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      Acute Stress May Facilitate Recovery from a Subcutaneous Bacterial Challenge

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          The effects of stress on the immune system vary with both the duration and type of stressor. Many studies suggest that stress may compromise an organism’s ability to recover from immune challenge. However, recent findings suggest that stress may actually enhance some aspects of immune function. For example, exposure to a single session (∼2 h) of intermittent inescapable tailshocks (IS) has been shown to activate the acute phase response and increase some aspects of macrophage function. Thus, the following experiments assessed whether IS exposure would alter local inflammation produced by peripheral injection of streptomycin-killed bacteria. Rats (Harlan Sprague Dawley) were exposed to IS (100 1.6-mA, 60 s variable intertrial interval) and injected with Escherichia coli (∼2.5 × 10<sup>8</sup> CFU s.c. posterior to the shoulder blades). The area of inflammation was measured until the inflammation had completely resolved (typically 7–8 days). When bacteria were administered immediately after IS, rats resolved inflammation significantly faster than did nonstressed rats. Since adrenalectomy did not reduce the effect of IS, it is unlikely that this effect is a result of elevated corticosterone levels. Furthermore, IS does not appear to alter the rat’s ability to sequester bacteria in the subcutaneous space since no swelling of lymph nodes or chronic activation of the hypothalamic-pituitary-adrenal axis was observed.

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          Most cited references 6

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          The acute phase response.

          Adult mammals respond to tissue damage by implementing the acute phase response, which comprises a series of specific physiological reactions. This review outlines the principal cellular and molecular mechanisms that control initiation of the tissue response at the site of injury, the recruitment of the systemic defense mechanisms, the acute phase response of the liver and the resolution of the acute phase response.
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            IL-6 and APPs: anti-inflammatory and immunosuppressive mediators.

            Acute inflammation is accompanied by changes in the concentrations of acute phase proteins (APPs). While much is known about the cytokines involved in the initiation of inflammation, less is known about the mediators involved in its resolution. Recent data suggest that interleukin 6 (IL-6) and IL-6-regulated APPs are anti-inflammatory and immuno-suppressive, and may negatively regulate the acute phase response.
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              The effects of psychological stress on plasma interleukin-6 activity in rats.

              The purpose of this study was to determine the effects of a particular psychological stress, exposure to an open-field, on plasma IL-6 activity in rats. Plasma IL-6 activity was 40.6 +/- 7.2 units/ml in control rats, 105 +/- 6.8 units/ml after 30 minutes exposure to an open-field, and 221 +/- 17 units/ml after 60 minutes of exposure (p = 0.0003). There was a positive correlation (r = .71, p = 0.043) between the change in plasma IL-6 activity and body temperature. However, we conclude, based on earlier data relating plasma IL-6 activity to body temperature changes following injection of lipopolysaccharide, that the plasma levels of IL-6 following exposure to an open-field are not high enough to account for the rise in body temperature observed in rats during this stress. In conclusion, these experiments indicate that exposure to psychological stress can elevate the plasma concentration of IL-6, a known mediator of the acute phase response.

                Author and article information

                S. Karger AG
                August 1999
                01 September 1999
                : 6
                : 5
                : 344-354
                aDepartment of Psychology and bDepartment of Kinesiology and Applied Physiology, University of Colorado, Boulder, Colo., USA
                26394 Neuroimmunomodulation 1999;6:344–354
                © 1999 S. Karger AG, Basel

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                Figures: 6, References: 59, Pages: 11
                Original Paper


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