The enhanced production of placental interleukin-1 during labor and intrauterine infection

Taniguchi, Takeshi; Matsuzaki, Noboru; Kameda, Takashi; Shimoya, K.; Jo, Takeo; Saji, Fumitaka; Takahashi, Osamu

doi:10.1016/0002-9378(91)90241-i

Cited by 113 publications

(65 citation statements)

References 19 publications

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“…Epithelial sodium channel and Na-K-ATPase subunit expressions were both increased by IL-1␤, but not further by oxytocin. Our results indicate that IL-1␤ release into the maternal blood circulation positively affects lung maturation due to the IL-1␤-induced release of cortisol and thus prepares the lungs for the epinephrine surge associated with labor.␤-adrenoceptors; cortisol; epinephrine; prenatal lung development; sodium transport CYTOKINES, SUCH AS INTERLEUKIN-1 (IL-1), can be important during pregnancy, because IL-1 has been detected in the placenta and amniotic fluid (12,44). In this regard, interleukins have been proposed as a signal for parturition onset, as cytokines can stimulate prostaglandin biosynthesis (41).…”

mentioning

confidence: 95%

“…␤-adrenoceptors; cortisol; epinephrine; prenatal lung development; sodium transport CYTOKINES, SUCH AS INTERLEUKIN-1 (IL-1), can be important during pregnancy, because IL-1 has been detected in the placenta and amniotic fluid (12,44). In this regard, interleukins have been proposed as a signal for parturition onset, as cytokines can stimulate prostaglandin biosynthesis (41).…”

mentioning

confidence: 99%

“…In this regard, interleukins have been proposed as a signal for parturition onset, as cytokines can stimulate prostaglandin biosynthesis (41). During normal pregnancies, IL-1 is present in the amniotic fluid in low concentrations, but during preterm labor much higher amniotic fluid IL-1 concentrations are present (44). Intrauterine infection/inflammation may further elevate cytokine levels, the highest activity being attributable to IL-1␤ (44).…”

mentioning

confidence: 99%

“…During normal pregnancies, IL-1 is present in the amniotic fluid in low concentrations, but during preterm labor much higher amniotic fluid IL-1 concentrations are present (44). Intrauterine infection/inflammation may further elevate cytokine levels, the highest activity being attributable to IL-1␤ (44). Many prematurely born infants suffer from fetal infection and/or respiratory distress syndrome (RDS), both of which are important reasons for mortality of premature babies.…”

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confidence: 99%

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Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Nair¹,

Li²,

Bhattacharjee³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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-We tested the hypothesis that oxytocin-induced labor augmented IL-1␤-induced/ -stimulated lung fluid absorption in preterm guinea pig fetuses. IL-1␤ was administered subcutaneously daily to timed-pregnant guinea pigs for 3 days with and without simultaneous cortisol synthesis inhibition by metyrapone. At day 3, oxytocin was administered, and fetuses were delivered by abdominal hysterotomy at 61 and by oxytocin-induced birth at 68 days gestation. Delivered fetuses were instilled with isosmolar 5% albumin into the lungs, and lung fluid movement was measured over 1 h by mass balance. Lung fluid absorption was induced in 61-day and stimulated in 68-day gestation lungs by IL-1␤. Labor induction by oxytocin augmented IL-1␤-induced/-stimulated lung fluid absorption. Metyrapone pretreatment did not affect oxytocin-induced/-stimulated lung fluid absorption, while completely blocking IL-1␤-induced/-stimulated fluid absorption. Fetal lung fluid absorption, when present, was always propranolol and amiloride sensitive, suggesting that ␤-adrenoceptor stimulation and amiloridesensitive sodium channels were critical for fluid absorption. Epithelial sodium channel and Na-K-ATPase subunit expressions were both increased by IL-1␤, but not further by oxytocin. Our results indicate that IL-1␤ release into the maternal blood circulation positively affects lung maturation due to the IL-1␤-induced release of cortisol and thus prepares the lungs for the epinephrine surge associated with labor.␤-adrenoceptors; cortisol; epinephrine; prenatal lung development; sodium transport CYTOKINES, SUCH AS INTERLEUKIN-1 (IL-1), can be important during pregnancy, because IL-1 has been detected in the placenta and amniotic fluid (12,44). In this regard, interleukins have been proposed as a signal for parturition onset, as cytokines can stimulate prostaglandin biosynthesis (41). During normal pregnancies, IL-1 is present in the amniotic fluid in low concentrations, but during preterm labor much higher amniotic fluid IL-1 concentrations are present (44). Intrauterine infection/inflammation may further elevate cytokine levels, the highest activity being attributable to IL-1␤ (44). Many prematurely born infants suffer from fetal infection and/or respiratory distress syndrome (RDS), both of which are important reasons for mortality of premature babies. Recent human data suggest that ion transport abnormalities across lung epithelial cells, i.e., an incomplete transition of lung fluid secretion to lung fluid absorption, can contribute to RDS development (1). Factors accelerating ion transport across alveolar cells may thus have benefits for the resolution of RDS. Recent experimental data have suggested that proinflammatory cytokines could also promote lung maturation (9,14,26,47). IL-1␣ increased mRNA surfactant protein expression and improved lung compliance in fetal rabbits (9). IL-1␣ also improved postnatal lung function with increased surfactant pool size without eliciting systemic inflammatory responses in lambs (14, 47). We recently reported that IL-...

