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Physiology and Pharmacology of Temperature Regulation

LPS-activated complement, not LPS per se, triggers the early release of PGE₂ by Kupffer cells

¹Departments of Physiology, University of Tennessee Health Science Center, Memphis, Tennessee; and ²Medicine and Rheumatology, Veterans Affairs Medical Center, Memphis, Tennessee

Submitted 20 August 2004 ; accepted in final form 24 March 2005

The intravenous injection of LPS rapidly evokes fever. We have hypothesized that its onset is mediated by prostaglandin (PG)E₂ quickly released by Kupffer cells (Kc). LPS, however, does not stimulate PGE₂ production by Kc as rapidly as it induces fever; but complement (C) activated by LPS could be the exciting agent. To test this hypothesis, we injected LPS (2 or 8 µg/kg) or cobra venom factor (CVF, an immediate activator of the C cascade that depletes its substrate, ultimately causing hypocomplementemia; 25 U/animal) into the portal vein of anesthetized guinea pigs and measured the appearance of PGE₂, TNF-, IL-1, and IL-6 in the inferior vena cava (IVC) over the following 60 min. LPS (at both doses) and CVF induced similar rises in PGE₂ within the first 5 min after treatment; the rises in PGE₂ due to CVF returned to control in 15 min, whereas PGE₂ rises due to LPS increased further, then stabilized. LPS given 3 h after CVF to the same animals also elevated PGE₂, but after a 30- to 45-min delay. CVF per se did not alter basal PGE₂ and cytokine levels and their responses to LPS. These in vivo effects were substantiated by the in vitro responses of primary Kc from guinea pigs to C (0.116 U/ml) and LPS (200 ng/ml). These results indicate that LPS-activated C rather than LPS itself triggers the early release of PGE₂ by Kc.

liver; fever; portal vein cannulation; cobra venom factor; pyrogenic cytokines

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