Lactoferrin in intrauterine infection, human parturition, and rupture of fetal membranes

2000 ◽  
Vol 183 (4) ◽  
pp. 904-910 ◽  
Author(s):  
Percy Pacora ◽  
Eli Maymon ◽  
Maria-Teresa Gervasi ◽  
Ricardo Gomez ◽  
Samuel S. Edwin ◽  
...  
Keyword(s):  
Intrauterine Infection ◽  
Fetal Membranes ◽  
Human Parturition

scholarly journals The Progesterone Receptor in Human Term Amniochorion and Placenta Is Isoform C

Endocrinology ◽  
2006 ◽  
Vol 147 (2) ◽  
pp. 687-693 ◽  
Author(s):  
Anthony H. Taylor ◽  
Penny C. McParland ◽  
David J. Taylor ◽  
Stephen C. Bell
Keyword(s):  
Progesterone Receptor ◽  
Western Blotting ◽  
Cell Types ◽  
Specific Role ◽  
Fetal Membranes ◽  
Rt Pcr ◽  
Reproductive Tissues ◽  
Pcr Techniques ◽  
Human Parturition ◽  
Extraembryonic Tissues

The mechanism that initiates human parturition has been proposed to be functional progesterone withdrawal whereby the 116-kDa B isoform of the progesterone receptor (PR-B) switches in favor of the 94-kDa A isoform (PR-A) in reproductive tissues. Recently other PR isoforms, PR-S, PR-C, and PR-M generated from the same gene have been identified and partially characterized. Using immunohistochemical, Western blotting, and RT-PCR techniques, evidence is provided that the major PR isoform present in human term fetal membranes (amnion and chorion) and syncytiotrophoblast of the placenta is neither of the classical nuclear PR-B or PR-A isoforms but is the N terminally truncated 60-kDa PR-C isoform. Evidence is also provided that the PR-C isoform resides in the cytoplasm of the expressing cell types. Data are also presented to show that PR-B, PR-A, and PR-S isoforms are essentially absent from the amnion and chorion, whereas PR isoforms A, B, C, and S are all present in the decidua, with PR-A being the major isoform. The syncytiotrophoblast of the placenta contains the cytoplasmic PR-C isoform but not PR-A, PR-B, or PR-S. The major PR isoform in the amnion, chorion, and placenta is PR-C, suggesting that the cytoplasmic PR-C isoform has a specific role in extraembryonic tissues and may be involved in the regulation of human parturition.

A clinical case of pregnancy with suspected trophoblastic disease in 3 trimester

2014 ◽  
Vol 63 (3) ◽  
pp. 66-70
Author(s):  
Yevgeniy Sergeyevich Mikhaylin ◽  
Lada Anatolyevna Ivanova ◽  
Alla Sergeyevna Lisyanskaya ◽  
Aleksey Gennadyevich Savitskiy ◽  
Anna Gennadyevna Minina ◽  
...  
Keyword(s):  
Clinical Case ◽  
Hydatidiform Mole ◽  
Intrauterine Infection ◽  
Fetal Membranes ◽  
Premature Rupture ◽  
Trophoblastic Disease ◽  
Preterm Premature Rupture ◽  
Placental Blood ◽  
Β Hcg ◽  
Placental Blood Flow

Cases of trophoblastic disease in the presence of the living fetus during 2-3 trimesters of pregnancy is a rare phenomenon. The description of the clinical case of suspected trophoblastic disease at term of 26 weeks is provided in article. The decision of pregnancy prolongation under control β- HCG was made. Therapy of gestosis, improvement of maternal-placental blood flow, anticoagulant therapy was carried out. Cesarean section was made at 30 weeks of pregnancy (preterm premature rupture of fetal membranes). In the postpartum period, a decrease of b-HCG to zero was within 1,5 months. In the postoperative period we did not receive convincing pathomorphological data for the presence of trophoblastic disease, so the question of whether there was in this case partial hydatidiform mole in combination with alive fetus, or received changes in the placenta and anomalously high values of b-HCG were the result of primary placental insufficiency with the intrauterine infection, remains open.

Are animal models relevant to key aspects of human parturition?

2009 ◽  
Vol 297 (3) ◽  
pp. R525-R545 ◽  
Author(s):  
Bryan F. Mitchell ◽  
Michael J. Taggart
Keyword(s):  
Immune System ◽  
Animal Models ◽  
Intrauterine Infection ◽  
Proinflammatory Response ◽  
Linear Sequence ◽  
Sequence Of Events ◽  
Novel Concept ◽  
Key Aspects ◽  
Human Parturition

Preterm birth remains the most serious complication of pregnancy and is associated with increased rates of infant death or permanent neurodevelopmental disability. Our understanding of the regulation of parturition remains inadequate. The scientific literature, largely derived from rodent animal models, suggests two major mechanisms regulating the timing of parturition: the withdrawal of the steroid hormone progesterone and a proinflammatory response by the immune system. However, available evidence strongly suggests that parturition in the human has significantly different regulators and mediators from those in most of the animal models. Our objectives are to critically review the data and concepts that have arisen from use of animal models for parturition and to rationalize the use of a new model. Many animal models have contributed to advances in our understanding of the regulation of parturition. However, we suggest that those animals dependent on progesterone withdrawal to initiate parturition clearly have a limitation to their translation to the human. In such models, a linear sequence of events (e.g., luteolysis, progesterone withdrawal, uterine activation, parturition) gives rise to the concept of a “trigger” mechanism. Conversely, we propose that human parturition may arise from the concomitant maturation of several systems in parallel. We have termed this novel concept “modular accumulation of physiological systems” (MAPS). We also emphasize the urgency to determine the precise role of the immune system in the process of parturition in situations other than intrauterine infection. Finally, we accentuate the need to develop a nonprimate animal model whose physiology is more relevant to human parturition. We suggest that the guinea pig displays several key physiological characteristics of gestation that more closely resemble human pregnancy than do currently favored animal models. We conclude that the application of novel concepts and new models are required to advance translational research in parturition.

