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      Physical training attenuates the stress-induced changes in rat T-lymphocyte function.

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          Abstract

          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.

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

          R M Sapolsky (2000)
          Article 0 comments Cited 489 times – based on 0 reviews     Review now
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            Glucocorticoids in T cell development and function*.

            Melanie S. Vacchio, Jonathan Ashwell, F. Lu (1999)
            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.

              Volker Stefanski, Harald Engler (1998)
              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
                Journal ID (iso-abbrev): Neuroimmunomodulation
                Title: Neuroimmunomodulation
                Publisher: S. Karger AG
                ISSN: 1021-7401
                ISSN (Print): 1021-7401
                Publication date (Electronic): 2006
                Volume: 13
                Issue: 2
                Affiliations
                [1 ] Superior School of Physical Education, Federal University of Pernambuco, Recife, Brazil.
                Article
                Publisher Item ID: 96432
                DOI: 10.1159/000096432
                PubMed ID: 17063041
                SO-VID: 30b81fdb-ea8b-419d-b208-0e9008eaf863
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