In response to pathogens, glial cells dynamically and differentially regulate Toll-like receptor gene expression

J Neuroimmunol. 2005 Dec;169(1-2):116-25. doi: 10.1016/j.jneuroim.2005.08.006. Epub 2005 Sep 6.

Abstract

The mechanisms that mediate innate immune recognition of CNS infections are unknown. This study provides a comparison of Toll-like receptor (TLR) gene expression in resting and virus infected CNS cells. N2a neuroblastoma cells expressed TLR 3 but demonstrated no change in TLR gene expression in response to either LPS or virus infection. N9 microglia and differentiated primary astrocytes expressed most TLR genes. TLR 2 expression was highest in N9 microglia and TLR 7 in astrocytes. In both glial cell types, LPS stimulation upregulated pro-inflammatory cytokines, TLR 2 and TLR 3 gene expression but down-regulated other TLR genes. RNA virus infection substantially increased levels of type-I interferon (IFN) and TLR 3 transcripts and to a lesser extent TLR 9 transcripts. Microglia and astrocytes thus have the ability to discriminate between pathogens and elicit an appropriate response.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alphavirus Infections / genetics
  • Alphavirus Infections / metabolism*
  • Animals
  • Animals, Newborn
  • Cells, Cultured
  • Gene Expression / physiology*
  • Lipopolysaccharides / toxicity*
  • Mice
  • Mice, Inbred C57BL
  • Neuroblastoma
  • Neuroglia / drug effects
  • Neuroglia / metabolism
  • Neuroglia / virology*
  • RNA, Messenger / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction / methods
  • Semliki forest virus / physiology*
  • Time Factors
  • Toll-Like Receptors / classification
  • Toll-Like Receptors / genetics*

Substances

  • Lipopolysaccharides
  • RNA, Messenger
  • Toll-Like Receptors