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Inducible IL-23p19 expression in human microglia via p38 MAPK and NF-kappaB signal pathways

Yonghai Li1, Niansheng Chu, Aihua Hu

  • 1Department of Neurology, Thomas Jefferson University, 300 JHN Building, 900 Walnut Street, Philadelphia, PA 19107, USA.

Experimental and Molecular Pathology
|December 7, 2007
PubMed

Insights

Interleukin-23 (IL-23) produced by microglia contributes to multiple sclerosis (MS) pathogenesis. Targeting the p38 MAP kinase and NF-kappaB pathways in microglia may offer new therapeutic strategies for MS.

Area of Science:

  • Neuroimmunology
  • Cellular Biology
  • Molecular Medicine

Background:

  • Activated microglia release proinflammatory cytokines crucial in multiple sclerosis (MS) pathogenesis.
  • Interleukin-23 (IL-23) is a key proinflammatory cytokine required for experimental autoimmune encephalomyelitis induction.
  • IL-23 is expressed in MS lesions, with microglia identified as a cellular source.

Purpose of the Study:

  • To investigate the inducible expression and regulation of IL-23's key subunit, p19, in human microglia.
  • To elucidate the signaling pathways controlling IL-23p19 expression in microglia.

Main Methods:

  • Stimulation of human microglial cells with lipopolysaccharide.
  • Utilizing signaling pathway-specific inhibitors (p38 MAP kinase, NF-kappaB).
  • Transduction of microglia with dominant-negative p38.

Main Results:

  • Lipopolysaccharide stimulation induced IL-23p19 expression in microglial cells.
  • Inhibition of p38 MAP kinase and NF-kappaB signaling pathways significantly reduced p19 expression.
  • Dominant-negative p38 further confirmed the regulatory role of p38 MAP kinase.

Conclusions:

  • The p38 MAP kinase and NF-kappaB signaling pathways are critical regulators of IL-23p19 expression in human microglia.
  • These pathways represent potential therapeutic targets for treating multiple sclerosis.

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