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1 Physiology and Biophysics, University of Calgary, Calgary, Alberta, Canada
* To whom correspondence should be addressed. E-mail: mouihate{at}ucalgary.ca.
Near term pregnant rats show a suppressed fever response to LPS that is associated with reduced induction of COX-2 in the hypothalamus. The objective of this study is to explore whether the LPS-activated signaling pathways in the fever-controlling region of the hypothalamus are specifically altered at near term. Three rat groups consisting of 15-day pregnant rats, near term 21-22 day pregnant rats and day 5 lactating rats, were injected with a febrile dose of LPS (50 µg/kg i.p.). The hypothalamic preoptic area and the organum vasculosum of the lamina terminalis (OVLT), was collected two hours post LPS injection. The activation of three transcription modulators; the Nuclear Factor 
B (NFB), the Extracellular Regulated Kinase (ERK1/2) and the Signal Transducer and Activator of Transcription 5 (STAT-5) were assessed by semi-quantitative Western Blot. LPS activated the NFB pathway in all rat groups and this response was not altered at near term. ERK1/2 and STAT-5 were constitutively activated during all reproductive stages and their levels were not significantly affected by LPS injection. Plasma levels of the pro-inflammatory (IL-1
, IL-6, TNF
, IFN
), the anti-inflammatory cytokines (IL-4, IL-10 and IL-1ra) and corticosterone were unaffected during the three reproductive stages after LPS challenge. We observed a sharp decrease in the expression of a prostaglandin-producing enzyme called lipocalin-prostaglandin D2 synthase (L-PGDS) in near term pregnant and lactating rats. Thus, fever suppression at near term is not due to an alteration in either LPS- activated intracellular signaling pathways or in LPS-induced pro- and anti-inflammatory cytokine production.
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