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Wishing Away Inflammation? New Links between Serotonin and TNF Signaling

Wishing Away Inflammation? New Links between Serotonin and TNF Signaling 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 http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Molecular Interventions Am. Soc for Pharma & Experimental Therapeutics

Wishing Away Inflammation? New Links between Serotonin and TNF Signaling

Molecular Interventions , Volume 9 (6): 299 – Dec 1, 2009

Wishing Away Inflammation? New Links between Serotonin and TNF Signaling

Molecular Interventions , Volume 9 (6): 299 – Dec 1, 2009

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

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Publisher
Am. Soc for Pharma & Experimental Therapeutics
Copyright
Copyright © Molecular Interventions
ISSN
1534-0384
eISSN
1543-2548
DOI
10.1124/mi.9.6.5
pmid
20048135
Publisher site
See Article on Publisher Site

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

Journal

Molecular InterventionsAm. Soc for Pharma & Experimental Therapeutics

Published: Dec 1, 2009

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