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Sterile-filtered saliva is a strong inducer of IL-6 and IL-8 in oral fibroblasts

Cvikl, Barbara ; Lussi, Adrian ; Moritz, Andreas ; Sculean, Anton ; Gruber, Reinhard

In: Clinical Oral Investigations, 2015, vol. 19, no. 2, p. 385-399

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    Titre
    • Sterile-filtered saliva is a strong inducer of IL-6 and IL-8 in oral fibroblasts
    Auteur
    • Cvikl, Barbara. Department of Preventive, Restorative and Pediatric Dentistry, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Lussi, Adrian. Department of Preventive, Restorative and Pediatric Dentistry, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Moritz, Andreas. Department of Conservative Dentistry and Periodontology, Medical University of Vienna, Vienna, Austria
    • Sculean, Anton. Department of Periodontology, School of Dental Medicine, University of Bern, Bern, Switzerland
    • Gruber, Reinhard. Department of Preventive, Restorative and Pediatric Dentistry, School of Dental Medicine, University of Bern, Bern, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • Clinical Oral Investigations, 2015, vol. 19, no. 2, p. 385-399. Springer Berlin Heidelberg
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:331137
    Summary
    Objectives: Saliva has been implicated to support oral wound healing, a process that requires a transient inflammatory reaction. However, definitive proof that saliva can provoke an inflammatory response remained elusive. Materials and methods: We investigated the ability of freshly harvested and sterile-filtered saliva to cause an inflammatory response of oral fibroblasts and epithelial cells. The expression of cytokines and chemokines was assessed by microarray, RT-PCR, immunoassays, and Luminex technology. The involvement of signaling pathways was determined by Western blot analysis and pharmacologic inhibitors. Results: We report that sterile-filtered whole saliva was a potent inducer of IL-6 and IL-8 in fibroblasts from the gingiva, the palate, and the periodontal ligament, but not of oral epithelial cells. This strong inflammatory response requires nuclear factor-kappa B and mitogen-activated protein kinase signaling. The pro-inflammatory capacity is heat stable and has a molecular weight of <40kDa. Genome-wide microarrays and Luminex technology further revealed that saliva substantially increased expression of other inflammatory genes and various chemokines. To preclude that the observed pro-inflammatory activity is the result of oral bacteria, sterile-filtered parotid saliva, collected under almost aseptic conditions, was used and also increased IL-6 and IL-8 expression in gingiva fibroblasts. The inflammatory response was, furthermore, independent of MYD88, an adapter protein of the Toll-like receptor signaling pathway. Conclusions: We conclude that saliva can provoke a robust inflammatory response in oral fibroblasts involving the classical nuclear factor-kappa B and mitogen-activated protein kinase signaling pathway. Clinical relevance: Since fibroblasts but not epithelial cells show a strong inflammatory response, saliva may support the innate immunity of defect sites exposing the oral connective tissue.