Abstract
We investigated the humoral mechanisms involved in tumour necrosis factor alpha (TNFα)-induced fever in rabbits. No change in lymphocyte-activating factor activity was detected in serum drawn during TNFα-induced fever. The pyrogenic activity of recombinant rabbit interleukin-1β (IL-1β) was entirely abolished by pre-incubation with anti-IL-1β antiserum from the goat. Fever induced by intravenous (i.v.) injection of IL-1β was significantly diminished by i.v. infusion of the antiserum. However, i.v. infusion of the antiserum for 1 h did not affect fever induced by i.v. injection of TNFα, when the antiserum infusion began either simultaneously with, or 2 h after, the injection of TNFα. Furthermore, intracerebroventricular injection of the antiserum did not affect TNFα-induced fever. The intracerebroventricular administration of naloxone (an opioid receptor antagonist) significantly diminished TNFα-induced fever. The results suggest that IL-1, both in the blood circulation and in the brain, may not be involved in TNFα-induced fever. Similar to the contribution of eicosanoids, the opioid system in the brain seems some-how to contribute to the mechanism of the development of fever induced by TNFα in rabbits.
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Hashimoto, M., Sakakibara, Y., Iriki, M. et al. Does interleukin-1 mediate tumour necrosis factor alpha-induced fever in rabbits?. Pflügers Arch 427, 365–372 (1994). https://doi.org/10.1007/BF00374546
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DOI: https://doi.org/10.1007/BF00374546