An experimental model for intraamniotic infection and preterm labor in rhesus monkeys

Gravett, Michael G.; Witkin, Steven S.; Haluska, George J.; Edwards, Jeffrey L.; Cook, Michael; Novy, Miles J.

doi:10.1016/0002-9378(94)90418-9

Cited by 324 publications

(216 citation statements)

References 16 publications

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“…In the primate, experimentally induced chorioamnionitis is also associated with contracture type activity and conversion to progressive, reversible contractions are rarely seen. It is hypothesized that the contractile pattern and premature delivery seen in the experimental model of chorioamnionitis in rhesus monkeys is due to increased concentrations of prostaglandins and cytokines in amniotic fluid associated with infection (Gravett et al 1994). Increases in IL-1, IL-6, tumor necrosis factor (TNF)-a, and high concentrations of prostaglandins E2 and F2a have been found in the amniotic fluid of women with intra-amniotic infection and preterm labor (Romero et al 1988, 1989a,b, 1990, Hillier et al 1993.…”

Section: Discussionmentioning

confidence: 99%

“…In 1998 -2000, five bi-polar Ag -AgCl electrodes constructed as described previously (Lester et al 1992) were implanted. In 2001, electrodes consisted of three sets of paired wires that were passed with an 18 gauge needle through the myometrium (Gravett et al 1994). A bi-polar electrode was made by placing the paired wires 3 mm apart.…”

Section: Surgical Instrumentation and Post-surgical Managementmentioning

confidence: 99%

“…These inflammatory processes result in prostaglandin production by amnionic cells and stimulation of myometrial cell contractility. In the primate, intra-amnionic inoculation with group B streptococcus results in sequential increase in amniotic fluid cytokines, prostaglandins, and uterine activity (Gravett et al 1994). Pro-inflammatory cytokines rise as early as 6 h after inoculation with an increase in uterine contractility (measured by intrauterine pressure; IUP) 14 -40 h later and delivery 55 -72 h after inoculation.…”

Section: Introductionmentioning

confidence: 99%

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Alteration in uterine contractility in mares with experimentally induced placentitis

McGlothlin

Lester²,

Hansen³

et al. 2004

Reproduction

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An experimental model of ascending placentitis was developed in the mare to characterize the uterine myoelectrical pattern in late gestation and determine how ascending placentitis altered this pattern. In experiment 1, myometrial electrical activity was analyzed during the early morning, late morning and evening hours in four mares in the last 15 days of gestation to identify patterns of activity. In experiment 2, nine mares received intra-cervical inoculations of Streptococcus equi subspecies zooepidemicus. Myoelectrical activity in the early morning and evening hours in these mares was compared with four control mares. In experiment 1, the number of spike burst clusters >30 s was greater in the evening than in the late morning hours (P < 0.04). Spike burst activity (number 3 duration) of mares in experiment 1 was similar during day and night recordings until the last 6 days of gestation when it gradually increased each evening until parturition (P < 0.05). In experiment 2, control mares experienced a gradual increase in the number of small spike burst clusters in the last 6 days (P 5 0.008) and an increase in large and small spike burst clusters in the evening hours in the last 4 days of gestation (P 5 0.03). Mares with experimentally induced placentitis never exhibited a rise in spike burst clusters but had an increase in the mean duration and activity index of large spike burst clusters in the 4 days before parturition (P < 0.04). In conclusion, control mares had a progressive, reversible rise in myoelectrical activity at night in the week preceding parturition. This was not observed in mares with experimentally induced placentitis. They exhibited an increase in the intensity and duration of large spike burst clusters possibly in response to local inflammation.

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Section: Discussionmentioning

confidence: 99%

Section: Surgical Instrumentation and Post-surgical Managementmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Alteration in uterine contractility in mares with experimentally induced placentitis

McGlothlin

Lester²,

Hansen³

et al. 2004

Reproduction

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“…IL-1␤ is a major factor in the initiation of infection-related preterm labor and delivery and has been associated with preeclampsia (24 -26). IL-1␤ levels are elevated in the amniotic fluid of pregnancies complicated by intraamniotic infection, and IL-1␤ may be capable of causing preterm labor by up-regulating PG production leading to myometrial contractions (27)(28)(29). Elevated IL-1␤ expression is also observed in the placentas of women with preeclampsia and may be associated with placental hypoxia (26).…”

Section: Il-1␤-mediated Proinflammatory Responsesmentioning

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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“…The direct evidence that infection provokes preterm labor was first shown in an animal study. When Group B streptococci were injected into the amnionic fluid in preterm rhesus monkeys, amnionic fluid cytokine concentrations increased, followed by production of the prostaglandins E 2 and F 2α and, finally, uterine contractions (Gravett et al, 1994). Similarly, in humans, preterm labor due to infection is thought to be initiated by cytokines, including interleukin-1 (IL-1), tumor necrosis factor, and interleukin-6, produced by macrophages (Cram et al, 2002;Narahara andJohnston 1993: Mitreski andRadeka 2002).…”

Section: Biological Mechanismmentioning

confidence: 99%

Air Pollution and Adverse Pregnancy Outcome

Leem¹,

Ha²

2011

Air Pollution - New Developments

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An experimental model for intraamniotic infection and preterm labor in rhesus monkeys

Cited by 324 publications

References 16 publications

Alteration in uterine contractility in mares with experimentally induced placentitis

Alteration in uterine contractility in mares with experimentally induced placentitis

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

Air Pollution and Adverse Pregnancy Outcome

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