scholarly journals Induction of PGF2α Synthesis by Cortisol Through GR Dependent Induction of CBR1 in Human Amnion Fibroblasts

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 3017-3024 ◽  
Author(s):  
Chunming Guo ◽  
Wangsheng Wang ◽  
Chao Liu ◽  
Leslie Myatt ◽  
Kang Sun
Keyword(s):  
Rna Polymerase Ii ◽  
Critical Role ◽  
Prostaglandin F2α ◽  
Fetal Membranes ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Human Amnion ◽  
Antagonist Ru486 ◽  
Human Parturition

Abundant evidence indicates a pivotal role of prostaglandin F2α (PGF2α) in human parturition. Both the fetal and maternal sides of the fetal membranes synthesize PGF2α. In addition to the synthesis of PGF2α from PGH2 by PGF synthase (PGFS), PGF2α can also be converted from PGE2 by carbonyl reductase 1 (CBR1). Here, we showed that there was concurrent increased production of cortisol and PGF2α in association with the elevation of CBR1 in human amnion obtained at term with labor versus term without labor. In cultured primary human amnion fibroblasts, cortisol (0.01–1μM) increased PGF2α production in a concentration-dependent manner, in parallel with elevation of CBR1 levels. Either siRNA-mediated knockdown of glucocorticoid receptor (GR) expression or GR antagonist RU486 attenuated the induction of CBR1 by cortisol. Chromatin immunoprecipitation (ChIP) showed an increased enrichment of both GR and RNA polymerase II to CBR1 promoter. Knockdown of CBR1 expression with siRNA or inhibition of CBR1 activity with rutin decreased both basal and cortisol-stimulated PGF2α production in human amnion fibroblasts. In conclusion, CBR1 may play a critical role in PGF2α synthesis in human amnion fibroblasts, and cortisol promotes the conversion of PGE2 into PGF2α via GR-mediated induction of CBR1 in human amnion fibroblasts. This stimulatory effect of cortisol on CBR1 expression may partly explain the concurrent increases of cortisol and PGF2α in human amnion tissue with labor, and these findings may account for the increased production of PGF2α in the fetal membranes prior to the onset of labor.

scholarly journals Immunolocalization of Proinflammatory Cytokines in Myometrium, Cervix, and Fetal Membranes During Human Parturition at Term1

2002 ◽  
Vol 66 (2) ◽  
pp. 445-449 ◽  
Author(s):  
Anne Young ◽  
Andrew J. Thomson ◽  
MarieAnne Ledingham ◽  
Fiona Jordan ◽  
Ian A. Greer ◽  
...  
Keyword(s):  
Proinflammatory Cytokines ◽  
Fetal Membranes ◽  
Human Parturition

Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions

1994 ◽  
Vol 130 (5) ◽  
pp. 478-484 ◽  
Author(s):  
Yasumasa Ohno ◽  
Masahide Kasugai ◽  
Osamu Kurauchi ◽  
Shigehiko Mizutani ◽  
Yutaka Tomoda
Keyword(s):  
Bacterial Infection ◽  
Prostaglandin E2 ◽  
Pregnant Women ◽  
Uterine Contraction ◽  
Interleukin 2 ◽  
Intrauterine Infection ◽  
Fetal Membranes ◽  
Prostaglandin E ◽  
Scatchard Analysis ◽  
Uterine Contractions

Ohno Y, Kasugai M, Kurauchi O, Mizutani S, Tomoda Y. Effect of interleukin 2 on the production of progesterone and prostaglandin E2 in human fetal membranes and its consequences for preterm uterine contractions. Eur J Endocrinol 1994;130:478–84. ISSN 0804–4643 Our objective was to clarify the mechanism of uterine contraction induced in pregnant women by intrauterine bacterial infection. The concentration of interleukin 2 (IL-2) was measured in amniotic fluids that had been obtained by amniocentesis, transvaginal amniotomy or by transuterine amniocentesis performed at cesarean section in 50 pregnant women. The concentration of IL-2 in those cases with intrauterine infection was significantly higher than that of those without intrauterine infection at preterm. The same tendency was found at term. Scatchard analysis demonstrated the presence of an IL-2 receptor in the fetal membranes. We collected the fetal membranes aseptically for the measurement of progesterone and prostaglandin E2 by radioimmunoassay following incubation with various concentrations of Interleukin I (IL-1) and IL-2 at 37°C for 16 h. The production of progesterone was inhibited significantly by 10 pmol/l IL-2 but not by 10 pmol/l IL-1. The production of prostaglandin E2 was accelerated significantly by either IL-1 or IL-2 at a dose of 10 pmol/l. The inhibitory effect of IL-2 on the production of progesterone was unaffected by indomethacin, which inhibits the production of arachidonate cycloxygenase metabolites such as prostaglandin E2. Our present data suggest that the presence of intrauterine bacterial infection may stimulate the intrauterine production of IL-2, and that the stimulation of IL-2 and the reduction of progesterone caused by IL-2 may in part explain the mechanism of uterine contraction associated with intrauterine infection during pregnancy. Yasumasa Ohno, Department of Obstetrics and Gynecology, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan

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