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Table of Contents
Vol. 13, No. 5-6, 2006
Issue release date: August 2007
Section title: Paper
Neuroimmunomodulation 2006;13:257–267
(DOI:10.1159/000104853)

Stress System – Organization, Physiology and Immunoregulation

Elenkov I.J.a · Chrousos G.P.b, c
aInstitute of Neurobiology and Molecular Medicine, Italian National Research Council, Rome, Italy; bFirst Department of Pediatrics, Athens University, Athens, Greece; cReproductive Biology and Medicine Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Md., USA

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Article / Publication Details

First-Page Preview
Abstract of Paper

Received: February 14, 2007
Accepted: June 20, 2007
Published online: August 22, 2007
Issue release date: August 2007

Number of Print Pages: 11
Number of Figures: 2
Number of Tables: 0

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM

Abstract

Stress is defined as a state of threatened homeostasis. The principal effectors of the stress system include corticotropin-releasing hormone, arginine vasopressin, the glucocorticoids, and the catecholamines norepinephrine and epinephrine. Activation of the stress system leads to adaptive behavioral and physical changes. The principal stress hormones glucocorticoids and catecholamines affect major immune functions such as antigen presentation, leukocyte proliferation and traffic, secretion of cytokines and antibodies, and selection of the T helper (Th) 1 versus Th2 responses. A fully fledged systemic inflammatory reaction results in stimulation of the stress response, which in turn, through induction of a Th2 shift protects the organism from systemic overshooting with Th1/pro-inflammatory cytokines. Stress is often regarded as immunosuppressive, but recent evidence indicates that stress hormones influence the immune response in a less monochromatic way – systemically they inhibit Th1/pro-inflammatory responses and induce a Th2 shift, whereas in certain local responses they promote pro-inflammatory cytokine production and activation of the corticotropin-releasing hormone-mast cell-histamine axis. Through this mechanism a hyper- or hypoactive stress system associated with abnormalities of the systemic anti-inflammatory feedback and/or hyperactivity of the local pro-inflammatory factors may play a role in the pathogenesis of chronic inflammation and immune-related diseases.

© 2006 S. Karger AG, Basel


Article / Publication Details

First-Page Preview
Abstract of Paper

Received: February 14, 2007
Accepted: June 20, 2007
Published online: August 22, 2007
Issue release date: August 2007

Number of Print Pages: 11
Number of Figures: 2
Number of Tables: 0

ISSN: 1021-7401 (Print)
eISSN: 1423-0216 (Online)

For additional information: http://www.karger.com/NIM


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Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.
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