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TLR2 hypersensitivity of astrocytes as functional consequence of previous inflammatory episodes

TLR2 hypersensitivity of astrocytes as functional consequence of previous inflammatory episodes

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HENN, Anja, Susanne KIRNER, Marcel LEIST, 2011. TLR2 hypersensitivity of astrocytes as functional consequence of previous inflammatory episodes. In: The Journal of Immunology. 186(5), pp. 3237-3247. ISSN 0022-1767. eISSN 1550-6606. Available under: doi: 10.4049/jimmunol.1002787

@article{Henn2011-03-01hyper-18152, title={TLR2 hypersensitivity of astrocytes as functional consequence of previous inflammatory episodes}, year={2011}, doi={10.4049/jimmunol.1002787}, number={5}, volume={186}, issn={0022-1767}, journal={The Journal of Immunology}, pages={3237--3247}, author={Henn, Anja and Kirner, Susanne and Leist, Marcel} }

<rdf:RDF xmlns:dcterms="http://purl.org/dc/terms/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:bibo="http://purl.org/ontology/bibo/" xmlns:dspace="http://digital-repositories.org/ontologies/dspace/0.1.0#" xmlns:foaf="http://xmlns.com/foaf/0.1/" xmlns:void="http://rdfs.org/ns/void#" xmlns:xsd="http://www.w3.org/2001/XMLSchema#" > <rdf:Description rdf:about="https://kops.uni-konstanz.de/rdf/resource/123456789/18152"> <dc:contributor>Kirner, Susanne</dc:contributor> <dcterms:available rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-02-02T13:55:21Z</dcterms:available> <dcterms:isPartOf rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <dcterms:bibliographicCitation>Publ. in: Journal of Immunology ; 186 (2011), 5. - pp. 3237-3247</dcterms:bibliographicCitation> <dc:creator>Kirner, Susanne</dc:creator> <foaf:homepage rdf:resource="http://localhost:8080/jspui"/> <void:sparqlEndpoint rdf:resource="http://localhost/fuseki/dspace/sparql"/> <dc:creator>Henn, Anja</dc:creator> <dc:creator>Leist, Marcel</dc:creator> <dc:rights>terms-of-use</dc:rights> <dcterms:title>TLR2 hypersensitivity of astrocytes as functional consequence of previous inflammatory episodes</dcterms:title> <dcterms:issued>2011-03-01</dcterms:issued> <dc:date rdf:datatype="http://www.w3.org/2001/XMLSchema#dateTime">2012-02-02T13:55:21Z</dc:date> <dcterms:rights rdf:resource="https://rightsstatements.org/page/InC/1.0/"/> <dc:language>eng</dc:language> <dc:contributor>Henn, Anja</dc:contributor> <dc:contributor>Leist, Marcel</dc:contributor> <dspace:isPartOfCollection rdf:resource="https://kops.uni-konstanz.de/rdf/resource/123456789/28"/> <bibo:uri rdf:resource="http://kops.uni-konstanz.de/handle/123456789/18152"/> <dcterms:abstract xml:lang="eng">Precedent inflammatory episodes may drastically modify the function and reactivity of cells. We investigated whether priming of astrocytes by microglia-derived cytokines alters their subsequent reaction to pathogen-associated danger signals not recognized in the quiescent state. Resting primary murine astrocytes expressed little TLR2, and neither the TLR2/6 ligand fibroblast-stimulating lipopeptide-1 (FSL1) nor the TLR1/2 ligand Pam(3)CysSK(4) (P3C) triggered NF-κB translocation or IL-6 release. We made use of single-cell detection of NF-κB translocation as easily detectable and sharply regulated upstream indicator of an inflammatory response or of c-Jun phosphorylation to measure restimulation events in astrocytes under varying conditions. Cells prestimulated with IL-1β, with a TLR3 ligand, with a complete cytokine mix consisting of TNF-α, IL-1β, and IFN-γ, or with media conditioned by activated microglia responded strongly to FSL1 or P3C stimulation, whereas the sensitivity of the NF-κB response to other pattern recognition receptors was unchanged. This sensitization to TLR2 ligands was associated with an initial upregulation of TLR2, displayed a "memory" window of several days, and was largely independent of the length of prestimulation. The altered signaling led to altered function, as FSL1 or P3C triggered the release of IL-6, CCL-20, and CXCL-2 in primed cells, but not in resting astrocytes. These data confirmed the hypothesis that astrocytes exposed to activated microglia assume a different functional phenotype involving longer term TLR2 responsiveness, even after the initial stimulation by inflammatory mediators has ended.</dcterms:abstract> </rdf:Description> </rdf:RDF>

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