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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-
(IFN-
) 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-
levels 2-4 days later in nonstressed control rats. In contrast, rats exposed to IS failed to increase cell number and IFN-
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-
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