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Articles in PresS, published online ahead of print August 29, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00396.2002
Submitted on July 5, 2002
Accepted on August 24, 2002
1 Department of Life and Health Sciences, Hyogo University of Teacher Education, Hyogo, Japan
2 Department of Intelligence Science and Technology, Graduate School of Informatics, Kyoto University, Kyoto, Japan
3 Molecular Neurobiology Laboratory, SRI International, Menlo Park, CA, USA
4 Department of Physiology, Osaka City University Graduate School of Medicine, Osaka, Japan
* To whom correspondence should be addressed. E-mail: matsu{at}i.kyoto-u.ac.jp.
Attenuation of fever occurs in pregnant animals. This study examined a hypothesis that brain production of prostaglandin E2 (PGE2), the final mediator of fever, is suppressed in pregnant animals. Near-term pregnant rats and age-matched non-pregnant female rats were injected with lipopolysaccharide (100 µg/kg) intraperitoneally. Four hours later, colonic temperature was measured, their cerebrospinal fluid (CSF) was sampled for PGE2 assay, and the brain was processed for immunohistochemistry of cyclooxygenase-2, an enzyme involved in PGE2 biosynthesis. In the pregnant rats, lipopolysaccharide injection resulted in significantly smaller elevations in both colonic temperature and CSF-PGE2 level than in non-pregnant rats. In the pregnant rats, lipopolysaccharide-induced cyclooxygenase-2 expression was blunted in terms of the number of positive cells. There was a significant correlation between PGE2 level in CSF and the number of cyclooxygenase-2-positive endothelial cells. These results suggest that suppressed PGE2 production in the brain is one cause for the attenuated fever response at near-term pregnancy, and that this suppressed PGE2 production is due to the suppressed induction of cyclooxygenase-2 in brain endothelial cells.
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