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

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.

• Authors: Clive S McKimmie, John K Fazakerley
• Journal: Journal of neuroimmunology (J Neuroimmunol) Vol. 169 Issue 1-2 Pg. 116-25 (Dec 2005) ISSN: 0165-5728 [Print] Netherlands
• PMID: 16146656 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Lipopolysaccharides
• RNA, Messenger
• Toll-Like Receptors

Topics

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