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      Effects of Cold Stress on Spleen Cell Proliferation and Cytokine Production during Chronic Toxoplasma gondii Infection

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          Background: Cell-mediated immunity is critical for controlling infection and preventing reactivation during the chronic phase of Toxoplasma gondii infection. In people suffering from AIDS, T. gondii is one of the major opportunistic infectious agents. Mechanisms regulating rapid development of clinical signs in previously asymptomatic patients remain unclear; however, cofactors such as stress are suspected to play a role in the susceptibility to opportunistic infections. Objective: This study examined the role of cold stress (CS) in splenocyte function during chronic T. gondii infection. Methods: Control mice and mice previously infected orally with T. gondii were subjected to CS during the chronic phase (CSchr), i.e. 90 days after infection, and in vitro cell proliferation and cytokine production were measured before (day 0) and 1, 15 and 25 days after CSchr. Splenocyte proliferation and cytokine production were measured after in vitro stimulation with concanavalin A (Con-A), anti-CD3 antibody (A-CD3) and Toxoplasma lysate antigen. Results: CSchr enhanced splenocyte proliferation in cells stimulated with Con-A and A-CD3, but it suppressed proliferation in cells stimulated with T. gondii antigens. Increased levels of interferon (IFN)-γ were detected independent of the type of stimulation after CSchr and remained high throughout the experiment. CS had similar results in noninfected animals. Conclusion: Although an overall increase in splenocyte function occurred after nonspecific stimulation, CS suppressed primed spleen cells from responding to T. gondii antigens which could lead to reactivation of latent infection. The increase in IFN-γ after CSchr could be a result of spleen cells being primed by released parasites by this stressor. IFN-γ is critical in the control of parasite reactivation.

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          Most cited references 12

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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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            Stress-induced enhancement of skin immune function: A role for gamma interferon.

            Contrary to the widespread belief that stress is necessarily immunosuppressive, recent studies have shown that, under certain conditions, stress can induce a significant enhancement of a skin cell-mediated immune response [delayed-type hypersensitivity (DTH) or contact hypersensitivity]. Adrenal stress hormones and a stress-induced trafficking of leukocytes from the blood to the skin have been identified as systemic mediators of this immunoenhancement. Because gamma interferon (IFNgamma) is an important cytokine mediator of DTH, the studies described here were designed to examine its role as a local mediator of the stress-induced enhancement of skin DTH. The effect of acute stress on skin DTH was examined in wild-type and IFNgamma receptor-deficient (IFNgammaR-/-) mice that had previously been sensitized with 2,4-dinitro-1-fluorobenzene. Acutely stressed wild-type mice showed a significantly larger DTH response than nonstressed mice. In contrast, IFNgammaR-/- mice failed to show a stress-induced enhancement of skin DTH. Immunoneutralization of IFNgamma in wild-type mice significantly reduced the stress-induced enhancement of skin DTH. In addition, an inflammatory response induced by direct IFNgamma administration to the skin was significantly enhanced by acute stress. Our results suggest that IFNgamma is an important local mediator of a stress-induced enhancement of skin DTH. These studies are clinically relevant because, depending on the nature of the antigen, DTH reactions mediate numerous protective (e.g., resistance to viral, bacterial, parasitic, and fungal infections) or pathological (e.g., autoimmune reactions and contact sensitivity reactions such as that to poison ivy) immune responses.
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              Stress-associated immune modulation: relevance to viral infections and chronic fatigue syndrome.

              The frequent association of an active viral infection with the symptoms of CFS led researchers to hypothesize that chronic fatigue syndrome (CFS) is induced by a virus. Results of these studies indicated that despite clinical support for this hypothesis, there were no clear data linking viruses to CFS. In this overview, we will explore the interrelation of the immune, endocrine, and central nervous systems, and the possibility that stress and/or the reactivation/replication of a latent virus (such as Epstein Barr virus) could modulate the immune system to induce CFS. Relevant research conducted in the developing field of psychoneuroimmunology will be reviewed, with a particular focus on cytokine synthesis, natural killer (NK) cell activity, and T-lymphocyte function, as they relate to CFS.

                Author and article information

                S. Karger AG
                February 2004
                06 February 2004
                : 11
                : 2
                : 93-102
                aDepartment of Microbiology, Biochemistry and Immunology, Morehouse School of Medicine, Atlanta, Ga., bTerre Haute Center for Medical Education, Indiana University School of Medicine, Terre Haute, Ind., and cDepartment of Biological Sciences, Northern Arizona University, Flagstaff, Ariz., USA
                75318 Neuroimmunomodulation 2004;11:93–102
                © 2004 S. Karger AG, Basel

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                Page count
                Figures: 5, Tables: 1, References: 50, Pages: 10
                Original Paper


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