Cyclooxygenase-2–Dependent Prostaglandin E2 Upregulates Interleukin (IL)-1α–Induced IL-6 Generation in Mouse Cementoblasts

• Autores: Kazuyuki Noguchi
• Localización: Journal of periodontology, ISSN 0022-3492, Vol. 78, Nº. 1, 2007, págs. 135-140
• Idioma: inglés
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• Resumen

  • Background: Prostaglandin E2 (PGE2), which exerts its biologic actions via EP receptors (EP1, EP2, EP3, and EP4), is a bioactive metabolite of arachidonic acid that is produced by cyclooxygenase (COX)-1 and/or COX-2. In the present study, we investigated whether a mouse cementoblast cell line, OCCM-30 cells, that was stimulated with interleukin (IL)-1α produced COX-2–dependent PGE2 and whether the produced PGE2 affected IL-1α–induced IL-6 production.

    Methods: OCCM-30 cells were stimulated with vehicle or IL-1α in the presence or absence of indomethacin (a COX-1/COX-2 inhibitor), NS-398 (a specific COX-2 inhibitor), PGE2, and EP receptor agonists. PGE2 and IL-6 levels were assayed by enzyme linked immunosorbent assay.

    Results: IL-1α induced PGE2 production in a time-dependent fashion. Indomethacin and NS-398 completely inhibited IL-1α–induced PGE2 production. 17-phenyl-ω-trinor PGE2 (an EP1 agonist) and an EP4 agonist mimicked PGE2 enhancement of IL-1α–induced IL-6 production in OCCM-30 cells.

    Conclusions: From these data, we suggest that IL-1α induced PGE2 production in a COX-2–dependent manner in OCCM-30 cells and that the COX-2–derived PGE2 upregulates IL-1α–elicited IL-6 production via EP1 and/or EP4 receptors. PGE2 and IL-6 produced by cementoblasts may be involved in the pathogenesis of periodontal disease.