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confidence: 95%

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confidence: 99%

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confidence: 99%

mentioning

confidence: 99%

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Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Nair¹,

Li²,

Bhattacharjee³

et al. 2005

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…One of the proposed underlying biochemical pathways by which bacterial infection may initiate preterm labour is via bacterial endotoxininduced formation of pro-inflammatory mediators that directly or indirectly promote myometrial responsiveness or activity. Bacterial endotoxins, such as lipopolysaccharide (LPS), induce inflammatory responses in human gestational tissues, resulting in increased release of proinflammatory cytokines, such as cytokine interleukin-1 (IL-1) (Taniguchi et al 1991, Kauma et al 1992 and phospholipid metabolites such as prostanoids (Romero et al 1988, Casey et al 1990, Mitchell et al 1990, Lundin-Schiller & Mitchell 1991, Nguyen et al 1994.…”

Section: Introductionmentioning

confidence: 99%

Effect of bacterial endotoxin on the in vitro release of Type II phospholipase-A2 and prostaglandin E2 from human placenta

Farrugia

Nicholls²,

Rice³

1999

Journal of Endocrinology

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The aim of this study was to establish the effect of bacterial endotoxin lipopolysaccharide (LPS) on the release of Type II phospholipase-A 2 (PLA 2 ) and prostaglandin E 2 (PGE 2 ) from late-pregnant human placental tissue incubated in vitro. Under basal conditions, immunoreactive Type II PLA 2 and PGE 2 were released from tissue explants in a time-dependent manner (up to 24 h, ANOVA, P<0·0001, n=6). The release of these mediators was not associated with a loss of cell membrane integrity, as indicated by concentrations of the intracellular enzyme, lactate dehydrogenase (LDH), in the incubation medium. Incubation of explants in the presence of LPS (0·001-100 µg LPS/ml) significantly decreased PLA 2 tissue content (P<0·02, n=6) and increased the accumulation of PLA 2 and PGE 2 in the incubation medium (P<0·0001, n=6). The data obtained in this study indicated that Type II PLA 2 and PGE 2 are released from term placenta under basal conditions and that LPS stimulated their release. The associated decrease in PLA 2 tissue content is consistent with the hypothesis that LPS induces the release of stored PLA 2 . This study identifies one pathway by which products of bacterial infection may induce the release of a pro-inflammatory, extracellularly active PLA 2 from intrauterine tissues that may promote the formation of phospholipid metabolites involved in the process of labour and delivery (e.g. the prostaglandins).

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Infectious Diseases

Pathology of the Human Placenta

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The enhanced production of placental interleukin-1 during labor and intrauterine infection

Cited by 113 publications

References 19 publications

Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Oxytocin-induced labor augments IL-1β-stimulated lung fluid absorption in fetal guinea pig lungs

Effect of bacterial endotoxin on the in vitro release of Type II phospholipase-A2 and prostaglandin E2 from human placenta

Infectious Diseases

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