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      Physical Training Attenuates the Stress-Induced Changes in Rat T-Lymphocyte Function

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          Abstract

          Backgorund/Aims: Modulations in the immune function by stress are a well-known phenomenon. Acute restraint stress may induce impaired T-lymphocyte responses. Moderate physical training is associated with beneficial effects on immunological functions. We investigated the effects of a moderate physical training on T-lymphocyte function in rats submitted to acute restraint stress. Methods: Thirty male Wistar rats weighing 210–226 g were randomly divided into four groups: non-trained rats (NT, n = 7), and non-trained rats submitted to stress (NT + S, n = 8); trained rats (T, n = 7), and trained rats submitted to stress (T + S, n = 8). Trained rats were submitted to a program of moderate running over a period of 8 weeks. Rats subjected to restraint stress were kept immobilized in glass cylinders (8 cm in diameter and 24 cm long) during 60 min. Plasma corticosterone concentration, peripheral blood leukocyte number, indicators of apoptosis of T lymphocytes in blood and lymphoid organs, and mitogen-induced proliferation of T lymphocytes in lymphoid organs were evaluated. Results: Acute stress exposure raised plasma corticosterone concentration (p < 0.001), but not in previously trained animals. Restraint stress induced an increase in the percentage of lymphocytes in apoptosis, and a decrease in the concanavalin-A-induced proliferation of lymphocytes from the thymus and lymph nodes, and an increase in lymphocytes of the spleen. Neither of these alterations was observed in trained animals submitted to acute restraint stress. Conclusions: Our data confirm that acute restraint stress is associated with changes in T-lymphocyte function. Moreover, moderate physical training attenuates the effects of acute stress by a mechanism that involves the hypothalamic-pituitary-adrenal axis and an increase in tolerance of leukocytes.

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          Most cited references 17

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          How Do Glucocorticoids Influence Stress Responses? Integrating Permissive, Suppressive, Stimulatory, and Preparative Actions

           R M Sapolsky (2000)
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            Glucocorticoids in T cell development and function*.

            Glucocorticoids are small lipophilic compounds that mediate their many biological effects by binding an intracellular receptor (GR) that, in turn, translocates to the nucleus and directly or indirectly regulates gene transcription. Perhaps the most recognized biologic effect of glucocorticoids on peripheral T cells is immunosuppression, which is due to inhibition of expression of a wide variety of activationinduced gene products. Glucocorticoids have also been implicated in Th lineage development (favoring the generation of Th2 cells) and, by virtue of their downregulation of fasL expression, the inhibition of activation-induced T cell apoptosis. Glucocorticoids are also potent inducers of apoptosis, and even glucocorticoid concentrations achieved during a stress response can cause the death of CD4(+)CD8(+ )thymocytes. Perhaps surprisingly, thymic epithelial cells produce glucocorticoids, and based upon in vitro and in vivo studies of T cell development it has been proposed that these locally produced glucocorticoids participate in antigen-specific thymocyte development by inhibiting activation-induced gene transcription and thus increasing the TCR signaling thresholds required to promote positive and negative selection. It is anticipated that studies in animals with tissue-specific GR-deficiency will further elucide how glucocorticoids affect T cell development and function.
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              Effects of acute and chronic social stress on blood cellular immunity in rats.

              The study compares the impact of acute and chronic social confrontation on aspects of blood cellular immunity in Long-Evans intruder rats. An adult male was introduced for either 2 h or 48 h into a male-female resident group, which resulted in fights for dominance. Thirty-eight of the 42 intruders became losers. For immunologic measurements, blood samples were taken from the intruders before confrontation (baseline) and 2 h or 48 h after the beginning of confrontation. Two h of confrontation resulted in increased granulocyte (+65%) and decreased lymphocyte numbers (-60%), as well as in differential reductions in CD4, CD8, and B cell numbers. CD4/CD8 and T/B ratios were elevated. T cell responsiveness to ConA was markedly suppressed in proliferation assays using either whole blood (-90%) or PBMC (-50%). The direction of changes in leukocyte and lymphocyte subsets after 48 h resembled in many aspects the 2 h changes, although with lower magnitude. In contrast to acute stress, a lowered T/B cells ratio and unaffected CD4/CD8 ratio was determined after 48 h. Proliferative response of T cells was lowered by about 25% in the whole blood assay; but unaffected in the PBMC assay. Significant correlations were found between the amount of submissive behavior displayed by the losers and several immunologic measures after 2 h of confrontation. The data suggest that acute and chronic stressful conditions may not necessarily result in similar effects on immune functioning. This should be considered when evaluating the biologic and evolutionary consequences of social stress-induced immune alterations.
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                Author and article information

                Journal
                NIM
                Neuroimmunomodulation
                10.1159/issn.1021-7401
                Neuroimmunomodulation
                S. Karger AG
                1021-7401
                1423-0216
                2006
                November 2006
                24 November 2006
                : 13
                : 2
                : 105-113
                Affiliations
                aSuperior School of Physical Education and Departments of bNutrition and cTropical Medicine, Federal University of Pernambuco, Recife, and dInstitute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil
                Article
                96432 Neuroimmunomodulation 2006;13:105–113
                10.1159/000096432
                17063041
                © 2006 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: 3, Tables: 2, References: 33, Pages: 9
                Categories
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