ABSTRACT
I. INTRODUCTION Neuroendocrine-immune interactions occur primarily through the hypothalamus-pituitaryadrenal (HPA) axis, the vagus nerve, and the innervation of the lymphoid organs. Lymphoid tissues are innervated by nerve fibers containing both neurotransmitters and neuropeptides. Some neuropeptides, such as vasoactive intestinal peptide (VIP), neuropeptide Y (NPY), somatostatin (SOM), and galanin (Gal), are present primarily in the noradrenergic autonomic and cholinergic innervation, whereas substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP) reside in the sensory innervation [1-7]. In addition, the immune cells express and release neuropeptides such as opioid peptides, -melanocyte-stimulating hormone (-MSH), SP, SOM, NPY, and VIP [8-19]. Although the factors that control neuronal or immune release of neuropeptides during an inflammatory response remain to be identified and characterized, neuropeptides such as VIP, SP, and CGRP were shown to be released in functionally relevant amounts during an immune response, both in patients and in animal models [20-24].
