Nature Neuroscience6, 1137 - 1138 (2003)
Published online: 19 October 2003; | doi:10.1038/nn1137
Microsomal prostaglandin E synthase-1 is the central switch during immune-induced pyresis
David Engblom1, Sipra Saha2, Linda Engström1, Marie Westman3, Laurent P Audoly4, Per-Johan Jakobsson3
& Anders Blomqvist1
1
Division of Cell Biology, Faculty of Health Sciences, University of Linköping, S-581 85 Linköping, Sweden.
2
Center for Structural Biochemistry, Karolinska Institute, 141 57 Huddinge, Sweden.
3
Department of Biochemistry and Biophysics, Karolinska Institute, 171 77 Stockholm, Sweden.
4
Inflammation Unit, Pfizer Global Research and Development, Groton Laboratories, Groton, Connecticut 06340, USA.
Correspondence should be addressed to Anders Blomqvist andbl@ibk.liu.se
We studied the febrile response in mice deficient in microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal isomerase expressed in cytokine-sensitive brain endothelial cells. These animals showed no fever and no central prostaglandin (PG) E2 synthesis after peripheral injection of bacterial-wall lipopolysaccharide, but their pyretic capacity in response to centrally administered PGE2 was intact. Our findings identify mPGES-1 as the central switch during immune-induced pyresis and as a target for the treatment of fever and other PGE2-dependent acute phase reactions elicited by the brain.
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