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Tumor necrosis factor-alpha and fever after peripheral inflammation in the rat.
Cooper A, Brouwer S, Turnbull A, Luheshi G, Hopkins S, Kunkel S, Rothwell NJ
Am J Physiol. 1994;267( 6 Pt 2):R1431-6.
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Abstract
The involvement of endogenous tumor necrosis factor-alpha (TNF-alpha) in the pyrogenic [i.e., rise in colonic temperature (Tc)] and thermogenic [increase in oxygen consumption (VO2)] responses to inflammation was investigated in rats subjected to an intramuscular injection of turpentine. Turpentine administration caused a rise in Tc and VO2 within 2 h (0.9 +/- 0.1 degrees C, 27 +/- 2%, respectively). Eighteen to twenty hours after turpentine, the magnitude of these responses had increased (2.3 degrees C fever and a 28% increase in metabolic rate compared with control animals) and was associated with marked inflammation in the injected limb. A rapid (by 4 h) and sustained rise in the plasma concentration of the endogenous pyrogen IL-6, but not TNF-alpha, was also observed. Intravenous pretreatment with a TNF-alpha antiserum attenuated the rise in Tc observed 2, 8, and 18 h after turpentine injection and almost abolished the hypermetabolic response observed at 18 h. In addition, the TNF-alpha antiserum inhibited the peak rise (8 h) in plasma IL-6 by 76%. These findings indicate that endogenous TNF-alpha is involved in fever and hypermetabolism during inflammation and that it may exert these effects by inducing the release of IL-6 into circulation.
Keyword(s)
Animals; Body Temperature; Colon; Kinetics; Male; Oxygen Consumption; Rats; Rats, Sprague-Dawley; Support, Non-U.S. Gov't; Turpentine; administration & dosage: Immune Sera; blood: Interleukin-6; chemically induced: Inflammation; immunology: Tumor Necrosis Factor; physiopathology: Fever