<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Belibasakis GN</dc:creator>
  <dc:creator>Bostanci N</dc:creator>
  <dc:creator>Reddi D</dc:creator>
  <dc:date>2010</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">Periodontal disease destroys the tooth-supporting tissues as a result of chronic inflammation elicited by bacterial accumulation on tooth surfaces. Porphyromonas gingivalis is a major periodontal pathogen, with a significant capacity to perturb connective tissue homeostasis and immune responses in the periodontium, attributed to its virulence factors, including a group of secreted cysteine proteases (gingipains). PAR-2 (protease-activated receptor-2) is a G-protein-coupled receptor activated upon proteolytic cleavage, mediating intracellular signalling events related to infection and inflammation, such as cytokine production. GF (gingival fibroblasts) and T cells have central roles in periodontal inflammation, which can potentially be mediated by PAR-2. The aims of this study were to investigate the effects of P. gingivalis on PAR-2 gene expression in human GF and Jurkat T cells, using quantitative real-time PCR, and to evaluate the involvement of gingipains. After 6 h of challenge with ascending concentrations of P. gingivalis, PAR-2 expression was up-regulated in both cell types by approximately 5-fold, compared with the control. The P. gingivalis concentration required for maximal PAR-2 induction was 4-fold greater in GF than Jurkat T cells. Heat inactivation or chemical inhibition of cysteine proteases abolished the capacity of P. gingivalis to induce PAR-2 expression in Jurkat T cells. In conclusion, P. gingivalis can induce PAR-2 expression in GF and Jurkat T cells, potentially attributed to its gingipains. These findings denote that P. gingivalis may perturb the host immune and inflammatory responses by enhancing PAR-2 expression, thus contributing to the pathogenesis of periodontal disease.</dc:description>
  <dc:format>application/pdf</dc:format>
  <dc:identifier>https://sonar.ch/global/documents/4558</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.1042/CBI20090290</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/19947912</dc:relation>
  <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
  <dc:source>Cell biology international. - 2010</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Cell Line</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Cysteine Proteases</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Fibroblasts</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Gingiva</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Jurkat Cells</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Porphyromonas gingivalis</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Receptor, PAR-2</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">T-Lymphocytes</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Up-Regulation</dc:subject>
  <dc:title xmlns:ns11="xml" ns11:lang="en">Regulation of protease-activated receptor-2 expression in gingival fibroblasts and Jurkat T cells by Porphyromonas gingivalis.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>