Prostaglandin E2 inhibits interleukin-6 release but not its transcription in human gingival fibroblasts stimulated with interleukin-1β or tumor necrosis factor-α

M. Takigawa, S. Takashiba, K. Takahashi, H. Arai, H. Kurihara, Y. Murayama

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Inflammatory mediators produced by human gingival fibroblasts (HGF) have been implicated in the initiation and progression of periodontal disease. The purpose of this study was to examine whether prostaglandin E2 (PGE2), which is produced in abundance from HGF after stimulation with interleukin (IL)-1β or tumor necrosis factor-α (TNF-α), could regulate IL-6 production by HGF. HGF stimulated with either IL-1β or TNF-α showed a rapid and dose-dependent increase in IL-6 mRNA accumulation and IL-6 secretion, as demonstrated by reverse transcription-polymerase chain reaction analysis and bioassay. IL-6 secretion from either IL-1β- or TNF-α-stimulated HGF was enhanced by the inhibition of PGE2 synthesis with indomethacin. Furthermore, the addition of PGE2 inhibited IL-6 secretion from these cells. In contrast, indomethacin or PGE2 did not affect the accumulation of IL-6 mRNA in IL-1β-stimulated HGF. These data indicate that IL-6 production by HGF is up-regulated by specific cytokines, IL-1β and TNF-α, and suggest that this production may be partially down-regulated by endogenous and exogenous PGE2 at the post-transcriptional level.

Original languageEnglish
Pages (from-to)1122-1127
Number of pages6
JournalJournal of periodontology
Volume65
Issue number12
DOIs
Publication statusPublished - 1994

Keywords

  • fibroblasts
  • interleukin-6
  • periodontal diseases/etiology
  • prostaglandins
  • tumor necrosis factor

ASJC Scopus subject areas

  • Periodontics

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