Elsevier

Brain Research Bulletin

Volume 27, Issues 3–4, September–October 1991, Pages 309-313
Brain Research Bulletin

Neuropeptides
Immune cytokines and regulation of body temperature, food intake and cellular immunity

https://doi.org/10.1016/0361-9230(91)90117-3Get rights and content

Abstract

Interleukin-1 (IL-1) and interferon α (IFNα), cytokines originally detected in immunological cells, now have been shown to produce nonimmunological host defense responses of central and peripheral origins. These cytokines are released from glial cells in the brain in pathological states. Local application of IL-1β and IFNα to thermosensitive neurons in the preoptic and anterior hypothalamus and glucose responsive neurons in the ventromedial hypothalamus in vivo and in vitro, altered the activity in appropriate ways to explain the cytokines-induced fever and anorexia, respectively. The responses to IL-1β, but not to IFNα, were blocked by sodium salicylate, suggesting the involvement of synthesis of prostaglandins, αMSH, an endogenous antipyretic and a possible antagonist of IL-1β at lymphocytes, specifically depressed the responses to IL-1β, but not those to IFNα. In contrast, the action of IFNα was reversibly blocked by naloxone, suggesting the opioid receptor mediation. Intracerebral injection of IFNα and β-endorphin in the rat and mouse resulted in the suppression of cytotoxic activity of natural killer cells in the spleen by activation of brain opioid receptor, which was shown to be mediated predominantly by splenic sympathetic nerves. The results suggest a view that immune cytokines may provide afferent links for the regulatory circuits between the brain and the immune system.

References (42)

  • T. Nakashima et al.

    Effects of interferon-α on the activity of preoptic thermosensitive neurons in tissue slices

    Brain Res.

    (1988)
  • T. Nakashima et al.

    Recombinant human interleukin-1β alters the activity of preoptic thermosensitive neurons in vitro

    Brain Res. Bull.

    (1989)
  • T. Nakayama et al.

    Effects of preoptic thermal stimulation on the ventromedial hypothalamic neurons in rats

    Neurosci. Lett.

    (1981)
  • D.M. Nance et al.

    Innervation of the spleen in the rat: evidence for absence of afferent innervation

    Brain Behav. Immun.

    (1989)
  • Y. Oomura

    Chemical and neuronal control of feeding motivation

    Physiol. Behav.

    (1988)
  • C.R. Plata-Salaman et al.

    Tumor necrosis factor and interleukin-1β: suppression of food intake by direct action in the central nervous system

    Brain Res.

    (1988)
  • J.E. Blalock

    A molecular basis for bidirectional communication between the immune and neuroendocrine systems

    Physiol. Rev.

    (1989)
  • C.D. Breder et al.

    Interleukin-1 immunoreactive innervation of the human hypothalamus

    Science

    (1988)
  • J.G. Cannon et al.

    αMelanocyte stimulating hormone inhibits immunostimulatory and inflammatory actions of interleukin 1

    J. Immunol.

    (1986)
  • W.I. Cranston et al.

    Intraventricular injection of drugs which inhibit phospholipase A2 suppress fever in rabbits

    J. Physiol. (Lond.)

    (1983)
  • A. Del Rey et al.

    Interleukin-1 affects glucose homeostasis

    Am. J. Physiol.

    (1987)
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