[Toll-like receptor 4 expression and cytokine secretion in microglial cells induced by IgG stimulation]

Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 Mar;25(3):201-3.
[Article in Chinese]

Abstract

Aim: To investigate the effects of immunoglobulin G (IgG) on the expression of toll-like receptor 4 (TLR4) and secretion of cytokines in microglial cells in vitro.

Methods: Cultured primary rat microglial cells were stimulated with different concentrations of rat IgG (2 mg/L, 20 mg/L, 200 mg/L) and lipopolysaccharide (LPS) 10 mg/L for 24 h, respectively. The TLR4 expression in the microglial cells was examined by immunofluorescence staining and tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) levels in the culture medium were assayed by ELISA.

Results: IgG stimulation induced a significant TLR4 expression and TNF-alpha secretion in cultured microglial cells in a dose-dependent manner, while IFN-gamma was not detected in the same medium samples. As a positive control, LPS caused increases of TLR4 expression and both IFN-gamma and TNF-alpha production in the microglial cells.

Conclusion: TLR4 expression could be induced in microglia in vitro by non-pathogenic protein, IgG from the same species. Therefore, congeneric IgG stimulation might lead to proinflammmatory cytokine production, probably via MyD88-dependent pathway. This finding suggests that TLR4 may play more roles than pathogen recognition of innate immune reactivity, at least in the central nervous system.

MeSH terms

  • Animals
  • Animals, Newborn
  • Cells, Cultured
  • Cytokines / metabolism*
  • Dose-Response Relationship, Drug
  • Enzyme-Linked Immunosorbent Assay
  • Fluorescent Antibody Technique
  • Immunoglobulin G / pharmacology*
  • Interferon-gamma / metabolism
  • Microglia / cytology
  • Microglia / drug effects*
  • Microglia / metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Toll-Like Receptor 4 / metabolism*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Cytokines
  • Immunoglobulin G
  • Tlr4 protein, rat
  • Toll-Like Receptor 4
  • Tumor Necrosis Factor-alpha
  • Interferon-gamma