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Central action sites of interleukin-1 beta for inducing fever in rabbits

N Murakami1, Y Sakata, T Watanabe

  • 1Department of Physiology, Yamaguchi University School of Medicine, Japan.

The Journal of Physiology
|September 1, 1990
PubMed

Insights

Interleukin-1 beta (IL-1 beta) induces biphasic fever in rabbits. Prostaglandin E2 (PGE2) is involved in the first phase, while other metabolites contribute to the second phase of IL-1 beta-induced fever.

Area of Science:

  • Neuroscience
  • Immunology
  • Physiology

Background:

  • Interleukin-1 beta (IL-1 beta) is a key mediator in inflammatory responses.
  • Fever is a complex physiological response involving central thermoregulatory pathways.
  • The precise mechanisms of IL-1 beta-induced fever, particularly its biphasic nature, require further elucidation.

Purpose of the Study:

  • To investigate the dose-dependent effects of IL-1 beta on thermoregulation in rabbits.
  • To differentiate the roles of prostaglandin E2 (PGE2) and other signaling pathways in the biphasic fever response.
  • To determine the central and peripheral mechanisms underlying IL-1 beta-induced fever.

Main Methods:

  • Administration of human recombinant IL-1 beta intravenously (I.V.), intracerebroventricularly (I.C.V.), and intrapreoptic-anterior hypothalamicly (IPOAH) in rabbits.
  • Pharmacological intervention using indomethacin, a prostaglandin synthesis inhibitor, administered subcutaneously and I.C.V.
  • Monitoring of rectal temperature to assess fever responses.

Main Results:

  • High-dose I.V. IL-1 beta induced a biphasic fever, while lower doses produced only the first phase.
  • I.C.V. or IPOAH administration of IL-1 beta rapidly increased rectal temperature.
  • Subcutaneous indomethacin partially inhibited the first phase and substantially reduced the second phase of I.V. IL-1 beta-induced fever.
  • Central indomethacin administration significantly inhibited fever induced by lower I.C.V. IL-1 beta doses, but only delayed the onset of fever with higher doses.

Conclusions:

  • The first phase of IL-1 beta-induced fever involves prostaglandin-independent pathways acting on extravascular components of the OVLT or circumventricular organs.
  • The second phase of fever is mediated by IL-1 beta acting at the blood-brain interface, releasing non-prostaglandin E2 (PGE2) metabolites.
  • These findings highlight distinct central and peripheral mechanisms contributing to the complex fever response induced by IL-1 beta.

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