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1 Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
* To whom correspondence should be addressed. E-mail: blatteis{at}physio1.utmem.edu.
Because the onset of fever induced by intravenously (iv) injected bacterial endotoxic lipopolysaccharides (LPS) precedes the appearance in the bloodstream of pyrogenic cytokines, the presumptive peripheral triggers of the febrile response, we have postulated previously that, in their stead, prostaglandin (PG)E2 could be the peripheral fever trigger because it appears in blood coincidentally with the initial body core temperature (Tc) rise. To test this hypothesis, we injected S. enteritidis LPS (2 µg/kg iv) into conscious guinea pigs and measured their plasma levels of LPS, PGE2, tumor necrosis factor (TNF)-
, interleukin (IL)-1
and IL-6 before and 15, 30, 60, 90, and 120 min after LPS administration; Tc was monitored continuously. The animals were untreated or Kupffer cells (KC)-depleted; the essential involvement of KC in LPS fever was shown previously. LPS very promptly (<10 min) induced a rise of Tc that was temporally correlated with the elevation of plasma PGE2. KC depletion prevented the Tc and plasma PGE2 rises and slowed the clearance of LPS from the blood. TNF- was not detectable in plasma until 30 min and IL-1 and IL-6 until 60 min after LPS injection. KC depletion did not alter the times of appearance or magnitudes of rises of these cytokines, excepting TNF-, the maximal level of which was increased ca. 2 fold in the KC-depleted animals. In a follow-up experiment, PGE2 antiserum administered iv 10 min before LPS significantly attenuated the febrile response to LPS. Together, these results support the view that, in guinea pigs, PGE2 rather than pyrogenic cytokines is generated by KC in immediate response to iv LPS and triggers the febrile response.
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