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Immune-to-brain communication dynamically modulates pain: physiological and pathological consequences.

Julie Wieseler-Frank1, Steven F Maier, Linda R Watkins

  • 1Department of Psychology & Center for Neuroscience, University of Colorado at Boulder, Boulder, CO 80309-0345, USA. frankjw@psych.colorado.edu

Brain, Behavior, and Immunity
|January 25, 2005
PubMed
Summary

Immune cells, specifically glial cells in the spinal cord, amplify pain by releasing inflammatory cytokines. This immune-driven pain modulation offers new therapeutic targets for chronic pain conditions.

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Area of Science:

  • Neuroimmunology
  • Pain Research
  • Cellular Neuroscience

Background:

  • Immunological processes play a recently recognized role in pain modulation.
  • Glial cells in the spinal cord can amplify pain by altering neuronal excitability.

Purpose of the Study:

  • To review the role of glial cells and immune responses in pain modulation.
  • To explore the implications for human chronic pain control.

Main Methods:

  • Review of recent literature on glial cell activation and immune signaling in pain.
  • Examination of neuroinflammatory pathways contributing to hyperalgesia.

Main Results:

  • Glial cell activation, triggered by infection, inflammation, or nerve injury, enhances pain (hyperalgesia).

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  • Proinflammatory cytokines released by activated glia are key mediators of this pain facilitation.
  • Immune-to-brain-to-spinal cord communication contributes to sickness-induced hyperalgesia.

    • Conclusions:

    • Spinal cord glia and their derived cytokines are powerful pain modulators.
    • Understanding these mechanisms may lead to novel therapies for difficult-to-treat chronic pain.