Prostaglandins E1 and E2 inhibit lipopolysaccharide-induced interleukin-18 production in monocytes.
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 E2 inhibited interleukin-18 production in human monocytes treated with lipopolysaccharide and prostanoid IP-, EP2- and EP4-receptor agonists mimicked the effects of prostaglandins E1 and E2. Therefore, prostanoid IP, EP2- and EP4-receptors might be involved in the decrease in interleukin-18 production during sepsis.
Department of Pharmacology, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, Okayama 700-8558, Japan.
Hideo K
HK
Takahashi
Hiromi
H
Iwagaki
Shuji
S
Mori
Tadashi
T
Yoshino
Noriaki
N
Tanaka
Masahiro
M
Nishibori
D000527:Alprostadil / Q000494:pharmacology*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism; D015232:Dinoprostone / Q000031:analogs & derivatives / Q000494:pharmacology*; D004797:Enzyme-Linked Immunosorbent Assay; D005434:Flow Cytometry; D006801:Humans; D020382:Interleukin-18 / Q000097:blood*; D007546:Isoquinolines / Q000494:pharmacology; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008562:Membrane Glycoproteins / Q000096:biosynthesis; D008738:Methyl Ethers / Q000494:pharmacology; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D011725:Pyridines / Q000494:pharmacology; D011956:Receptors, Cell Surface / Q000096:biosynthesis; D044006:Receptors, Epoprostenol / Q000819:agonists / Q000502:physiology; D018078:Receptors, Prostaglandin E / Q000819:agonists / Q000502:physiology; D058307:Receptors, Prostaglandin E, EP2 Subtype; D058309:Receptors, Prostaglandin E, EP4 Subtype; D013449:Sulfonamides / Q000494:pharmacology; D051193:Toll-Like Receptors
C499423:9-deoxy-9-chloro-15-deoxy-16-hydroxy-17,17-trimethylene-19,20-didehydroprostaglandin E2; D020382:Interleukin-18; D007546:Isoquinolines; D018950:Lipopolysaccharide Receptors; D008070:Lipopolysaccharides; D008562:Membrane Glycoproteins; D008738:Methyl Ethers; C461399:ONO-AE1-329; C545644:PTGER2 protein, human; C545650:PTGER4 protein, human; D011725:Pyridines; D011956:Receptors, Cell Surface; D044006:Receptors, Epoprostenol; D018078:Receptors, Prostaglandin E; D058307:Receptors, Prostaglandin E, EP2 Subtype; D058309:Receptors, Prostaglandin E, EP4 Subtype; D013449:Sulfonamides; D051193:Toll-Like Receptors; C105488:ONO 1301; D017868:Cyclic AMP-Dependent Protein Kinases; D000527:Alprostadil; D015232:Dinoprostone; C063509:N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide