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The EAE-associated behavioral syndrome: I. Temporal correlation with inflammatory mediators.

Y Pollak1, H Ovadia, E Orion

  • 1Department of Psychology, The Hebrew University of Jerusalem, Mount Scopus, Jerusalem 91905, Israel.

Journal of Neuroimmunology
|April 2, 2003
PubMed
Summary

Inflammation drives sickness behavior in experimental autoimmune encephalomyelitis (EAE). Pro-inflammatory cytokines like interleukin-1 beta correlate with EAE-associated behavioral syndrome (EBS) onset and recovery.

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Area of Science:

  • Neuroimmunology
  • Behavioral Neuroscience
  • Inflammatory Diseases

Background:

  • Experimental autoimmune encephalomyelitis (EAE) is an animal model for multiple sclerosis.
  • EAE is characterized by central nervous system inflammation and neurological deficits.
  • A distinct behavioral syndrome (EBS) is associated with EAE, but its underlying mechanisms are not fully understood.

Purpose of the Study:

  • To investigate the temporal relationship between behavioral changes and inflammatory processes in EAE.
  • To identify the specific inflammatory mediators involved in EAE-associated behavioral syndrome (EBS).

Main Methods:

  • Examined temporal correlation between behavioral alterations and inflammatory markers in EAE models.
  • Measured mRNA expression of key cytokines (IL-1 beta, TNF-alpha).

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  • Assessed protein production of IL-1 beta and prostaglandin E(2) (PGE(2)).

    • Main Results:

    • EBS onset correlated with brain infiltration and increased expression of IL-1 beta and TNF-alpha.
    • Sickness behavior symptoms peaked with maximal cytokine expression.
    • Behavioral recovery was linked to reduced cytokine expression, but not reduced infiltration or PGE(2) levels.

    Conclusions:

    • Inflammatory processes, particularly pro-inflammatory cytokines, play a crucial role in mediating sickness behavior during EAE.
    • Cytokine production appears critical for the manifestation and resolution of EAE-associated behavioral changes.