ABSTRACT
It has been known for some time that there is a two-way communication link between the immune and nervous systems. Accumulating evidence has led to the conclusion that the nervous system regulates immune responses. In most cases this regulation involves negative feedback loops that result in dampening down of immune (inflammatory) responses and reestablishment of homeostasis. In response to the production of pro-inflammatory cytokines through infection or other stimulants of inflammation, the hypothalamus-pituitary-adrenal axis (HPA) stimulates the release of glucocorticoids from the adrenal cortex that together with epinephrine (adrenaline) produced by the adrenal medulla, result in immune suppression. In addition, norepinephrine (noradrenaline) and neuro-peptide Y released from sympathetic nerve endings, and acetylcholine from parasym-pathetic fibers, are also suppressive. In contrast, sensory peripheral nerves involved in pain, touch, and temperature perception release a number of neuropeptides, including corticotropin-releasing hormone (CRH), calcitonin gene-related peptide (CGRP), and substance P that are generally pro-inflammatory. The various neurotransmitters released from nerve endings, and those acting systemically, are thought to regulate immune responses through receptors that the cells of the immune system have for these transmitters. In most cases regulation is through modulation of the levels of pro-inflammatory cytokines produced and their effects on both the innate and adaptive immune systems.
