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These data support the hypothesis that maternal-fetal ..

In mammals is associated/incorporated with connecting stalk/placental cord fetal-maternal interface.

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The Journal of Maternal-Fetal & Neonatal Medicine

N2 - The interactions taking place between mother and embryo have been the focus of detailed studies in recent years, where pregnancy is considered as an in vivo transplant. The immune systems of the mother and the embryo together establish a condition of tolerance, which lasts throughout the pregnancy. Alongside immunogenetic components, a contribution is provided by the ectoenzyme network, a chain of surface molecules mainly operating in closed environments and potentially providing inhibitory or activator signals. One of the soluble products of the ectoenzyme network with immunosuppressory potential is adenosine, a purine nucleoside that plays multiple roles in almost all tissues and organs. The hypothesis behind the work was studied in patients with recurrent pregnancy loss (RPL), an event which remains unexplained in over 50% of cases. To this aim, we analyzed the expression of CD39 (ectonucleoside triphosphate diphosphohydrolase 1, ENTPD1) and CD73 (ecto-5′-nucleotidase, NT5E), the main pathway for adenosine generation, in samples obtained from women with RPL. The study included the evaluation of the expression of TNF-α (a pro-inflammatory cytokine) and of an alternative pathway of adenosine generation run by CD38 (ADP-ribosyl cyclase/cyclic ADP-ribose hydrolase) and PC-1 (ectonucleotide pyrophosphatase/phosphodiesterase 1, ENPP1). The results of this study highlight the existence of a network of surface enzymes expressed at the maternal/fetal interface and addressed to the production of adenosine. Perturbation of this network may induce a rescue pathway driven by CD38 and ENPP1. Ectoenzyme and inflammation may be considered now key elements in orchestrating the events leading to the interruption of pregnancy in the RPL sample analyzed and at the same potentially becoming therapeutic targets.

11/10/2017 · Synthesis of T-Helper 2-Type cytokines at the maternal–fetal ..

Congenital disease was first reported in a 3 days old baby girl in New York, 1938 who developed seizure and eyes lesion and died after one month of birth (). Congenital toxoplasmosis is mostly a subclinical infection in about 85% of the infants whose mothers have been treated for Toxoplasma during pregnancy (). Theses proportions are influenced by factors such as, the time of maternal infection, treatment given to the mother, organism load and the genetics of the host and the strain ofToxoplasma. The incidence of fetal infection is estimated 2% if the maternal infection occur before week 10 and 90% in the last weeks of pregnancy. However, early maternal infection is reported to cause higher risk of disease and brain damage. Congenital toxoplasmosis manifests with spontaneous miscarriage and abortion, fetal growth retardation, encephalomyelitis, intracranial calcifications, hydrocephalus, neurological, mental illnesses, retinochoroiditis, visual and auditory inflammatory disorders, cardiovascular abnormalities (, , , , ), gastrointestinal complications and pain (, , , , , ). The severity of complications depends on the gestation period when the fetus is infected, and the earlier the infection the more severe the complications (, ). Those fetuses infected late in gestation may born normal, but develop symptoms of CNS and retinochoroiditis later in life and the new lesions may occur in untreated as well as treated children (). Retrospective trials (2000–2011) reviled 18% (2206/12035) prevalence rate of anti-Toxoplasma antibody in pregnant women. Thirty eight per 10,000 of these women had acute infection and 5.8% transplacentally infected their neonates as reported in Argentina ().

and Th1/Th2 cytokine profiles at the maternal-fetal …

We hypothesize that maternal immunodeficiencies play a role in susceptibility to fetal malformations following gestational exposure to fumonisin.

Discussion: This small study suggests that fetal-maternal microchimerism is associated with a statistically significant improvement in anti-tumor effect of activated haplo-PBSC treatment.

AB - Sleep duration in the population has been declining. Women occupy an increasingly prominent place in the work force without reducing most of their responsibilities at home. Consequently, sleep needs are often pushed to the bottom of women's daily priority list. Prior research has indicated that sleep deprivation is associated with higher levels of pro-inflammatory serum cytokines. This is important because higher plasma concentrations of pro-inflammatory serum cytokine levels are associated with postpartum depression and adverse birth outcomes such as preterm delivery. However, little research has directly examined how sleep deprivation may affect maternal and fetal outcomes. This review summarizes the existing data on the effect of sleep deprivation during pregnancy on maternal and fetal outcomes. We review supporting evidence for the hypotheses that sleep deprivation during pregnancy increases the risk of preterm delivery and postpartum depression, and that systemic inflammation is the causal mechanism in the association. Prior research on sleep in pregnancy has been limited by varying data collection methods, subjective self-reported sleep measures, small and non-representative samples, cross-sectional designs; descriptive or non-hypothesis driven studies. Future research with longitudinal study designs is needed to allow examination of the effect of sleep deprivation on adverse maternal and fetal outcomes.

Toxoplasma gondii (Toxoplasmosis) - Infectious Disease …

and it supports the supposition that fetal cytokine levels are related to maternal ..

