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Am J Physiol Regul Integr Comp Physiol 275: R2028-R2034, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 6, R2028-R2034, December 1998

IL-6 is essential in TNF-alpha -induced fever

Anna K. Sundgren-Andersson, Pernilla Östlund, and Tamas Bartfai

Department of Neurochemistry and Neurotoxicology, Arrhenius Laboratories for Natural Sciences, Stockholm University, S-10691 Stockholm, Sweden

Tumor necrosis factor-alpha (TNF-alpha ) is a pleiotropic cytokine that orchestrates an array of local and systemic effects. For instance, acute exposure to a high dose of TNF-alpha results in septic shock and fever. We have used interleukin-1beta (IL-1beta )- and interleukin-6 (IL-6)-deficient mice, along with their wild-type equivalents, to define a role for TNF-alpha in fever. Briefly, the mice produced prostaglandin E2-dependent fevers in response to recombinant murine TNF-alpha (rmTNF-alpha ). Furthermore, rmTNF-alpha (12 µg/mouse ip) triggered a febrile response in IL-1beta -deficient mice as well as in their corresponding wild-type controls. In contrast, the IL-6-deficient mice were resistant to rmTNF-alpha (4.5 µg/mouse ip), although their wild-type counterparts readily mounted a fever. In the IL-6-deficient mice, moreover, the febrile response to rmTNF-alpha could be restored by a central administration of rat recombinant IL-6 (500 ng/mouse icv). We thus conclude that TNF-alpha can trigger fever independent of IL-1beta but dependent on IL-6. We also suggest that central, rather than peripheral, IL-6 (plasma IL-6 was measured 2 h after pyrogenic challenge) is essential in TNF-alpha -induced fever.

interleukin-1beta ; interleukin-1beta -deficient mice; interleukin-6-deficient mice; lipopolysaccharide; indomethacin


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