Prostaglandins E1 and E2 inhibit lipopolysaccharide- induced interleukin-18 production in monocytes

Hideo K. Takahashi, Hiromi Iwagaki, Shuji Mori, Tadashi Yoshino, Noriaki Tanaka, Masahiro Nishibori

Research output: Contribution to journalArticlepeer-review

14 Citations (Scopus)


The purpose of this present study was to explore the therapeutic potential of prostaglandins E1 and E2 on the systemic inflammatory response evoked by endotoxin. Since interleukin-18, a monocyte-derived cytokine, is increased during sepsis, decreasing the production of interleukin-18 is important in treating this condition. Prostaglandin E1 and E 2 inhibited interleukin-18 production in human monocytes treated with lipopolysaccharide and prostanoid IP-, EP2- and EP 4-receptor agonists mimicked the effects of prostaglandins E 1 and E2. Therefore, prostanoid IP, EP2- and EP4-receptors might be involved in the decrease in interleukin-18 production during sepsis.

Original languageEnglish
Pages (from-to)252-256
Number of pages5
JournalEuropean Journal of Pharmacology
Issue number3
Publication statusPublished - Jul 11 2005


  • Adhesion molecule
  • Monocyte
  • Prostaglandin

ASJC Scopus subject areas

  • Pharmacology


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