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 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.
McKimmie
Clive S
CS
Virology, Centre for Infectious Diseases, College of Medicine and Veterinary Medicine, University of Edinburgh, Summerhall, Edinburgh EH9 1QH, UK.
Fazakerley
John K
JK
D018354:Alphavirus Infections / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D000831:Animals, Newborn; D002478:Cells, Cultured; D015870:Gene Expression / Q000502:physiology*; D008070:Lipopolysaccharides / Q000633:toxicity*; D051379:Mice; D008810:Mice, Inbred C57BL; D009447:Neuroblastoma; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism / Q000821:virology*; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012672:Semliki forest virus / Q000502:physiology*; D013997:Time Factors; D051193:Toll-Like Receptors / Q000145:classification / Q000235:genetics*
D008070:Lipopolysaccharides; D012333:RNA, Messenger; D051193:Toll-Like Receptors