Interleukin-1 mediates behavioural but not metabolic effects of tumor necrosis factor alpha in mice

Eur J Pharmacol. 1991 Dec 17;209(3):281-3. doi: 10.1016/0014-2999(91)90184-r.


Recombinant human tumor necrosis factor alpha (TNF alpha) decreases social exploration and induces weight loss in mice in a dose- and time-dependent manner (2.5-40 micrograms/mouse). To assess the role of interleukin-1 (IL-1) in these effects, mice pretreated with IL-1 receptor antagonist (IL-1ra, 500 micrograms/mouse, i.p.) were injected with 25 micrograms TNF alpha. Pretreatment with IL-1ra antagonized the depressive effects of TNF alpha on behaviour but only partially attenuated the weight loss induced by this cytokine. These results suggest that TNF alpha-induced sickness behaviour is mediated mainly by endogenously released IL-1 whereas metabolic changes are dependent on the release of other additional cytokines.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Behavior, Animal / drug effects*
  • Body Weight / drug effects
  • Dose-Response Relationship, Drug
  • Exploratory Behavior / drug effects
  • Humans
  • Interleukin-1 / pharmacology*
  • Male
  • Mice
  • Mice, Inbred DBA
  • Receptors, Immunologic / antagonists & inhibitors
  • Receptors, Interleukin-1
  • Recombinant Proteins / pharmacology
  • Social Behavior
  • Tumor Necrosis Factor-alpha / antagonists & inhibitors*
  • Tumor Necrosis Factor-alpha / metabolism
  • Tumor Necrosis Factor-alpha / physiology


  • Interleukin-1
  • Receptors, Immunologic
  • Receptors, Interleukin-1
  • Recombinant Proteins
  • Tumor Necrosis Factor-alpha