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dc.contributor.authorStevens, Niall T
dc.contributor.authorSadovskaya, Irina
dc.contributor.authorJabbouri, Said
dc.contributor.authorSattar, Tafiq
dc.contributor.authorO'Gara, James P
dc.contributor.authorHumphreys, Hilary
dc.contributor.authorGreene, Catherine M
dc.date.accessioned2011-04-07T10:46:01Z
dc.date.available2011-04-07T10:46:01Z
dc.date.issued2009-03
dc.identifier.citationStaphylococcus epidermidis polysaccharide intercellular adhesin induces IL-8 expression in human astrocytes via a mechanism involving TLR2. 2009, 11 (3):421-32 Cell. Microbiol.en
dc.identifier.issn1462-5822
dc.identifier.pmid19016779
dc.identifier.doi10.1111/j.1462-5822.2008.01264.x
dc.identifier.urihttp://hdl.handle.net/10147/127675
dc.description.abstractStaphylococcus epidermidis is an opportunistic biofilm-forming pathogen associated with neurosurgical device-related meningitis. Expression of the polysaccharide intercellular adhesin (PIA) on its surface promotes S. epidermidis biofilm formation. Here we investigated the pro-inflammatory properties of PIA against primary and transformed human astrocytes. PIA induced IL-8 expression in a dose- and/or time-dependent manner from U373 MG cells and primary normal human astrocytes. This effect was inhibited by depletion of N-acetyl-beta-d-glucosamine polymer from the PIA preparation with Lycopersicon esculentum lectin or sodium meta-periodate. Expression of dominant-negative versions of the TLR2 and TLR4 adaptor proteins MyD88 and Mal in U373 MG cells inhibited PIA-induced IL-8 production. Blocking IL-1 had no effect. PIA failed to induce IL-8 production from HEK293 cells stably expressing TLR4. However, in U373 MG cells which express TLR2, neutralization of TLR2 impaired PIA-induced IL-8 production. In addition to IL-8, PIA also induced expression of other cytokines from U373 MG cells including IL-6 and MCP-1. These data implicate PIA as an important immunogenic component of the S. epidermidis biofilm that can regulate pro-inflammatory cytokine production from human astrocytes, in part, via TLR2.
dc.language.isoenen
dc.subject.meshAstrocytes
dc.subject.meshCell Line
dc.subject.meshCells, Cultured
dc.subject.meshChemokine CCL2
dc.subject.meshHumans
dc.subject.meshInterleukin-6
dc.subject.meshInterleukin-8
dc.subject.meshPolysaccharides, Bacterial
dc.subject.meshStaphylococcus epidermidis
dc.subject.meshToll-Like Receptor 2
dc.subject.meshUp-Regulation
dc.titleStaphylococcus epidermidis polysaccharide intercellular adhesin induces IL-8 expression in human astrocytes via a mechanism involving TLR2.en
dc.typeArticleen
dc.contributor.departmentDepartment of Clinical Microbiology, Royal College of Surgeons in Ireland Education & Research Centre, Beaumont Hospital, Dublin, Ireland. nstevens@rcsi.ieen
dc.identifier.journalCellular microbiologyen
dc.description.provinceLeinster
html.description.abstractStaphylococcus epidermidis is an opportunistic biofilm-forming pathogen associated with neurosurgical device-related meningitis. Expression of the polysaccharide intercellular adhesin (PIA) on its surface promotes S. epidermidis biofilm formation. Here we investigated the pro-inflammatory properties of PIA against primary and transformed human astrocytes. PIA induced IL-8 expression in a dose- and/or time-dependent manner from U373 MG cells and primary normal human astrocytes. This effect was inhibited by depletion of N-acetyl-beta-d-glucosamine polymer from the PIA preparation with Lycopersicon esculentum lectin or sodium meta-periodate. Expression of dominant-negative versions of the TLR2 and TLR4 adaptor proteins MyD88 and Mal in U373 MG cells inhibited PIA-induced IL-8 production. Blocking IL-1 had no effect. PIA failed to induce IL-8 production from HEK293 cells stably expressing TLR4. However, in U373 MG cells which express TLR2, neutralization of TLR2 impaired PIA-induced IL-8 production. In addition to IL-8, PIA also induced expression of other cytokines from U373 MG cells including IL-6 and MCP-1. These data implicate PIA as an important immunogenic component of the S. epidermidis biofilm that can regulate pro-inflammatory cytokine production from human astrocytes, in part, via TLR2.


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