The mechanisms of immune suppression by high-pressure stress in mice

The effects of high-pressure stress on the induction of anti-sheep red bloo d cells (SRBC) and of plaque-forming cells (PFC), and on thymus weight, wer e studied in BALB/c mice in-vivo and in-vitro. The efficacy of high-pressure stress in suppressing PFC and thymic involuti on was maximum when the stress was applied 1 h day(-1) for 2 days before im munization with SRBC. Both effects were blocked by administration of indome thacin, atropine, naloxone or phentolamine before the first application of stress, whereas hexamethonium and propranolol had no such effect. Hexametho nium, naloxone and propranolol administered before the second application o f high-pressure stress blocked both effects. Prostaglandin and acetylcholin e given 24 h before application of high-pressure stress caused a marked red uction in PFC count, but not in thymus weight. The reduced PFC count caused by acetylcholine was blocked by pretreatment with indomethacin. When adren aline was injected 24 h after application of high-pressure stress a marked reduction in PFC was observed, but without thymic involution. When adrenali ne was injected 24 h after prostaglandin injection the PFC count was also m arkedly reduced, but not thymus weight. The decrease in PFC caused by two e xposures to stress or one exposure to stress plus injection of adrenaline w as blocked by diethylcarbamazine before the second exposure to stress or th e injection of adrenaline. In addition, normal spleen cells were induced as suppressor cells when incubated with the serum of stressed mice, but not w hen supplemented with anti-leukotriene C-4, D-4 antibody. These data suggest that mice fall into a pre-stress condition via the relea se of prostaglandin after the first stress, and then immunosuppression is i nduced in these prestressed mice via the release of leukotriene C-4, D4, ca used by the activation of the autonomic nervous system by the second exposu re to stress.