Wishing Away Inflammation? New Links between Serotonin and TNF Signaling
Abstract
Wishing Away Inflammation? New Links between Serotonin and TNF Signaling — MI var callbackToken='473510DBCF3CF60'; Skip to main page content HOME CURRENT ISSUE ARCHIVE FEEDBACK SUBSCRIPTIONS ALERTS HELP Keywords GO Advanced » Institution: DeepDyve User Name Password Sign In Wishing Away Inflammation? New Links between Serotonin and TNF Signaling Martin Pelletier and Richard M. Siegel Immunoregulation Section, Autoimmunity Branch, NIAMS, NIH, Bethesda, MD 20814 The idea that emotional states can influence health has been widely accepted in medicine since Roman times ( 1 ) . This idea has been validated in the modern era; several neuroendocrine pathways have been elucidated that link neural and immune responses ( 2 ) . These links function reciprocally: a number of neural signaling pathways trigger the release of immunomodulators, and cells of the nervous system sense inflammation through receptors for immune cytokines. The Hypothalamic-Pituitary-Adrenal Axis “translates” psychological stressors into glucocorticoid synthesis by the adrenal cortex and epinephrine synthesis by the adrenal medulla, leading to an immediate epinephrine-activated vasoactive response. Glucocorticoid-mediated immune modulation may provide the short-term advantage of suppressing inflammation during stress, whereas chronic endogenous production or exogenous administration of glucocorticoids results in immunosuppression. Both the benefits and detriments of these effects are