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Articles in PresS, published online ahead of print July 25, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00347.2002
Submitted on June 13, 2002
Accepted on July 23, 2002
1 Trauma Research, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA
2 Neurology Research, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, Phoenix, Arizona, USA
* To whom correspondence should be addressed. E-mail: aromanov{at}chw.edu.
The febrile response to lipopolysaccaharide (LPS) consists of three phases (Phases I-III), all requiring de novo synthesis of prostaglandin (PG) E2. The major mechanism for activation of PGE2-synthesizing enzymes is transcriptional up-regulation. The triphasic febrile response of Wistar Kyoto rats to intravenous LPS (50 µg/kg) was studied. Using real-time RT-PCR, the expression of seven PGE2-synthesizing enzymes in the LPS-processing organs (liver and lungs) and the brain "febrigenic center" (hypothalamus) was quantified. Phase I involved transcriptional up-regulation of the functionally coupled cyclooxygenase (COX)-2 and microsomal (m) PGE synthase (PGES) in the liver and lungs. Phase II entailed robust up-regulation of all enzymes of the major inflammatory pathway, i.e., secretory (s) phospholipase (PL) A2 IIA 
COX-2 mPGES, in both the periphery and brain. Phase III was accompanied by the induction of cytosolic (c) PLA2 
in the hypothalamus, further up-regulation of sPLA2 IIA and mPGES in the hypothalamus and liver, and a decrease in the expression of COX-1 and COX-2 in all tissues studied. Neither sPLA2 V nor cPGES was induced by LPS. The high magnitude of up-regulation of mPGES and sPLA2 IIA (1,257 and 133 fold, respectively) makes these enzymes attractive targets for anti-inflammatory therapy.
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