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Am J Physiol Regul Integr Comp Physiol 275: R870-R878, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 3, R870-R878, September 1998

Acute stressor exposure both suppresses acquired immunity and potentiates innate immunity

Monika Fleshner1, Kien T. Nguyen2, Crystal S. Cotter2, Linda R. Watkins2, and Steven F. Maier2

1 Department of Kinesiology and Applied Physiology and 2 Department of Psychology, University of Colorado, Boulder, Colorado 80309

Acute stressor exposure alters immune function. Rats exposed to inescapable tail shock stress (IS) generate less antibody to a benign, antigenic protein, keyhole limpet hemocyanin (KLH). The following studies examined the effect of IS on peritoneal cavity, spleen, and mesenteric lymph node cell number, interferon-gamma (IFN-gamma ) production, and nitrite production. Rats were injected intraperitoneally with KLH (200 µg) or saline immediately before IS exposure and killed 0, 48, and 96 h after IS termination. KLH immunization resulted in elevated cell numbers and IFN-gamma levels 2-4 days later in nonstressed control rats. In contrast, rats exposed to IS failed to increase cell number and IFN-gamma levels in response to KLH. The T cell subpopulations affected were CD4 T cells, specifically the Th1-like subset. In addition, in rats exposed to IS + KLH, nitrite production was potentiated 2-4 days after stressor termination. IS had little effect on these measures in saline-injected rats. These data support the conclusion that exposure to IS suppresses the expansion of anti-KLH lymphocytes, possibly anti-KLH Th1 cells. In addition, stressor exposure potentiates the production of nitrite. Importantly, this potentiated response occurred only in KLH-immunized animals, suggesting that macrophages may be primed by stressor exposure and thus respond more vigorously to antigen. The potential links between these changes are discussed.

stress; Th1 cells; CD4 T cells; nitric oxide; keyhole limpet hemocyanin; interferon-gamma


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