IL-18 in pregnancy; the elevation of IL-18 in maternal peripheral blood during labour and complicated pregnancies

Ida, Akinori; Tsuji, Yoshiyuki; Muranaka, Junko; Kanazawa, Riichiro; Nakata, Yoshitaka; Adachi, Susumu; Okamura, Haruki; Koyama, Koji

doi:10.1016/s0165-0378(00)00058-9

Cited by 75 publications

(56 citation statements)

References 17 publications

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“…Therefore, mouse uterus may possess an IL-18 system, and IL-18 plays roles in the regulation of the immune response and uterine functions, although it is difficult to specify physiological roles of IL-18 in the mouse uterus. We investigated IL-18 mRNA expression in the mouse uterus since sever al recent studies suggested that IL-18 was involved in the regulation of uterine functions [14][15][16][17][18] and there are no reports on sex steroid hormone actions on IL-18 gene expression. In the mouse uterus, expressions of IL-1 8 a n d I L -1 8 R α m R N A s w er e d e t e c t e d i n separately cultured endometrial epithelial and stromal cells by RT-PCR.…”

Section: Discussionmentioning

confidence: 99%

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Estrogen Inhibits Interleukin-18 mRNA Expression in the Mouse Uterus

Murakami

Otsuki

Kusumoto

et al. 2005

Journal of Reproduction and Development

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Abstract. ) is a proinflammatory cytokine expressed in female reproductive organs in humans, rats and mice. The physiological roles of uterine IL-18 and the regulatory mechanisms of IL-18 gene expression are unclear. The present study aimed to clarify the effects of estradiol-17β (E2) and progesterone (P4) on IL-18 mRNA expression in the mouse uterus. Distribution and expression levels of IL-18 mRNA were studied using an RNase protection assay. Expression of IL-18 mRNA was observed in all organs studied, including testes, ovaries and uteri. The uterine IL-18 mRNA level of estrous mice was higher than that of diestrous mice. E2 treatment (1, 5, 25 or 250 ng/ mouse) decreased uterine IL-18 mRNA levels in ovariectomized mice dose-dependently. E2 treatment acutely decreased IL-18 mRNA levels 3 h after injection, but these levels returned to the initial level after 48 h. P4 treatment (1 mg/mouse) decreased uterine IL-18 mRNA levels after 12 h, but levels returned to the initial level after 48 h. Both uterine IL-18 and IL-18Rα mRNAs were detected in cultured endometrial epithelial and stromal cells. These results suggest that uterine IL-18 expression is reduced by sex steroid hormones and that IL-18 acts on endometrial cells in a paracrine or autocrine manner.

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Section: Discussionmentioning

confidence: 99%

“…In human endometrium, IL-18 protein and mRNA were both expressed throughout the menstrual cycle [14]. In human sera and amniotic fluid, IL-18 protein levels increased during pregnancy, and increased further at delivery [15,16]. On the other hand, IL-18 mRNA levels in human blood decreased during pregnancy [17].…”

mentioning

confidence: 99%

Estrogen Inhibits Interleukin-18 mRNA Expression in the Mouse Uterus

Murakami

Otsuki

Kusumoto

et al. 2005

Journal of Reproduction and Development

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“…To determine the acute effect of ovariectomy, uteri from the first group of animals were collected at 1, 3, and 14 days after ovariectomy. To determine the effects of estradiol-17β (E2), the second group of ovariectomized mice were rested for 14 days, and then treated with single injection of E2 (0, 25, or 250 ng/mouse; Sigma-Aldrich, St. Louis, MO, USA), and uteri were collected at 0, 3,6,12,24,48,72, or 96 h after initiation of the E2 treatment. To examine v a r i o u s d o s e s o f E 2 , t h e t h i r d g r o u p o f ovariectomized animals was treated with a single injection of E2 (0, 1, 5, 25, or 250 ng/mouse), and their uteri were collected 12 h after the E2 treatment.…”

