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Related Experiment Videos

Molecular basis of sickness behavior

Robert Dantzer1, Rose-Marie Bluthé1, Gilles Gheusi1

  • 1Neurobiologie intégrative, INSERM U394, Rue Camille Saint-Saens, 33077 Bordeaux Cédex, France.

Annals of the New York Academy of Sciences
|January 26, 1999
PubMed
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Lipopolysaccharide (LPS) and cytokines like IL-1 beta induce sickness behavior, reducing food intake and social activity. These effects are mediated by brain cytokine pathways activated by peripheral signals.

Area of Science:

  • Neuroimmunology
  • Behavioral Neuroscience
  • Molecular Biology

Background:

  • Proinflammatory cytokines, such as interleukin-1 beta (IL-1 beta), and lipopolysaccharide (LPS) are known to induce sickness behavior.
  • Sickness behavior manifests as reduced food intake and social interaction, representing a coordinated motivational state.

Purpose of the Study:

  • To investigate the molecular and neural mechanisms underlying cytokine-induced sickness behavior.
  • To elucidate the role of central and peripheral cytokine compartments in mediating behavioral changes.

Main Methods:

  • Administration of peripheral and central lipopolysaccharide (LPS) and recombinant proinflammatory cytokines.
  • Pharmacological interventions including cytokine receptor antagonists and neutralizing antibodies.

Related Experiment Videos

  • Gene targeting techniques to investigate cytokine receptor function.

    • Main Results:

    • Cytokine-induced sickness behavior is mediated by an inducible brain cytokine compartment.
    • Peripheral cytokines activate central pathways via neural afferent signaling.
    • Centrally produced cytokines interact with brain cytokine receptors analogous to peripheral ones.

    Conclusions:

    • Sickness behavior is a complex, organized motivational state driven by cytokine signaling in the brain.
    • Distinct cytokines may mediate different aspects of sickness behavior.
    • The relative importance of cytokines differs between central and peripheral compartments.