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contributes to antibody suppression produced
by stress
1 Department of Kinesiology and Applied Physiology, 2 Department of Psychology, and 3 Center for Neuroscience, University of Colorado at Boulder, Boulder, Colorado 80309; and 4 Ethicon, Somerville, New Jersey 08876
Acute stressor
exposure can facilitate innate immunity and suppress acquired
immunity. The present study further characterized the potentiating
effect of stress on innate immunity, interleukin-1
(IL-1
), and
demonstrated that stress-induced potentiation of innate immunity may
contribute to the stress-induced suppression of acquired immunity. The
long-term effect of stress on IL-1
was measured by using an ex vivo
approach. Sprague-Dawley rats were challenged with lipopolysaccharide
(LPS) in vivo, and the IL-1
response was measured in vitro.
Splenocytes, mesenteric lymphocytes, and peritoneal cavity cells had a
dose- and time-dependent ex vivo IL-1
response to LPS. Rats that
were exposed to inescapable shock (IS, 100 1.6 mA, 5-s tail shocks,
60-s intertrial interval) and challenged with a submaximal dose
of LPS 4 days later had elevated IL-1
measured ex vivo. To test
whether the acute stress-induced elevation in IL-1
contributes to
the long-term suppression in acquired immunity, IL-1
receptors were
blocked for 24 h after stress. Serum anti-keyhole limpet
hemocyanin (KLH) immunoglobulin (Ig) was measured. In addition, the
acute elevation (2 h post-IS) of splenic IL-1
in the absence of
antigen was verified. Interleukin-1 receptor antagonist prevented
IS-induced suppression in anti-KLH Ig. These data support the
hypothesis that stress-induced increases in innate immunity (i.e.,
IL-1
) may contribute to stress-induced suppression in acquired
immunity (i.e., anti-KLH Ig).
interleukin-1
; interleukin-1 receptor antagonist; keyhole limpet
hemocyanin; lipopolysaccharide
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