Section: Ovariectomy and Hormone Treatmentmentioning

confidence: 99%

“…In situ hybridization analysis demonstrated that IL-18 mRNA is mainly detected in glandular epithelial cells and stromal cells in the adult mouse uterus [10]. In women, the serum IL-18 level is elevated during labor [12]. Hence, we hypothesized that IL-18 would be involved in the regulation of mouse uterine functions, although the physiological roles of IL-18 and the target cells of IL-18 actions in the mouse endometrium are not well known.…”

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confidence: 99%

Expression of Interleukin-18 Receptor mRNA in the Mouse Endometrium

Otsuki

Kusumoto

Murakami

et al. 2007

Journal of Reproduction and Development

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Abstract. ) is a proinflammatory cytokine involved in chronic inflammation, autoimmune diseases, and a variety of cancers, and is expressed in mouse uteri. Our previous study suggested that IL-18 acts as a paracrine factor, regulating endometrial function. To elucidate the physiological roles of IL-18 in the mouse endometrium, the expression of the IL-18 receptor (IL-18R) α subunit was analyzed. IL-18Rα mRNA was expressed in several mouse organs in addition to the endometrium. In situ hybridization analysis using a biotin-labeled mouse IL-18Rα riboprobe demonstrated that IL-18Rα mRNA expression was detected in glandular epithelial cells, stromal cells around uterine glands, and myometrial cells in the mouse uterus, suggesting that these cells are targets for IL-18. The uterine IL-18Rα mRNA expression level changed with the estrous cycle. The uterine IL-18Rα mRNA levels of estrous mice were higher than those of diestrous mice. In addition, the IL-18Rα mRNA levels in uteri at 3 and 14 days after ovariectomy were higher than those at diestrus and decreased following treatment with estradiol-17β or progesterone. These findings suggest that IL-18Rα gene expression is regulated by estrogen and progesterone and that the uterine IL-18 system is involved in the regulation of uterine functions in a paracrine manner.

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“…Amniotic fluid levels of TNF-a and IL-10 are elevated 11,12 , however, placental TNF-a mRNA levels are reported to be unaltered in fetal growth restriction 13 . Maternal circulating levels of TNF-a, IL-6 and IL-8 are unaltered in fetal growth restriction 11 , but those of IL-18 are increased 14 . Similarly, there are limited data with regards to adhesion molecule levels in fetal growth restriction.…”

Section: Introductionmentioning

confidence: 99%

Does endothelial cell activation occur with intrauterine growth restriction?

Johnson

2002

BJOG: An International Journal of Obstetrics and Gynaecology

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It is possible that in fetal growth restriction without pre-eclampsia endothelial cell activation does not occur. This might be either because there is no release of 'factor X' or because of maternal resistance to its effects. To test this hypothesis, we took blood samples from 26 women with pre-eclampsia (without fetal growth restriction), 13 women with fetal growth restriction (without pre-eclampsia) and 24 normal pregnant controls, and measured the circulating levels of three markers of endothelial cell activation (soluble VCAM, ICAM and E-selectin) and three cytokines [tumour necrosis factor-a (TNF-a), interleukin-6 (IL-6) and -8 (IL-8)]. The levels of the markers of endothelial cell activation were raised in both pre-eclampsia and fetal growth restriction pregnancies compared with controls; however, the levels of TNF-a, IL-6 and IL-8 were significantly raised in pregnancies complicated by pre-eclampsia, but not in fetal growth restriction, compared with controls. These data show that endothelial cell activation is common to both pre-eclampsia and fetal growth restriction, but that the circulating levels of cytokines are elevated only in pre-eclampsia. Thus, it seems likely that endothelial cell activation is a consequence of a failure of trophoblast invasion and that a further step is required, possibly involving cytokine release, for the expression of the full clinical picture of pre-eclampsia.

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IL-18 in pregnancy; the elevation of IL-18 in maternal peripheral blood during labour and complicated pregnancies

Cited by 75 publications

References 17 publications

Estrogen Inhibits Interleukin-18 mRNA Expression in the Mouse Uterus

Estrogen Inhibits Interleukin-18 mRNA Expression in the Mouse Uterus

Expression of Interleukin-18 Receptor mRNA in the Mouse Endometrium

Does endothelial cell activation occur with intrauterine growth restriction?

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