Systemic administration of interleukin-1 induces preterm parturition in mice

Romero, Roberto; Mazor, Moshe; Tartakovsky, Boris

doi:10.1016/0002-9378(91)90450-6

Cited by 319 publications

(173 citation statements)

References 13 publications

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“…Among these, prostaglandins and interleukins have attracted the most attention. 22,23 Our results show a remarkable stability in circulating concentrations of oxytocin before and in the hour after the administration of epidural analgesia. These observations are consistent with previous reports that observed similar unchanged plasma oxytocin concentrations following epidural labour analgesia, ll,12 In contrast to the small variation in plasma oxytocin levels in individual patients, we found large inter-patient variations indicating that different patients may vary considerably with respect to oxytocin secretion and/or degradation, but this process was not affected by epidural analgesia.…”

Section: Discussionmentioning

confidence: 51%

Epidural analgesia in early labour blocks the stress response but uterine contractions remain unchanged

Scull¹,

Hemmings

Carli³

et al. 1998

Can J Anaesth

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Purpose: To determine the effect of epidural analgesia on biochemical markers of stress, plasma oxytocin concentrations and frequency of uterine contractions during the first stage of labour. Methods: Nine nulliparous women, in spontaneous labour, with a singleton fetus and cervical dilatation < 5 cm were enrolled. Epidural bupivacaine 0.25% (range I 0 -14 ml) was administered and bilateral sensory blockade to ice 0-8 -L4) achieved. Blood samples were collected before the epidermal block and every I0 min for one hour after the block was achieved for the measurement of plasma beta-endorphin, cortical, glucose, lactate and oxytocin concentrations. No exogenous oxytocin was given. Intensity of pain was assessed at the time of the blood sampling using a I0 cm visual analogue scale (VAS). The frequency of uterine contractions was recorded for 60 rain before and after the epidural block.Results: There was a decrease in plasma beta-endorphin and cortisol concentrations after epidural block (P < 0.01).There were no changes in plasma glucose and lactate concentrations. The mean VAS for pain decreased I0 rain after epidural block was achieved and remained < 2 throughout the study period (P < 0.001 ). Mean plasma oxytocin concentrations did not change. The frequency of uterine contractions before and after the epidural block was similar. Condusions: The metabolic stress response to the pain of labour was attenuated by epidural analgesia. In contrast, plasma oxytocin concentration and frequency of uterine contractions were unaffected by the attenuation of metabolic stress response.Object~ : D&erminer reffet de l'analg&ie p&idurale sur les marqueurs biochimiques de stress, les concentrations plasmatiques d'oxytocine et la frdquence des contractions ut&ines pendant le premier stade du travail. M&hode : Neuf femmes nullipares, en travail spontan6, porteuse d'un seul foetus et pr&entant une dilatation du col de l'ut&us < 5 cm, ont dtd recrut&s. On a administrd de la bupivaca'ine p&idurale ~ 0,25 % (de I0 ~ 14 ml) et on a procddd ~ un blocage sensoriel bilat&al ~ la glace (-I-8 -I_4). On a prdlevd des &hantillons de sang avant le point dermique et ~ toutes les I0 minutes pendant une heure apt& le bloc afin de mesurer les concentrations plasmatiques de 13-endorphine, de cortisol, de glucose, de lactate et d'oxytocine. On n'a pas administrd d'oxytocine exog~ne. l'intensitd de la douleur a 6td dvalu6e au moment des prdl~vements sanguins en utilisant une &helle visuelle analogique (EVA) de 10 cm. La frdquence des contractions ut&ines a &d enregistr6e pendant 60 minutes avant et apr& I'analg6sie p&idurale. R&ultats : On a observd une baisse de la 13-endorphine plasmatique et des concentrations de cortisol apr& ranalg&ie p&idurale (P < 0,01). II n'y a pas eu de changements dans les concentrations de glucose et de lactate. La moyenne de rEVA pour la dou~eur a diminu~, I0 minutes apr~s le bloc p6ridural et est demeur& < 2 pendant toute la dur& de l'&ude (m < 0,00 I). Les concentrations moyennes d'oxytocine front pas changd. La frdquence...

