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

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 resp...

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Bibliographic Details
Published in:Journal of neuroimmunology 2005-12, Vol.169 (1), p.116-125
Main Authors: McKimmie, Clive S., Fazakerley, John K.
Format: Article
Language:English
Subjects:
Alphavirus Infections - genetics
Alphavirus Infections - metabolism
Animals
Animals, Newborn
Astrocyte
Cells, Cultured
Gene Expression - physiology
Innate immunity
Lipopolysaccharides - toxicity
LPS
Mice
Mice, Inbred C57BL
Microglia
Neuroblastoma
Neuroglia - drug effects
Neuroglia - metabolism
Neuroglia - virology
Reverse Transcriptase Polymerase Chain Reaction - methods
RNA, Messenger - metabolism
Semliki forest virus - physiology
Time Factors
Toll-like receptor
Toll-Like Receptors - classification
Toll-Like Receptors - genetics
Virus
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Summary: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.
ISSN:0165-5728
1872-8421
DOI:10.1016/j.jneuroim.2005.08.006