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      Modulation of Early Immune Responses and Suppression of Trypanosoma brucei brucei Infections by Surgical Denervation of the Spleen

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          Objective: To examine critical interactions between the nervous system and the immune system during experimental African trypanosomiasis. Methods and Results: Inoculation of Trypanosoma brucei brucei resulted in early interferon (IFN)-γ production, elevated corticosterone and prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) levels and increased splenocyte proliferation, as measured by enzyme-linked immunospot assay, radioimmunoassay and thymidine incorporation assay, respectively. Splenic denervation suppressed IFN-γ, corticosterone and PGE<sub>2</sub> production, enhanced splenocyte proliferation, and significantly reduced parasitemia and prolonged rat survival. Conclusions: Our data show substantial effects of the nervous system on early immune responses that may influence the outcome of this disease. These effects were not dependent on cytokine inhibitory mediators such as prostaglandins or stress hormones. More investigations are required to understand the evident neural control over the immune system during infectious challenges, which may assist in novel therapeutic approaches.

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          Most cited references 3

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          Reverse ELISPOT assay for clonal analysis of cytokine production. I. Enumeration of gamma-interferon-secreting cells.

          A reverse modification of ELISPOT assay using nitrocellulose membranes and epitope-specific monoclonal antibodies is described for the detection of single lymphokine-secreting cells. As a model, the production of gamma-interferon by mitogen stimulated human peripheral blood lymphocytes has been examined. The assay can also be modified to permit microscopic examination of spot-forming cells.
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            Update on the mechanisms of immune suppression of injury and immune modulation.

             S Zimmer,  E Faist,  C Schinkel (1996)
            Major trauma results in massive impairment of immunologic reactivity, the clinical consequence of which consists in the high susceptibility of the traumatized individual toward serious infection. Whereas parts of the immune system are stimulated within a systemic, nondiscriminant, excessive whole-body inflammation, other functions within the complex of cell-mediated immunity (CMI) are dramatically paralyzed. Immune abnormalities in the aftermath of trauma occur in a sequence of states of cellular activation and within a complex order of events that is not yet well understood. Traumatic stress is causing disintegration of the intact monocyte (Mphi)-T cell interaction, which is associated with profound changes in Mphi forward-regulatory capacities and substantial depression of T cell function. Extensive tissue destruction results in the generation of numerous stimuli, such as phagocytosis, immune complexes, complement split products, and endo- and exotoxins, all of which contribute to excessive Mphi activation. Mphi then rapidly produce and release prostaglandin E2 (PGE2), a powerful endogenous immune suppressant. PGE2 is an inhibitor of T cell mitogenesis, interleukin 2 (IL-2) production, and IL-2 receptor expression; and it has a massive impact on the quality of B cell antibody synthesis. Most importantly, PGE2 represents an important cofactor for the induction of T-helper lymphocyte (TH) activity toward the TH2 direction. TH2 cells are associated with the synthesis of immunosuppressive cytokines, such as IL-4 and IL-10. Although immunosuppressive substrates are inhibitory for TH1 cells-the functional carriers of CMI-they support TH2 activity, which predisposes the host to develop infection. The endogenous ability of the organism to survive overwhelming trauma is insufficient and requires major exogenous support. Immune modulatory interventions, depending on the immune abnormalities seen in the traumatized host, should be started as early as possible after trauma in a preventive fashion to protect against organ tissue destruction. Ideally, it should protect all cellular host defense compartments from hyperactivation as well as from exhaustion. We do believe that only a combination of drugs can effectively control the posttraumatic dyshomeostasis of the various cell systems.
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              T cell immunity and interferon-γ secretion during experimental allergic encephalomyelitis in Lewis rats


                Author and article information

                S. Karger AG
                June 2000
                08 June 2000
                : 8
                : 1
                : 31-38
                Departments of aInfectious Diseases, bPedodontics, cNeurology and dGeriatrics, Karolinska Institute, Huddinge University Hospital, Stockholm, Sweden; eDepartment of Radiotherapy and Oncology, Kreft Clinic, R.I.T., Trondheim University Hospital, Trondheim, Norway
                26450 Neuroimmunomodulation 2000;8:31–38
                © 2000 S. Karger AG, Basel

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                Page count
                Figures: 6, References: 18, Pages: 8
                Original Paper


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