Although a considerable amount of evidence has shown that physical and psychological stress elevates the plasma interleukin 6 (IL-6) levels, the physiological significance of such an elevation remains to be elucidated. In this study, in order to determine whether the restraint stress-induced elevation of plasma IL-6 contributes to the activation of the hypothalamic-pituitary-adrenal axis, and whether or not such elevation can affect the inflammatory processes, the plasma levels of ACTH, corticosterone, interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-alpha) in mice pretreated with anti-IL-6 antibody (MP5-20F3 monoclonal antibody) were compared with those in mice pretreated with rat IgG (control antibody) both during and after stress. Both the anti-IL-6-antibody- and control-antibody-pretreated mice showed the same extent of plasma ACTH and corticosterone increases during stress, and no significant difference was found between the two groups of animals. On the other hand, the level of plasma TNF-alpha in the anti-IL-6-treated animals was also significantly higher than that in the control animals both immediately after cessation of stress and 60 min after the cessation of the 120-min period of restraint. Plasma IL-1 activity, however, did not reach a detectable level in either group of animals at any time point examined. These results thus indicate that the restraint-stress-induced elevation of plasma IL-6 negatively regulates the plasma TNF-alpha levels and may thus contribute to the maintenance of homeostasis.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Restraint stress causes tissue-specific changes in the immune cell distribution.

In this study, the effect of restraint stress on alterations in the immune cell distribution was examined in bone marrow, liver, thymus, and spleen. In bone marrow, stress induced a striking increase in both the proportion and number of CD3+CD4+, CD3+CD8+, B220brightIgM+, CD3-IL-2R beta + and CD3intIL-2R beta + cells. Such an increase was partially reversed by pretreatment with RU-486, a steroid receptor antagonist, while it was profoundly enhanced by either sympathectomy with 6-hydroxydopamine hydrobromide or by a beta-adrenergic blockade with propranolol, a beta-adrenergic receptor antagonist; this suggests that corticosteroids and catecholamines may act in opposition with regard to such an immune-cell accumulation in bone marrow. In the liver, stress decreased the proportions of CD3intIL-2R beta +, CD3-IL-2R beta +, and B220brightIgM+ cells, while it increased the proportion of CD3brightIL-2R beta-cells, thus demonstrating that different subpopulations were differentially affected. In the thymus and spleen, stress only slightly affected the proportions of lymphocyte subpopulations, although both tissues showed a drastic reduction in the number of lymphocytes. Taken together, these results suggest that restraint stress induces tissue-specific changes in the immune-cell distribution.

Animals↗