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

Clive S McKimmie, John K Fazakerley

Research output: Contribution to journalArticlepeer-review

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.
Original languageEnglish
Pages (from-to)116-25
Number of pages10
JournalJournal of Neuroimmunology
Volume169
Issue number1-2
DOIs
Publication statusPublished - Dec 2005

Keywords

  • Alphavirus Infections
  • Animals
  • Animals, Newborn
  • Cells, Cultured
  • Gene Expression
  • Lipopolysaccharides
  • Mice
  • Mice, Inbred C57BL
  • Neuroblastoma
  • Neuroglia
  • RNA, Messenger
  • Reverse Transcriptase Polymerase Chain Reaction
  • Semliki forest virus
  • Time Factors
  • Toll-Like Receptors

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