Changes in the activation level of NF-kappa B in lymphocytes of MS patients during glucocorticoid pulse therapy

J Neurol Sci. 2008 Jan 15;264(1-2):145-50. doi: 10.1016/j.jns.2007.08.026. Epub 2007 Sep 24.

Abstract

Nuclear factor-kappaB activity was analyzed in multiple sclerosis (MS) patients during the course of a methylprednisolone pulse therapy. Molecular effects were evaluated using lymphocytes derived from 20 MS patients before and after therapy and 24 healthy individuals. All patients responded to treatment clinically. The mean level of DNA-binding p65 in MS was proportionate to that of healthy controls, but was significantly decreased directly after therapy whereas the level of DNA-binding p50 was significantly elevated prior to therapy and remained unchanged. In summary, pulse therapy resulted in a decreased level of activated p65 NF-kappaB subunits leading to decreased levels of transcriptionally active pro-inflammatory NF-kappaB.

Publication types

  • Clinical Trial

MeSH terms

  • Adult
  • Aged
  • Biomarkers / analysis
  • Biomarkers / blood
  • DNA-Binding Proteins / drug effects
  • DNA-Binding Proteins / metabolism
  • Down-Regulation / drug effects
  • Down-Regulation / genetics
  • Drug Administration Schedule
  • Female
  • Glucocorticoids / administration & dosage*
  • Humans
  • Immunosuppressive Agents / administration & dosage
  • Inflammation / genetics
  • Inflammation / immunology
  • Inflammation / physiopathology
  • Lymphocytes / drug effects*
  • Lymphocytes / metabolism*
  • Male
  • Middle Aged
  • Multiple Sclerosis / blood*
  • Multiple Sclerosis / drug therapy*
  • Multiple Sclerosis / genetics
  • NF-kappa B / drug effects*
  • NF-kappa B / metabolism
  • Transcription Factor RelA / drug effects
  • Transcription Factor RelA / metabolism
  • Transcriptional Activation / drug effects
  • Transcriptional Activation / immunology
  • Treatment Outcome

Substances

  • Biomarkers
  • DNA-Binding Proteins
  • Glucocorticoids
  • Immunosuppressive Agents
  • NF-kappa B
  • RELA protein, human
  • Transcription Factor RelA