Silencing of miR155 promotes the production of inflammatory mediators in Guillain-Barré syndrome in vitro

Inflammation. 2013 Apr;36(2):337-45. doi: 10.1007/s10753-012-9551-5.

Abstract

MicroRNA-155 (miR155) has been demonstrated as a central regulator of immune responses induced by inflammatory mediators. Previous studies suggest that miR155 may play adverse effects in various diseases. We hereby explored the roles of miR155 in the pathogenesis of Guillain-Barré syndrome (GBS). Peripheral blood mononuclear cells (PBMCs) were separated from GBS patients and healthy controls. Expression of miR155 in PBMCs was detected by quantitative PCR. An inhibitor of miR155 was transfected into the cultured PBMCs and the GBS-related cytokines were detected. Significantly, our study demonstrated that miR155 was downregulated in PBMCs from GBS patients and silencing of miR155 profoundly promoted the production of Th1-type cytokines in vitro. Our data effectively demonstrate a protective role of miR155 in GBS, which suggests that miR155 may be a promising target for the therapy of the disease.

MeSH terms

  • Adult
  • Female
  • Guillain-Barre Syndrome / genetics*
  • Humans
  • Inflammation / genetics*
  • Inflammation Mediators / metabolism*
  • Interferon-gamma / analysis
  • Interleukin-12 / analysis
  • Interleukin-1beta / analysis
  • Interleukin-4 / analysis
  • Leukocytes, Mononuclear / cytology
  • Leukocytes, Mononuclear / metabolism*
  • Male
  • MicroRNAs / genetics*
  • RNA Interference
  • RNA, Small Interfering
  • Tumor Necrosis Factor-alpha / analysis

Substances

  • Inflammation Mediators
  • Interleukin-1beta
  • MIRN155 microRNA, human
  • MicroRNAs
  • RNA, Small Interfering
  • Tumor Necrosis Factor-alpha
  • Interleukin-12
  • Interleukin-4
  • Interferon-gamma