Stressor-specific alterations in corticosterone and immune responses in mice
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- 作者：Stephanie L. Bowers ; Staci D. Bilbo ; Firdaus S. Dhabhar ; R ; y J. Nelson
- 关键词：Restraint ; Glucocorticoids ; Low temperature ; Stressors ; Stress ; Isolation ; Mice ; Delayed-type hypersensitivity
- 刊名：Brain, Behavior, and Immunity
- 出版年：2008
- 出版时间：January 2008
- 年：2008
- 卷：22
- 期：1
- 页码：105-113
- 全文大小：259 K
文摘
Different stressors likely elicit different physiological and behavioral responses. Previously reported differences in the effects of stressors on immune function may reflect qualitatively different physiological responses to stressors; alternatively, both large and subtle differences in testing protocols and methods among laboratories may make direct comparisons among studies difficult. Here we examine the effects of chronic stressors on plasma corticosterone concentrations, leukocyte redistribution, and skin delayed-type hypersensitivity (DTH), and the effects of acute stressors on plasma corticosterone and leukocyte redistribution. The effects of several commonly used laboratory stressors including restraint, forced swim, isolation, and low ambient temperatures (4 °C) were examined. Exposure to each stressor elevated corticosterone concentrations, with restraint (a putative psychological stressor) evoking a significantly higher glucocorticoid response than other stressors. Chronic restraint and forced swim enhanced the DTH response compared to the handled, low temperature, or isolation conditions. Restraint, low temperature, and isolation significantly increased trafficking of lymphocytes and monocytes compared to forced swim or handling. Generally, acute restraint, low temperature, isolation, and handling increased trafficking of lymphocytes and monocytes. Considered together, our results suggest that the different stressors commonly used in psychoneuroimmunology research may not activate the physiological stress response to the same extent. The variation observed in the measured immune responses may reflect differential glucocorticoid activation, differential metabolic adjustments, or both processes in response to specific stressors.