Abstract
Toll-like receptors (TLR) play a key role in the recognition of microbial components. We investigated the differential regulation of TLR mRNA expression in bacterial and viral mouse models of central nervous system infection. Streptococcus pneumoniae meningitis led to an enhanced expression of TLR2, TLR4 and TLR9 mRNA. In Escherichia coli meningitis, TLR2, TLR4 and TLR7 mRNA expression was increased and Herpes simplex encephalitis caused a rise of TLR4 mRNA. In organotypic hippocampal cultures treatment with S. pneumoniae R6 led to increased expression of TLR2 and TLR3 mRNA. Our data provide evidence that regulation of TLR mRNA is not fully specific for the molecular patterns of the infectious pathogen. The TLR mRNA regulation observed probably represents a combination of specific response to the causative pathogen and non-specific activation of the innate immune system.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Central Nervous System Infections / genetics
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Central Nervous System Infections / immunology*
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Encephalitis, Herpes Simplex / genetics
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Encephalitis, Herpes Simplex / immunology
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Gene Expression Regulation
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Hippocampus / immunology*
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Membrane Glycoproteins / biosynthesis*
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / immunology*
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Meningitis, Escherichia coli / genetics
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Meningitis, Escherichia coli / immunology
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Meningitis, Pneumococcal / genetics
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Meningitis, Pneumococcal / immunology
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Organ Culture Techniques
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RNA, Messenger / analysis*
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Receptors, Cell Surface / biosynthesis*
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / immunology*
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Reverse Transcriptase Polymerase Chain Reaction
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Toll-Like Receptor 2
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Toll-Like Receptor 3
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Toll-Like Receptor 4
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Toll-Like Receptor 7
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Toll-Like Receptors
Substances
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Membrane Glycoproteins
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RNA, Messenger
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Receptors, Cell Surface
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Toll-Like Receptor 2
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Toll-Like Receptor 3
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Toll-Like Receptor 4
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Toll-Like Receptor 7
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Toll-Like Receptors