Effects of pro-inflamatory cytokines on polarized rat parotid Par-C10 monolayers [abstract]

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Effects of pro-inflamatory cytokines on polarized rat parotid Par-C10 monolayers [abstract]

Please use this identifier to cite or link to this item: http://hdl.handle.net/10355/1851

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dc.contributor.author Zimmerman, Danielle en
dc.contributor.author Camden, Jean M. en
dc.contributor.author Weisman, Gary A. en
dc.contributor.author Baker, Olga J. en
dc.date 2007 en
dc.date.accessioned 2009-06-25T15:30:42Z en
dc.date.available 2009-06-25T15:30:42Z en
dc.date.issued 2007 en
dc.identifier.uri http://hdl.handle.net/10355/1851
dc.description Abstract only available en
dc.description.abstract Sjögren's syndrome (SS), an autoimmune disorder, is distinguished by inflammation and salivary gland cell death, leading to xerostomia (dry mouth). The G protein-coupled P2Y2 receptor (P2Y2R) is up-regulated in response to damage or stress in salivary epithelium. Pro-inflammatory cytokines associated with SS can be produced by infiltrating lymphocytes or salivary epithelium. Correlations have been found between lymphocytic infiltration and increased production of pro-inflammatory cytokines such as interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-Éø (TNFα) and interferon-γ (IFNγ) and decreased function of exocrine glands in SS. Recent data has shown that P2Y2R activation enhances the activity of metalloproteases that release TNFα. OBJECTIVES: To study the effects of cytokines on polarized salivary epithelium. METHODS: Polarized rat parotid (Par-C10) monolayers were used to perform these studies. Cytokines released by UTP-induced P2Y2R activation were identified by ELISA. To evaluate the role of cytokines associated with SS on epithelial integrity, epithelial resistance was determined and correlated with the expression and distribution of tight junction (TJ) proteins by immunofluorescence and Western analysis, respectively. RESULTS: Activation of P2Y2Rs in Par-C10 monolayers induced the release of TNFα. The cytokines TNFα and IFNγ, but not IL-6 or IL1β, decreased the resistance of Par-C10 cells. However, the expression/distribution of the TJ protein ZO-1 was unaffected. CONCLUSIONS: The data support a hypothesis that P2Y2R expression and activation in salivary gland cells contribute to epithelial dysfunction in SS by generating pro-inflammatory cytokines that regulate ion transport and epithelial integrity in salivary glands. Future studies will determine the role of cytokines on the expression and distribution of other TJ molecules including occludin, claudins and junctional adhesion molecules. These studies may lead to better therapeutic strategies for minimizing autoimmune-associated dysfunction of salivary gland that contributes to xerostomia in SS patient. en
dc.description.sponsorship Life Sciences Undergraduate Research Opportunity Program en
dc.language en_US en
dc.language.iso en_US en
dc.publisher University of Missouri--Columbia. Office of Undergraduate Research en
dc.relation.ispartof 2007 Undergraduate Research and Creative Achievements Forum (MU) en
dc.source.uri http://undergradresearch.missouri.edu/forums-conferences/abstracts/abstract-detail.php?abstractid= en
dc.subject Sjögren's syndrome (SS) en
dc.subject autoimmune disorder en
dc.subject salivary epithelium en
dc.subject tight junction (TJ) proteins en
dc.title Effects of pro-inflamatory cytokines on polarized rat parotid Par-C10 monolayers [abstract] en
dc.type Presentation en
dc.contributor.meetingname Undergraduate Research and Creative Achievements Forum (2007 : University of Missouri--Columbia) en
dc.contributor.corporatename University of Missouri-Columbia. Office of Undergraduate Research en
dc.relation.ispartofcommunity University of Missouri-Columbia. Office of Undergraduate Research. Undergraduate Research and Creative Achievements Forum


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