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      Beta-Adrenergic Receptor Blockade Attenuates the Exercise-Induced Suppression of TNF-Alpha in Response to Lipopolysaccharide in Rats

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          Stressful exercise has been found to reduce the proinflammatory cytokine response to lipopolysaccharide (LPS). In this study, we aimed to determine whether receptor antagonists for corticosterone or catecholamines would increase the LPS-induced tumor necrosis factor-α (TNF-α) response after exhaustive exercise. Female F344 rats were randomly assigned to one of five groups: control (vehicle), RU-486 (glucocorticoid receptor antagonist, 30 mg/kg)-, propranolol [nonselective β-adrenergic receptor (AR) blockade, 30 mg/kg]-, atenolol (β<sub>1</sub>-AR blockade, 30 mg/kg)-, or ICI 118551 (β<sub>2</sub>-AR blockade, 30 mg/kg)-treated groups. Each antagonist was given intraperitoneally 30 min prior to exercise or control period. Exercised rats ran until exhaustion on a treadmill at gradually increasing speeds, from 10 to 36 m/min at 15% grade. Immediately postexercise or control period all rats were injected with LPS (1 mg/kg, i.v.). Plasma TNF-α was reduced by prior exercise to approximately 10% of that of sedentary controls (p < 0.01). Plasma TNF-α concentration in exercised RU-486-treated rats was significantly different than that of nonexercised rats (19.2%, p < 0.01) and not different from exercised rats. However, pretreatment of rats with the nonselective β-AR blocker propranolol almost completely reversed the exercise-induced suppression of plasma TNF-α in response to LPS. β<sub>1</sub>-AR pretreatment almost completely attenuated the exercise-induced suppression of LPS-induced plasma TNF-α while β<sub>2</sub>-antagonism had a partial effect. These results indicate that exercise-induced catecholamines, acting through β-ARs (especially the β<sub>1</sub>-AR), are responsible for the exercise-induced suppression of plasma TNF-α after LPS administration.

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          Most cited references 15

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          Acute stress enhances while chronic stress suppresses cell-mediated immunity in vivo: a potential role for leukocyte trafficking.

          Delayed type hypersensitivity (DTH) reactions are antigen-specific, cell-mediated immune responses which, depending on the antigen involved, mediate beneficial (resistance to viruses, bacteria, fungi, and certain tumors) or harmful (allergic dermatitis, autoimmunity) aspects of immune function. We have shown that acute stress administered immediately before antigenic challenge results in a significant enhancement of a skin DTH response in rats. A stress-induced trafficking or redeployment of leukocytes to the skin may be one of the factors mediating this immunoenhancement. Here we investigate the effects of varying the duration, intensity, and chronicity of stress on the DTH response and on changes in blood leukocyte distribution and glucocorticoid levels. Acute stress administered for 2 h prior to antigenic challenge, significantly enhanced the DTH response. Increasing the duration of stress from 2 h to 5 h produced the same magnitude enhancement in cutaneous DTH. Moreover, increasing the intensity of acute stress produced a significantly larger enhancement of the DTH response which was accompanied by increasing magnitudes of leukocyte redeployment. In contrast, chronic stress suppressed the DTH response when it was administered for 3 weeks before sensitization and either discontinued upon sensitization, or continued an additional week until challenge, or extended for one week after challenge. The stress-induced redeployment of peripheral blood lymphocytes was attenuated with increasing exposure to chronic stress and correlated with attenuated glucocorticoid responsivity. These results suggest that stress-induced alterations in lymphocyte redeployment may play an important role in mediating the bi-directional effects of acute versus chronic stress on cell-mediated immunity in vivo.
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            Stress hormones, proinflammatory and antiinflammatory cytokines, and autoimmunity.

            Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)-12, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-gamma, whereas they stimulate the production of antiinflammatory cytokines, such as IL-10, IL-4, and transforming growth factor (TGF)-beta. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an "overshoot" of proinflammatory cytokines and other products of activated macrophages with tissue-damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF-alpha, IL-1, and IL-8, and by inhibiting TGF-beta production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.
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              NK cell response to physical activity: possible mechanisms of action.

              Natural killer (NK) cells are highly influenced by physical exercise. The possible important mechanisms behind exercise-induced changes in NK cell function are cytokines, hyperthermia, and stress hormones, including catecholamines, growth hormone, cortisol, and beta-endorphins. Infusion studies mimicking stress hormone levels in blood during exercise indicate that increased plasma-adrenaline accounts for at least part of the exercise-induced modulation of NK cell function. During moderate as well as severe acute exercise, the NK cell activity is enhanced, but severe exercise is followed by immunodepression, at least in part caused by prostaglandins. Elite athletes have at rest elevated NK cell activity. However, due to frequent severe exercise the NK cell function is often temporarily severely depressed. It is suggested that during the time of immunodepression microorganisms, especially virus, invade the host, whereby infections can be established. However, in those who perform regular moderate exercise the immune system will often be temporarily enhanced and this will protect these from infections.

                Author and article information

                S. Karger AG
                September 2007
                21 August 2007
                : 14
                : 2
                : 91-96
                aDepartment of Health and Nutrition, Wayo Women’s University, Chiba, and bDepartment of Health and Sports Science, Kawasaki University of Medical Welfare, Okayama, Japan; cDepartment of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Champaign, Ill., USA
                107424 Neuroimmunomodulation 2007;14:91–96
                © 2007 S. Karger AG, Basel

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                Page count
                Figures: 2, Tables: 2, References: 26, Pages: 6
                Original Paper


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