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Am J Physiol Regul Integr Comp Physiol (October 24, 2002). doi:10.1152/ajpregu.00230.2002
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Articles in PresS, published online ahead of print October 24, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00230.2002
Submitted on April 23, 2002
Accepted on October 18, 2002

Effects of prior stress on LPS-induced cytokine and sickness responses

John D Johnson1*, Kevin A O'Connor1, Michael K Hansen2, Linda R Watkins1, and Steven F Maier1

1 Pyschology and Center for Neuroscience, University of Colorado, Boulder, CO, USA
2 Pyschology and Center for Neuroscience, University of Colorado, Boulder, CO, USA; High Throughput Biology, GlaxoSmithKline Pharmaceuticals, King of Prussia, PA, USA

* To whom correspondence should be addressed. E-mail: john.johnson{at}colorado.edu.

It has recently been reported that exposure to inescapable tailshock (IS) enhances the release of proinflammatory cytokines following bacterial challenge. However, it is not known whether the level of potentiation of proinflammatory cytokines is sufficient to exaggerate any of the physiological processes that are regulated by these cytokines. Thus, lipopolysaccharide (LPS) was administered and fever, activity, HPA responses, and proinflammatory cytokine release were assessed during both the light and dark phases of the light cycle following IS. Exposure to IS resulted in elevated basal core body temperature during the light phase but not the dark phase and decreased activity during the dark phase but not the light phase. IS animals had significantly greater fever, corticosterone, and ACTH responses following LPS during both the light and dark phases, while enhanced proinflammatory cytokine responses were only observed during the light phase. These data suggest that enhanced proinflammatory cytokine responses are not necessary to observe enhanced HPA or fever responses.




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