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ERK-MAP-kinases differentially regulate expression of IL-23 p19 compared with p40 and IFN-beta in Theiler's

Thomas M Petro1

  • 1Department of Oral Biology, the Nebraska Center for Virology, University of Nebraska Medical Center, Lincoln, NE 68583, USA. tpetro@unmc.edu

Immunology Letters
|January 1, 2005
PubMed

Insights

Theiler

Area of Science:

  • Neuroimmunology
  • Virology
  • Cellular Biology

Background:

  • Theiler's murine encephalomyelitis virus (TMEV) infection in mice causes a demyelinating disease (DD) analogous to human multiple sclerosis.
  • Interleukin-23 (IL-23) subunits (p19 and p40) and Interferon-beta (IFN-beta) expression by macrophages following TMEV infection may contribute to DD pathogenesis.
  • Mitogen-activated protein kinases (MAPKs), including p38 and Extracellular signal-regulated kinases (ERK), are implicated in TMEV-induced cytokine expression.

Purpose of the Study:

  • To investigate the specific roles of p38 and ERK MAPKs in regulating TMEV-induced IL-23 and IFN-beta expression in macrophages.
  • To elucidate the differential regulation of IL-23 p19, p40 subunits, and IFN-beta by distinct MAPK pathways during TMEV infection.

Main Methods:

  • RAW264.7 macrophage cell line was utilized for in vitro studies.
  • Cells were pretreated with specific MAPK inhibitors: SB203580 (p38 inhibitor) and U0126 (ERK inhibitor).
  • Expression levels of IL-23 p19, p40, and IFN-beta were quantified post-TMEV infection.
  • Activation of the p38 substrate ATF-2 was monitored over time.

Main Results:

  • SB203580 (p38 inhibitor) increased IL-23 p19 expression but decreased p40 expression.
  • U0126 (ERK inhibitor) decreased IL-23 p19 expression while increasing p40 and IFN-beta expression.
  • U0126 treatment prolonged the activation of ATF-2 induced by TMEV infection.

Conclusions:

  • ERK MAPKs differentially regulate the expression of TMEV-induced IL-23 p19 compared to p40 and IFN-beta.
  • The distinct effects of ERK inhibition on cytokine expression suggest potential therapeutic strategies for TMEV-induced demyelinating disease.

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