Cortisol mediates redistribution of CD8+but not of CD56+cells after the psychological stress of public speaking

The present study investigated the question if a pharmacological blockade o f cortisol release with stress affects lymphocyte redistribution in healthy volunteers. It was expected that the well known increases in the number of CD8+ (T-suppressor/cytotoxic cells) and CD56+ (natural killer cells) after stress would not be downregulated in the absence of an appropriate cortiso l response, since redistribution is markedly influenced by glucocorticoids. In a double blind design, forty healthy male volunteers were exposed to a b rief psychological stressor (public speaking) and received a single oral do se of dexamethasone [DEX] (N=20) or placebo (N=20) the evening before the m ain experiment. Ratings on emotional states and blood samples for determina tion of hormones, CD8+, and CD56+ cell counts were obtained at different ti me points during the experiment. Stress of public speaking led to highly significant increases in catecholam ine and cortisol concentrations, to subjective discomfort and, most pronoun ced, to high increases in the number of CD8+ and CD56+ cells. DEX neither i nfluenced baseline levels of mood, catecholamines and cell numbers nor stre ss induced responses of mood and catecholamines. However, during the whole experiment cortisol concentrations were suppressed in the DEX-condition and the number of CD8+, but not CD56+, cells remained elevated at the end of t he session, while in the placebo condition the numbers of these cells were decreased to baseline levels. The data demonstrate that cortisol seems to play an important role in stres s induced redistribution patterns of CD8+ but not CD56+ cells. This, howeve r, can be explained by different migration processes between those cells (e .g. different targets of migration) and, therefore, different glucocorticoi d influences on target tissues. (C) 2001 Elsevier Science Ltd. All rights r eserved.