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      Are adhesion molecules involved in stress-induced changes in lymphocyte distribution?

      Life Sciences

      Acute Disease, Adrenal Glands, cytology, physiology, Animals, Antigens, CD18, metabolism, Cell Count, Chronic Disease, Corticosterone, blood, Immunophenotyping, Killer Cells, Natural, Lymphocyte Function-Associated Antigen-1, biosynthesis, Lymphocyte Subsets, Macrophage-1 Antigen, Male, Organ Size, Rats, Rats, Sprague-Dawley, Restraint, Physical, psychology, Stress, Psychological, T-Lymphocytes, Helper-Inducer, Thymus Gland, Time Factors, Up-Regulation

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          Acute psychological stress is associated with important changes in circulating cell populations and reductions in cell-mediated immune responses. However, the mechanisms underlying these phenomena are poorly understood. In this study, we investigated (i) acute and chronic restraint stress effects in Sprague-Dawley rats on peripheral lymphocyte subsets and (ii) adhesion molecule (beta2 integrins) expression and (iii) also determined whether glucocorticoids could underlie stress-related changes in cellular redistribution. We observed time-dependent changes in lymphocyte distribution including decreased (-21%) percentages of peripheral T helper cells and increased (88%) NK cell numbers following acute brief restraint. Acute stress was also found to overall upregulate beta2-integrin (CD11a and CD11b) expression on T cells and to raise (1049%) plasma corticosterone levels. However, this stress response was found habituated (-75% vs. acute) in the animals previously exposed to chronic restraint stress. Stress effects on circulating lymphocytes were not observed in animals previously exposed to chronic intermittent restraint stress or chronically stressed animals re-exposed to the same stressor. Our results indicate that 1) stress alters lymphocyte distribution, 2) that adhesion molecules may be involved in stress-induced alterations of T-cell distribution and 3) that these changes may be related to circulating glucocorticoids and subjected to adaptation with repeated stress exposure.

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