Central activation of thermogenesis and fever by interleukin-1 beta and interleukin-1 alpha involves different mechanisms.

N Busbridge, M Dascombe, F Tilders, Oers J van, E Linton, NJ. Rothwell

Research output: Contribution to journalArticlepeer-review

Abstract

Interleukin-1 exists in two forms (alpha and beta) which are assumed to act on the same receptor. Both forms of the molecule stimulated fever and thermogenesis in the rat when injected into the brain, but interleukin-1 beta was more effective, and combined injection of alpha and beta elicited additive responses. The actions of interleukin-1 beta were inhibited by pretreatment of the animals with either a receptor antagonist or monoclonal antibody to corticotrophin releasing factor. The effects of interleukin-1 alpha were unaltered by these treatments. The results indicate that brain corticotrophin releasing factor mediates thermogenesis and fever induced by interleukin-1 beta but not by interleukin-1 alpha.
Original languageEnglish
JournalBiochemical and biophysical research communications
Volume162
Issue number2
Publication statusPublished - 31 Jul 1989

Keywords

  • Animals
  • Antibodies, Monoclonal
  • Body Temperature
  • Body Temperature Regulation
  • Brain
  • Comparative Study
  • antagonists & inhibitors: Corticotropin-Releasing Hormone
  • Immunization, Passive
  • administration & dosage: Interleukin-1
  • Male
  • Oxygen Consumption
  • Rats
  • Rats, Inbred Strains
  • Support, Non-U.S. Gov't

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