Maternal intraperitoneal LPS acutely induces placental inflammation and congestion. This may increase fetal cardiac afterload, leading to cardiac failure. Six hours after maternal LPS, proinflammatory cytokines were not induced in fetal tissues.

AB - Both villous and extravillous trophoblast contact maternal blood. This juxtaposition should result inplacental rejection. However, detrimental anti-placental reactivity is uncommon. First trimesterplacental samples obtained by chorion villous sampling(CVS) were assayed for the presence IL-4 and IL-10. Tissue lysates were prepared and assayed RT-PCR and ELISA and sections were analyzed byhistochemical techniques. By both approaches these cytokines were detected. Reproducible amount of IL-4 or IL-10 were observed by ELISA and RT_PCR showed that specific sequences were associated with pregnancy tissue. RNA isolated from the JEG-3 cell line also contained IL-4 andIL-10. These findings were confirmed by immunohistology and by insitu hybridization. Preliminary evidence suggests that these cytokines are secreted by JEG-3 cells and there production is not inducible but is constitutive in these cells. Isolated tropho blast also produce these cytokines in culture. These data support the hypothesis that maternal-fetal tolerance is maintained at the uteroplacental interface by anti-inflammatory cytokine synthesis by atypical fetal-derived trophoblast.

Our overall hypothesis is that embryonic/fetal and maternal-derived ..
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  • Tumor-Infiltrating Immune Cells Promoting Tumor …

    The prolactin and growth hormone families: Pregnancy-specific hormones/cytokines at the maternal-fetal interface

  • Nutrients | March 2017 - Browse Articles

    Prenatal exposure to maternal infection alters cytokine expression in the placenta, amniotic fluid, and fetal brain

  • Nutrients, an international, peer-reviewed Open Access journal.

    PapersTwins and maternal smoking: ordeals for the fetal origins hypothesis? A cohort study The BMJ

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cytokine levels influence fetal growth in pregnant women with RA

Sleep duration in the population has been declining. Women occupy an increasingly prominent place in the work force without reducing most of their responsibilities at home. Consequently, sleep needs are often pushed to the bottom of women's daily priority list. Prior research has indicated that sleep deprivation is associated with higher levels of pro-inflammatory serum cytokines. This is important because higher plasma concentrations of pro-inflammatory serum cytokine levels are associated with postpartum depression and adverse birth outcomes such as preterm delivery. However, little research has directly examined how sleep deprivation may affect maternal and fetal outcomes. This review summarizes the existing data on the effect of sleep deprivation during pregnancy on maternal and fetal outcomes. We review supporting evidence for the hypotheses that sleep deprivation during pregnancy increases the risk of preterm delivery and postpartum depression, and that systemic inflammation is the causal mechanism in the association. Prior research on sleep in pregnancy has been limited by varying data collection methods, subjective self-reported sleep measures, small and non-representative samples, cross-sectional designs; descriptive or non-hypothesis driven studies. Future research with longitudinal study designs is needed to allow examination of the effect of sleep deprivation on adverse maternal and fetal outcomes.

Endocan-1 concentrations in maternal and fetal plasma …

Both villous and extravillous trophoblast contact maternal blood. This juxtaposition should result inplacental rejection. However, detrimental anti-placental reactivity is uncommon. First trimesterplacental samples obtained by chorion villous sampling(CVS) were assayed for the presence IL-4 and IL-10. Tissue lysates were prepared and assayed RT-PCR and ELISA and sections were analyzed byhistochemical techniques. By both approaches these cytokines were detected. Reproducible amount of IL-4 or IL-10 were observed by ELISA and RT_PCR showed that specific sequences were associated with pregnancy tissue. RNA isolated from the JEG-3 cell line also contained IL-4 andIL-10. These findings were confirmed by immunohistology and by insitu hybridization. Preliminary evidence suggests that these cytokines are secreted by JEG-3 cells and there production is not inducible but is constitutive in these cells. Isolated tropho blast also produce these cytokines in culture. These data support the hypothesis that maternal-fetal tolerance is maintained at the uteroplacental interface by anti-inflammatory cytokine synthesis by atypical fetal-derived trophoblast.

Endocan-1 concentrations in maternal and fetal ..

As epidemiologic studies continue to note a striking increase in rates of autism spectrum disorder (ASD) diagnosis around the world, the lack of identified causative agents in most cases remains a major hindrance to the development of treatment and prevention strategies. Published observations of immune system abnormalities in ASD have increased recently, with several groups identifying fetal protein reactive IgG antibodies in plasma from mothers of children with autism. Furthermore, other gestational immune parameters, including maternal infection and dysregulated cytokine signaling, have been found to be associated with ASD in some cases. While detailed pathogenic mechanisms remain to be determined, the hypothesis that some cases of ASD may be influenced, or even caused, by maternal fetal brain-reactive antibodies or other in utero immune-related exposures is an active area of investigation. This article reviews the current literature in this area and proposes several directions for future research.

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