not only mediated via the hypothalamopituitary-adrenal axis (HPA), but also by direct neuronal control (Besedovsky and Del Rey, 1996; James et al. 1996; Elenkov et al., 2000). The sympathetic branch of the autonomic nervous system (ANS) is able to regulate blood flow and cytokine production. Besides the primary (thymus, bone marrow) and secondary lymphoid organs (spleen, tonsils, and lymph nodes), many other tissues involved in immune responses are heavily influenced by incoming chemical signals via norepinephrine (NE) derived from varicose axon terminals of the sympathetic nervous system (Vizi, 1998; Elenkov et al., 2000). In addition to NE released from nonsynaptic varicosities of noradrenergic terminals (Vizi, 2000), circulating catecholamines (epinephrine, NE) are able to influence the production of pro-and anti-inflammatory cytokines by different immune cells (Table 13.1) (Mire-Sluis and Thorpe, 1998).
