Prostaglandin E2 production by endogenous secretion of interleukin-1 in decidual cells obtained before and after the labor.
Previous reports revealed that interleukin-1 (IL-1) was involved in the process of premature labor in the cases with intrauterine infection. However, the roles of the cytokine in normal spontaneous labor remain uncertain. The present studies aimed at determining the involvement of the cytokine in prostaglandin (PG)E2 production during labor by the third trimester decidual cells. The cells were obtained at the time of normal spontaneous delivery (NVD) and elective cesarean section (ECS). The NVD cells produced significantly more amount of PGE2 than the ECS cells and the both cells responded to the addition of IL-1 beta to increase PGE2 production. A specific inhibitor of cyclooxygenase-2 (COX-2), NS398, decreased basal PGE2 production and inhibited the stimulatory effect of IL-1 beta in a dose dependent manner in NVD cells. The NVD cells secreted more amount of IL-1 beta than the ECS cells and contained more amount of preprocessed 31kD IL-1 beta inside the cells. The addition of recombinant soluble human IL-1 receptor (type I) not only blocked the effect of IL-1 beta on PG secretion, but significantly reduced the basal production of PGE2 by NVD cells. These results indicate that decidual PG production depends upon COX-2 after the onset of labor. Besides it seems likely that endogenously produced IL-1 beta may be involved in autocrine or paracrine fashion in inducing COX-2 after the onset of labor.
Ishihara
O
O
Department of Obstetrics and Gynaecology, Saitama Medical Centre, Saitama Medical School, Kawagoe, Japan.
Numari
H
H
Saitoh
M
M
Arai
Y
Y
Takanashi
H
H
Kitagawa
H
H
Kinoshita
K
K
D015153:Blotting, Western; D002585:Cesarean Section; D051546:Cyclooxygenase 2; D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003656:Decidua / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D015232:Dinoprostone / Q000096:biosynthesis*; D004305:Dose-Response Relationship, Drug; D005260:Female; D006801:Humans; D007375:Interleukin-1 / Q000378:metabolism* / Q000494:pharmacology; D007527:Isoenzymes / Q000187:drug effects / Q000378:metabolism; D007743:Labor, Obstetric / Q000378:metabolism*; D008565:Membrane Proteins; D009578:Nitrobenzenes / Q000494:pharmacology; D011247:Pregnancy; D011451:Prostaglandin-Endoperoxide Synthases / Q000187:drug effects / Q000378:metabolism; D017472:Receptors, Interleukin-1; D013449:Sulfonamides / Q000494:pharmacology
D052246:Cyclooxygenase 2 Inhibitors; D016861:Cyclooxygenase Inhibitors; D007375:Interleukin-1; D007527:Isoenzymes; D008565:Membrane Proteins; D009578:Nitrobenzenes; D017472:Receptors, Interleukin-1; D013449:Sulfonamides; C080955:N-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamide; D051546:Cyclooxygenase 2; C496540:PTGS2 protein, human; D011451:Prostaglandin-Endoperoxide Synthases; D015232:Dinoprostone