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

doi:10.1016/j.ejphar.2005.05.020

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 journal › Article › peer-review

14 Citations (Scopus)

Abstract

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 language	English
Pages (from-to)	252-256
Number of pages	5
Journal	European Journal of Pharmacology
Volume	517
Issue number	3
DOIs	https://doi.org/10.1016/j.ejphar.2005.05.020
Publication status	Published - Jul 11 2005

Keywords

Adhesion molecule
Monocyte
Prostaglandin

ASJC Scopus subject areas

Pharmacology

Access to Document

10.1016/j.ejphar.2005.05.020

Cite this

@article{52952d056acd493ca20d61e69c56dde0,

title = "Prostaglandins E1 and E2 inhibit lipopolysaccharide- induced interleukin-18 production in monocytes",

abstract = "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.",

keywords = "Adhesion molecule, Monocyte, Prostaglandin",

author = "Takahashi, {Hideo K.} and Hiromi Iwagaki and Shuji Mori and Tadashi Yoshino and Noriaki Tanaka and Masahiro Nishibori",

note = "Funding Information: This study was supported in part by a grant for the promotion of research from Okayama University (No.21 to M.N.), a grant from the Okayama Medical Foundation (to H.K.T.) and a grant-in-aid for scientific research (C) (15590467 to H.K.T. and 15590228 to M.N.). The authors thank Ono Pharmaceutical Co. (Tokyo, Japan) for their generous donation of ONO-DI-004, ONO-AE1-259-01, ONO-AE-248, ONO-AE1-329 and ONO-1301.",

year = "2005",

month = jul,

day = "11",

doi = "10.1016/j.ejphar.2005.05.020",

language = "English",

volume = "517",

pages = "252--256",

journal = "European Journal of Pharmacology",

issn = "0014-2999",

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TY - JOUR

T1 - Prostaglandins E1 and E2 inhibit lipopolysaccharide- induced interleukin-18 production in monocytes

AU - Takahashi, Hideo K.

AU - Iwagaki, Hiromi

AU - Mori, Shuji

AU - Yoshino, Tadashi

AU - Tanaka, Noriaki

AU - Nishibori, Masahiro

N1 - Funding Information: This study was supported in part by a grant for the promotion of research from Okayama University (No.21 to M.N.), a grant from the Okayama Medical Foundation (to H.K.T.) and a grant-in-aid for scientific research (C) (15590467 to H.K.T. and 15590228 to M.N.). The authors thank Ono Pharmaceutical Co. (Tokyo, Japan) for their generous donation of ONO-DI-004, ONO-AE1-259-01, ONO-AE-248, ONO-AE1-329 and ONO-1301.

PY - 2005/7/11

Y1 - 2005/7/11

N2 - 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.

AB - 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.

KW - Adhesion molecule

KW - Monocyte

KW - Prostaglandin

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