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Abstract
Delayed-type hypersensitivity (DTH) reactions represent cell-mediated immune responses
that exert important immunoprotective (resistance to viruses, bacteria, and fungi)
or immunopathological (allergic or autoimmune hypersensitivity) effects. We initially
utilized the skin DTH response as an experimental in vivo model to study neuro-endocrine-immune
interactions in rodents. We hypothesized that just as an acute stress response prepares
the cardiovascular and musculoskeletal systems for fight or flight, it may also prepare
the immune system for challenges which may be imposed by a stressor. The skin DTH
model allowed us to examine the effects of stress at the time of primary and secondary
exposure to antigen. Studies showed that acute (2h) stress experienced before primary
or secondary antigen exposure induces a significant enhancement of skin DTH. Importantly,
this enhancement involved innate as well as adaptive immune mechanisms. Adrenalectomy
eliminated the stress-induced enhancement of DTH. Acute administration of physiological
(stress) concentrations of corticosterone and/or epinephrine to adrenalectomized animals
enhanced skin DTH. Compared with controls, DTH sites from acutely stressed or hormone-injected
animals showed significantly greater erythema and induration, numbers of infiltrating
leukocytes, and levels of cytokine gene expression. In contrast to acute stress, chronic
stress was immunosuppressive. Chronic exposure to corticosterone, or acute exposure
to dexamethasone significantly suppressed skin DTH. These results suggest that during
acute stress, endogenous stress hormones enhance skin immunity by increasing leukocyte
trafficking and cytokine gene expression at the site of antigen entry. While these
results are discussed from a mechanistic and clinical relevance perspective, it is
acknowledged that much work remains to be done to elucidate the precise mechanisms
mediating these bi-directional effects of stress and stress hormones and their clinical
ramifications.