Effects of the 120 days of head-down bed rest on cytokine secretion and its in vitro modulation by glucocorticoids.

Antiorthostatic hypokinesia or head-down bed rest (HDBR), is a ground-based model system used to simulate some of the physioloical responses observed during space flight. Several studies involving humans and animals have demonstrated the effects of HDBR on different physioloical systems. HDBR produced a large thoracic fluid shift similar to that reported for space flight. Exposure to the combination of -6 degrees HDBR, emotional stress, and hypergravity led to an elevation of plasma histamine and serotinin and a dramatic decrease in the concentration of prostaglandins E, F2-alpha, and erthropoietin. These responses indicated the HDBR produces significant alterations in the neuroendocrine regulatory pathways. The proliferative response of immune cells in response to activators was significantly enhanced in antiorthostatically suspended mice; plasma corticosterone also was higher but splenic natural killer cell cytotoxicity remained unchanged after suspension. Bone-resporbing activity of supernatatants increased in mitogen-stimulated PBMC cultures of subjects exposed to -5 degrees HDBR for 370 days of HDBR. Proliferative activity of PBMCs had declined at the end of a 320-day HDBR and during the initial days of recovery, but the numbers of active rosette-forming T cells increased. These and other results suggest that most stress-induced immune changes are neuroendocrine modulated, and that corticosteroids play a significant role in this modulation. It is expected that HDBR-induced immune changes could result from similar mechanisms. In this study, we investigated the effect of 120 days of HDBR on Type-1 vs. Type-2 cytokine equilibrium in mitogen-activated PBMC culture, and how these reactions may correlate with changes in the neuroendocrine status.