Interleukin-I? intra-amniotic infusion induces tumor necrosis factor-?, prostaglandin production, and preterm contractions in pregnant rhesus monkeys

BAGGIA, S; Gravett, Michael G.; Witkin, Steven S.; Haluska, George J.; Novy, Miles J.

doi:10.1016/1071-5576(96)00002-0

Cited by 106 publications

(75 citation statements)

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“…IL-1␤ plays a major role in the initiation of infection-related preterm labor and delivery (24,25). Although normal term labor directly correlates with the expression levels of IL-1␤, IL-6, and CXCL8 (60 -64), premature induction of these proinflammatory factors often results in preterm delivery (65).…”

Section: Discussionmentioning

confidence: 99%

IL-1β-Mediated Proinflammatory Responses Are Inhibited by Estradiol via Down-Regulation of IL-1 Receptor Type I in Uterine Epithelial Cells

Schaefer

Wright

Pioli

et al. 2005

The Journal of Immunology

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The objective of this study was to examine the effects of sex hormones on IL-1β-mediated responses by uterine epithelial cells. The mRNA expression and secretion of human β-defensin-2 and CXCL8 by uterine epithelial cells was examined following stimulation with IL-1β in the presence of estradiol or progesterone. Estradiol inhibited the IL-1β-mediated mRNA expression and secretion of human β-defensin-2 and CXCL8 by uterine epithelial cells while progesterone had no effect. Inhibition of the IL-1β-mediated response by estradiol was dose dependent, with maximal inhibition observed using 10−7 to 10−10 M, and was shown to be mediated through the estrogen receptor because addition of a pure estrogen receptor antagonist abrogated this effect. The mechanism by which estradiol inhibits IL-1β-mediated responses by uterine epithelial cells appears to be the down-modulation of the IL-1R type I, thereby reducing the uterine epithelial cell’s ability to respond to IL-1β. These results suggest that the inhibitory effect of estradiol on IL-1β-mediated inflammatory responses by uterine epithelial cells indicates a link between the endocrine and immune systems and may be crucial for dampening proinflammatory responses during the time of ovulation or pregnancy.

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Section: Discussionmentioning

confidence: 99%

IL-1β-Mediated Proinflammatory Responses Are Inhibited by Estradiol via Down-Regulation of IL-1 Receptor Type I in Uterine Epithelial Cells

Schaefer

Wright

Pioli

et al. 2005

The Journal of Immunology

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“…The IL-6 level has been proposed as a marker for the prediction of preterm delivery (24). TNF-␣, IL-1␤, and IL-6 can induce the production of both prostaglandins and metalloproteases leading to preterm delivery (19,20). Double knockouts for TNF-␣ and IL-1␤ receptors are refractory to bacterially induced preterm labor (22).…”

Section: Discussionmentioning

confidence: 99%

“…To assess that the onset of preterm labor in LPS-injected dams was concomitant to an intrauterine inflammation and that this phenomenon was prevented in the presence of rolipram, we measured the concentration of cytokines in amniotic fluids, namely TNF-␣, IL-1␤, IL-6, and IL-10, which have been reported to be involved in inflammation-induced preterm delivery (19,20). As depicted in Fig.…”

Section: Decrease Of Inflammation-induced Cytokines Level Rises In Ammentioning

confidence: 99%

PDE4 Inhibition Prevents Preterm Delivery Induced by an Intrauterine Inflammation

Schmitz

Souil

Hervé

et al. 2007

The Journal of Immunology

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The aim of this study was to explore the anti-inflammatory properties of phosphodiesterase-4 (PDE4) inhibitors in vivo and their potential ability to prevent inflammation-induced preterm delivery. Indeed, intrauterine inflammation is the major etiology of very preterm delivery, the leading cause of neonatal mortality and morbidity. Intrauterine injection of Escherichia coli LPS in 15-day-pregnant mice induced an increase of PDE4 activity and PDE4B expression at the maternofetal interface, a rise of amniotic fluid levels of TNF-α, IL-1β, IL-6, and IL-10 and provoked massive preterm delivery and fetal demise. Selective PDE4 inhibition by rolipram prevented the rise in the proinflammatory cytokines. Following the nuclear translocation of the transcription factor NFκB, as a marker of cellular activation after the inflammatory challenge, showed a time-dependent sequential activation of the gestational tissues, from the uterine mesometrial to the fetal compartment, particularly in the glycogen-trophoblastic cells of the placenta. This activation was disrupted by PDE4 inhibition, and inflammation-induced preterm delivery and fetal demise were prevented. PDE4 selective inhibitors may thus represent a novel effective treatment to delay inflammation-induced preterm delivery and to prevent adverse outcomes in infants.

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“…IL-1beta is able to induce the secretion of several inflammatory factors, such as IL-6, IL-8, tumor necrosis factor-alpha (TNF-alpha), matrix metalloproteinases (MMPs) by many different cell types including vaginal epithelial cells, macrophages, neutrophils, peripheral blood mononuclear cells (PBMC), fibroblasts, endothelial and muscle cells [42,43]. The expression of cytokines such as IL-1beta, IL-6, IL-8, and TNF-alpha by either the fetal or maternal tissues has been demonstrated Volume 5 Issue 4 -2016 to upregulate the activity of a number of uterine and cervical factors (e.g., prostaglandin hormones and their receptors, MMPs, vascular endothelial growth factor and elafin) and leukocytes leading to premature initiation of the parturition process [42][43][44]. The crucial role of IL-1beta was recently highlighted by a study aimed to determine the relative contributions of individual proinflammatory cytokines and chemokines to the triggering of preterm labor.…”

Section: Introductionmentioning

confidence: 99%

Local Interleukin-1beta in Pregnant Women with Bacterial Vaginosis and Adverse Pregnancy Outcomes

Cauci¹

2016

OGIJ

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Objective: To assess if vaginal interleukin-(IL)-1beta in early pregnancy is associated with adverse outcome among BV-positive women.Study Design: 1,806 women were enrolled at <20 weeks' gestation. 800 women were BV-positive (Nugent 7-10), 707 of them had birth outcome data. Vaginal IL1beta concentrations were measured in 105 BV-positive women who had an adverse preterm outcome, including 66 preterm births (20-<37 weeks, of which 52 were spontaneous) and 14 late miscarriages (12-<20 weeks), and in 295 BV controls (term normal birth weight infants). The upper (>66 th percentile) and lower (<33 rd percentile) tertiles of IL-1beta concentrations were compared with the middle tertile (33 rd to 66 th percentile). Results:None of the IL-1beta tertiles was associated with increased risk for any adverse preterm outcome, nor preterm birth and miscarriage with or without exclusion of women with concurrent STDs.Conclusion: IL-1beta is not a risk marker for preterm birth among BV-positive women in early gestation.

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Interleukin-I? intra-amniotic infusion induces tumor necrosis factor-?, prostaglandin production, and preterm contractions in pregnant rhesus monkeys

Cited by 106 publications

References 0 publications

IL-1β-Mediated Proinflammatory Responses Are Inhibited by Estradiol via Down-Regulation of IL-1 Receptor Type I in Uterine Epithelial Cells

IL-1β-Mediated Proinflammatory Responses Are Inhibited by Estradiol via Down-Regulation of IL-1 Receptor Type I in Uterine Epithelial Cells

PDE4 Inhibition Prevents Preterm Delivery Induced by an Intrauterine Inflammation

Local Interleukin-1beta in Pregnant Women with Bacterial Vaginosis and Adverse Pregnancy Outcomes

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