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Prostaglandin E 2 (PGE 2 ) downregulates interleukin (IL)‐1 α ‐induced IL‐6 production via EP 2 /EP 4 subtypes of PGE 2 receptors in human periodontal ligament cells
Author(s) -
Noguchi K,
Maeda M,
Ruwanpura SMPM,
Ishikawa I
Publication year - 2005
Publication title -
oral diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.953
H-Index - 87
eISSN - 1601-0825
pISSN - 1354-523X
DOI - 10.1111/j.1601-0825.2005.01059.x
Subject(s) - prostaglandin e , prostaglandin e2 , chemistry , interleukin , endocrinology , medicine , cytokine , biochemistry
Objectives: Prostaglandin E 2 (PGE 2 ) exerts its biological actions via EP receptors, which are divided into four subtypes, EP 1 , EP 2 , EP 3 and EP 4 . In the present study, we examined whether PGE 2 regulated interleukin (IL)‐1 α ‐induced IL‐6 production in human periodontal ligament (PDL) cells and if so, which subtypes of PGE 2 receptors were involved. Methods: PDL cells were stimulated with vehicle or IL‐1 α in the presence or absence of indomethacin (a cylooxygenase inhibitor), PGE 2 or various EP agonists. IL‐6 and PGE 2 levels were measured by enzyme‐linked immunosorbent assay. EP receptor mRNA expression was examined by reverse transcription‐polymerase chain reaction (RT‐PCR). Results: Indomethacin significantly enhanced IL‐1 α ‐induced IL‐6 production by PDL cells, although it completely inhibited IL‐1 α ‐induced PGE 2 production. Exogenous PGE 2 significantly suppressed IL‐1 α ‐induced IL‐6 production. Butaprost, a selective EP 2 agonist, and ONO‐AE1‐329, a selective EP 4 agonist, significantly inhibited IL‐1 α ‐induced IL‐6 production, although 17‐phenyl‐ ω ‐trinor PGE 2 , an EP 1 agonist, and ONO‐AP‐324, an EP 3 agonist, did not affect it. RT‐PCR analysis showed that EP 2 and EP 4 mRNA was expressed in PDL cells. Conclusions: We suggest that PGE 2 downregulates IL‐1 α ‐induced IL‐6 production via EP 2 /EP 4 receptors in human PDL cells.