ACUTE STRESSOR EXPOSURE BOTH SUPPRESSES ACQUIRED-IMMUNITY AND POTENTIATES INNATE IMMUNITY

Acute stressor exposure alters immune function. Rats exposed to inesca pable tail shock stress (IS) generate less antibody to a benign, antig enic protein, keyhole limpet hemocyanin (KLH). The following studies e xamined the effect of IS on peritoneal cavity, spleen, and mesenteric lymph node cell number, interferon-gamma (IFN-gamma) production, and n itrite production. Rats were injected intraperitoneally with KLH (200 mu g) or saline immediately before IS exposure and killed 0, 48, and 9 6 h after IS termination. KLH immunization resulted in elevated cell n umbers and IFN-gamma levels 2-4 days later in nonstressed control rats . In contrast, rats exposed to IS failed to increase cell number and I FN-gamma levels in response to KLH. The T cell subpopulations affected were CD4 T cells, specifically the Th1-like subset. In addition, in r ats exposed to IS + KLH, nitrite production was potentiated 2-4 days a fter stressor termination. IS had little effect on these measures in s aline-injected rats. These data support the conclusion that exposure t o IS suppresses the expansion of anti-KLH lymphocytes, possibly anti-K LH Th1 cells. In addition, stressor exposure potentiates the productio n of nitrite. Importantly, this potentiated response occurred only in KLH-immunized animals, suggesting that macrophages may be primed by st ressor exposure and thus respond more vigorously to antigen. The poten tial Links between these changes are discussed.