Article

Diurnal and Acute Stress-Induced Changes in Distribution of Peripheral Blood Leukocyte Subpopulations

Laboratory of Neuroendocrinology, Rockefeller University, New York, New York 10021.
Brain Behavior and Immunity (Impact Factor: 6.13). 04/1994; 8(1):66-79. DOI: 10.1006/brbi.1994.1006
Source: PubMed

ABSTRACT In this study, we examined hormonal regulation of the distribution profiles of leukocyte subpopulations in the peripheral blood of rats. Flow cytometric analysis revealed significant and selective changes in the numbers and the percentages of peripheral blood leukocyte subpopulations which were a function of diurnal variations in hormone secretion and hormonal changes induced by acute stress. Changes in numbers and percentages of leukocyte subpopulations, which varied with time of day, were similar to changes observed under stress conditions. At the beginning of the rat's active period, and after 1 h of restraint stress, there was a significant reduction in numbers of leukocytes and lymphocytes. This reduction was primarily accounted for by a decrease in numbers of B cells, natural killer cells, monocytes (diurnal study), and helper T cells (diurnal study). There was also a significant decrease in the percentage of lymphocytes which was mirrored by an increase in the percentage of neutrophils in the peripheral blood. Peripheral blood leukocyte numbers were inversely related to plasma corticosterone levels. These results suggest that the endocrine system plays a role in the regulation of immune cell turnover and/or redistribution between immune compartments under conditions of normal daily experiences, namely, the diurnal cycle, and mild acute stress. They also suggest that these effects are selective for certain subpopulations of leukocytes.

0 Bookmarks
 · 
58 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: The release of the pituitary hormones, prolactin and growth hormone (GH), and of adrenal corticosteroids is subject to a profound regulation by sleep. In addition these hormones are known to be involved in the regulation of the immune response. Here, we examined their role for in vitro production of T-cell cytokines. Specifically, we hypothesized that increased concentrations of prolactin and GH as well as a decrease in cortisol, i.e., hormonal changes characterizing early nocturnal sleep, could be responsible for a shift towards T helper 1 (Th1) cytokines during this time. Whole blood was sampled from 15 healthy humans in the morning after regular sleep and was activated in vitro with ionomycin and two concentrations of phorbol myrestate acetate (PMA, 8 and 25 ng/ml) in the absence or presence of prolactin, prolactin antibody, GH, glucocorticoid receptor (GR) antagonist RU-486, or mineralocorticoid receptor (MR) antagonist spironolactone. Hormones were examined at physiological concentrations. Production of T-cell derived cytokines was measured at the single cell level using multiparametric flow cytometry. Generally, effects were more pronounced after stimulation with 8 rather than 25 ng/ml PMA. The following changes reached significance (p<.05): prolactin (versus prolactin antibody) increased tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) producing CD4+ and CD8+ cells and interleukin-2 (IL-2) producing CD8+ cells. Compared with control, prolactin antibody decreased, whereas GH increased IFN-γ + CD4+ cells. RU-486 increased TNF-α, IFN-γ, and IL-2 producing CD4+ and CD8+ cells. Surprisingly strong effects were found after MR blocking with spironolactone which increased TNF-α, IFN-γ, and IL-2 producing CD4+ and CD8+ cells. No effects on IL-4 + CD4+ cells were observed, while the IFN-γ/IL-4 ratio shifted towards Th1 after spironolactone and after RU-486 plus GH. Results suggest that enhanced prolactin and GH concentrations as well as low cortisol levels during early nocturnal sleep synergistically act to enhance Th1 cytokine activity.
    Brain Behavior and Immunity 07/2004; 18(4):368-374. DOI:10.1016/S0889-1591(03)00170-3 · 6.13 Impact Factor
  • Source
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Sickness behavior, a coordinated set of behavioral changes in response to infection, lies at the intersection of immunology, endocrinology, and evolutionary biology. Sickness behavior is elicited by pro-inflammatory cytokines, is thought to be an adaptive means of redirecting energy away from disadvantageous behaviors and toward mounting an effective immune response, and may be modulated by hormones, including testosterone and oxytocin. Research on sickness behavior in humans has lagged behind non-human animal research due to methodological complexities. Here we review what is known about sickness behavior in humans, the effects of various hormones on sickness behavior, the possible role of cytokine gene variation in influencing sickness behavior responses, and the ways in which culture and gender norms could similarly influence these behavioral changes. We also propose methodologies for advancing further studies of sickness behavior in humans.
    American Journal of Physical Anthropology 01/2015; DOI:10.1002/ajpa.22698 · 2.51 Impact Factor