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      Comparable Effects of Adrenalectomy and C Fiber Depletion on Delayed-Type Hypersensitivity in Rats

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          Abstract

          Objective: To determine the influence of the hypothalamic-pituitary-adrenal (HPA) axis and sensory C fibers on cell-mediated immunity, the time course of allergic contact dermatitis (ACD) was examined in normal, adrenalectomized (ADX) and capsaicin (CAP)-treated rats. Methods: Five days after sensitization with 2,4-dinitro-1-fluorobenzene (DNFB) onto the back, rats were challenged with DNFB on the pinna. ADX or CAP treatment was performed a week before the sensitization. Results: Ear swelling in normal rats reached a peak 24 h after the challenge and subsided gradually to about half of this peak 72 h afterwards. Plasma ACTH levels increased about 9 times more than those of nonsensitized rats 72 h after the challenge. ADX rats, in which the plasma corticosterone level was significantly lower than that in sham-operated animals, exhibited more rapid development of ACD, which reached a peak 12 h after the challenge. However, the swelling returned to about half of the maximum within 48 h. In CAP-treated rats, ACD reached a peak 6 h after the challenge and recovered quickly as in ADX rats. Plasma ACTH levels in CAP- treated rats were significantly lower than those in vehicle-treated rats. Conclusions: The rapid development of and recovery from ACD in ADX and CAP-treated rats, both of which showed suppression of the HPA axis, indicated a biphasic action of the HPA axis on ACD, i.e. inhibitory in the early phase but augmentative in the late phase of ACD.

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          Most cited references 5

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          Enhancing versus suppressive effects of stress hormones on skin immune function.

          Delayed-type hypersensitivity (DTH) reactions are antigen-specific cell-mediated immune responses that, depending on the antigen, mediate beneficial (e.g., resistance to viruses, bacteria, and fungi) or harmful (e.g., allergic dermatitis and autoimmunity) aspects of immune function. Contrary to the idea that stress suppresses immunity, we have reported that short-duration stressors significantly enhance skin DTH and that a stress-induced trafficking of leukocytes to the skin may mediate this immunoenhancement. Here, we identify the hormonal mediators of a stress-induced enhancement of skin immunity. Adrenalectomy, which eliminates the glucocorticoid and epinephrine stress response, eliminated the stress-induced enhancement of skin DTH. Low-dose corticosterone or epinephrine administration significantly enhanced skin DTH and produced a significant increase in the number of T cells in lymph nodes draining the site of the DTH reaction. In contrast, high-dose corticosterone, chronic corticosterone, or low-dose dexamethasone administration significantly suppressed skin DTH. These results suggest a role for adrenal stress hormones as endogenous immunoenhancing agents. These results also show that hormones released during an acute stress response may help prepare the immune system for potential challenges (e.g., wounding or infection) for which stress perception by the brain may serve as an early warning signal.
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            Effects of stress on the immune system.

            Stress, distress and a variety of psychiatric illnesses, notably the affective disorders, are increasingly reported to be associated with immunosuppression. The concept that psychic distress may predispose to medical illness is centuries old but has only recently attracted the attention of the scientific community at large. Interdisciplinary collaboration has established psychoneuroimmunology, or neuroimmunomodulation, as a new field of investigation with the goal of rigorous scientific research into the elusive mind-body connection. This has resulted in the rapid accumulation of information which falls across the boundary lines of psychiatry, immunology, neurosciences and endocrinology. Here David Khansari, Anthony Murgo and Robert Faith review the effects of stress on the endocrine and central nervous systems and the interactions between these systems and the immune response after exposure to stress signals.
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              Sensory denervation with capsaicin attenuates inflammation and nociception in arthritic rats.

              The relatively few studies that have investigated the effects of the nervous system on chronic joint disease have reported conflicting results. We have reassessed the effects of capsaicin on experimental polyarthritis with particular reference to the relationship between changes in nociception and changes in process and outcome measures of disease activity. Capsaicin pretreatment significantly attenuated both joint swelling and disease outcome as determined by quantitative radiology and histology. There was a close correlation between process measures of inflammation and mechanical hyperalgesia in both the untreated and capsaicin treated arthritic groups. The results confirm a suppression of inflammation by capsaicin and imply that the nociceptive and pro-inflammatory (neurogenic inflammation) activities of capsaicin-sensitive fibres are closely linked such that stimuli which cause pain will also induce neurogenic inflammation and vice versa.
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                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                2001
                December 2001
                13 December 2001
                : 9
                : 3
                : 157-162
                Affiliations
                Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan
                Article
                49020 Neuroimmunomodulation 2001;9:157–162
                10.1159/000049020
                11752889
                © 2001 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. 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. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 5, References: 16, Pages: 6
                Categories
                Original Paper

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