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Section: Discussionmentioning

confidence: 51%

Epidural analgesia in early labour blocks the stress response but uterine contractions remain unchanged

Scull¹,

Hemmings

Carli³

et al. 1998

Can J Anaesth

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“…(1) stimulation of IL-1R induces the transcription of numerous pro-labor genes via MAPK p38, JNK, c-jun and small GTPase Rho in myometrial smooth muscle cells, which results in increased myometrial contractility (Tribe et al 2003, Chevillard et al 2007, Nadeau-Vallee et al 2015b; and preterm labor in mice and non-human primates (Romero et al 1991, Sadowsky et al 2006; (2) antagonism of IL-1R prevents all of these events (Romero & Tartakovsky 1992, Nadeau-Vallee et al 2015b; (3) IL-1α amniotic fluid levels are elevated in women that deliver preterm (Figueroa et al 2005); (4) preterm labor is associated with increased IL-1α activity in amniotic fluids (Romero et al 1989); and (5) maternal polymorphisms and haplotypes in the IL-1α gene (Sata et al 2009), as well as fetal polymorphism in the endogenous IL-1R antagonist (Witkin et al 2003), have been associated with increased risk of preterm birth. The critical role of IL-1 in preterm labor has been reviewed elsewhere (Nadeau-Vallee et al 2015a).…”

Section: Preterm Labormentioning

confidence: 99%

“…In animals, sterile inflammation is sufficient to recreate major features of common reproductive diseases (Romero et al 1991, Scharfe-Nugent et al 2012, Gomez-Lopez et al 2016, whereas in humans, a significant part of patients suffering from preeclampsia, preterm labor or other inflammatory diseases during pregnancy display no clinical signs of infection. This has been extensively studied in the context of preterm birth; although observational, correlational and causal data accumulated for >30 years have linked infection to preterm labor, preterm birth without infection is more prevalent (Romero et al 2001).…”

Section: Introductionmentioning

confidence: 99%

Sterile inflammation and pregnancy complications: a review

Nadeau-Vallée¹,

Obari²,

Palacios³

et al. 2016

Reproduction

216

161

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Inflammation is essential for successful embryo implantation, pregnancy maintenance and delivery. In the last decade, important advances have been made in regard to endogenous, and therefore non-infectious, initiators of inflammation, which can act through the same receptors as pathogens. These molecules are referred to as damage-associated molecular patterns (DAMPs), and their involvement in reproduction has only recently been unraveled. Even though inflammation is necessary for successful reproduction, untimely activation of inflammatory processes can have devastating effect on pregnancy outcomes. Many DAMPs, such as uric acid, high-mobility group box 1 (HMGB1), interleukin (IL)-1 and cell-free fetal DNA, have been associated with pregnancy complications, such as miscarriages, preeclampsia and preterm birth in preclinical models and in humans. However, the specific contribution of alarmins to these conditions is still under debate, as currently there is lack of information on their mechanism of action. In this review, we discuss the role of sterile inflammation in reproduction, including early implantation and pregnancy complications. Particularly, we focus on major alarmins vastly implicated in numerous sterile inflammatory processes, such as uric acid, HMGB1, IL-1α and cell-free DNA (especially that of fetal origin) while giving an overview of the potential role of other candidate alarmins.Reproduction (2016) 152 R277-R292

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“…Concentrations of IL-1b, IL-8, IL-6 and TNF-a are elevated in amniotic fluid and uterine tissues in association with preterm and term labour (Keelan et al 2003) and mediate infection-induced preterm labour (Romero et al 2002). Furthermore, systemic administration of IL-1b can induce preterm parturition in pregnant mice (Romero et al 1991). The high levels of pro-inflammatory cytokines detected in uterine tissues may derive, in part, from infiltrating leukocytes (Young et al 2002, Osman et al 2003, but decidual, myometrial, amnion and placental cells can themselves all produce pro-inflammatory cytokines.…”

Section: Nf-kb Is Activated By and Regulates Pro-inflammatory Cytokinesmentioning

confidence: 99%

The role of nuclear factor kappa B in human labour

Lindström

Bennett²

2005

Reproduction

272

237

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Preterm birth remains the leading cause of perinatal mortality and morbidity, largely as a result of a poor understanding of the precise mechanisms controlling labour onset in humans. Inflammation has long been recognised as a key feature of both preterm and term labour, with an influx of inflammatory cells into the uterus and elevated levels of pro-inflammatory cytokines observed during parturition. Nuclear factor kappa B (NF-kB) is a transcription factor family classically associated with inflammation. Accumulating evidence points to a role for NF-kB in the physiology and pathophysiology of labour. NF-kB activity increases with labour onset and is central to multiple pro-labour pathways. Premature or aberrant activation of NF-kB may thus contribute to preterm labour. The current understanding of NF-kB in the context of human labour is discussed here.

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Systemic administration of interleukin-1 induces preterm parturition in mice

Cited by 319 publications

References 13 publications

Epidural analgesia in early labour blocks the stress response but uterine contractions remain unchanged

Epidural analgesia in early labour blocks the stress response but uterine contractions remain unchanged

Sterile inflammation and pregnancy complications: a review

The role of nuclear factor kappa B in human labour

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