Stressor-specific alterations in corticosterone and immune responses in mice.

Published

Journal Article

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 degrees 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.

Full Text

Cited Authors

  • Bowers, SL; Bilbo, SD; Dhabhar, FS; Nelson, RJ

Published Date

  • January 2008

Published In

Volume / Issue

  • 22 / 1

Start / End Page

  • 105 - 113

PubMed ID

  • 17890050

Pubmed Central ID

  • 17890050

Electronic International Standard Serial Number (EISSN)

  • 1090-2139

International Standard Serial Number (ISSN)

  • 0889-1591

Digital Object Identifier (DOI)

  • 10.1016/j.bbi.2007.07.012

Language

  • eng