Homo sapiens
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PROVIDER: PRJNA297709 | ENA |
REPOSITORIES: ENA
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Project description:RNA-Seq of human placenta: spontaneous preterm birth in the presence of intra-amniotic infection/inflammation and controls
| PRJNA297708 | ENA
Project description:RNA-Seq and miRNA-Seq of human placenta: spontaneous preterm birth in the presence of intra-amniotic infection/inflammation and controls
| PRJNA297707 | ENA
Project description:Chorioamnionitis (CA), resulting from intra-amniotic inflammation, is a frequent cause of preterm birth and exposes the immature intestine to bacterial toxins and/or inflammatory mediators before birth via fetal swallowing. This may affect intestinal immune development, interacting with the effects of enteral feeding and gut microbiota colonization just after birth. Using preterm pigs as model for preterm infants, we hypothesized that prenatal exposure to gram-negative endotoxin influences postnatal bacterial colonization and gut immune development. Pig fetuses were given intra-amniotic lipopolysaccharide (LPS) 3 d before preterm delivery by cesarean section, and were compared with litter-mate controls (CON) at birth and after 5 d of formula feeding and spontaneous bacterial colonization. Amniotic fluid was collected for analysis of leukocyte counts and cytokines, and the distal small intestine was analyzed for endotoxin level, morphology and immune cell counts. Intestinal gene expression and microbiota were analyzed by transcriptomics and metagenomics, respectively. At birth, LPS-exposed pigs showed higher intestinal endotoxin, neutrophil/macrophage density and shorter villi. About 1.0% of intestinal genes were affected at birth and DMBT1, a regulator of mucosal immune defense, was identified as the hub gene in the co-expression network. Genes related to innate immune response (TLR2, LBP, CD14, C3, SFTPD), neutrophil chemotaxis (C5AR1, CSF3R, CCL5) and antigen processing (MHC II, CD4) were also affected and expression levels correlated with intestinal neutrophil/macrophage density and amniotic fluid cytokine levels. On day 5, LPS and CON pigs showed similar necrotizing enterocolitis (NEC) lesions, endotoxin levels, morphology, immune cell counts, gene expressions and microbiota (except for difference in some low-abundant species). Our results show that CA markedly affects intestinal genes at preterm birth, including genes related to immune cell infiltration. However, a few days later, following the physiological adaptations to preterm birth, CA had limited effects on intestinal structure, function, gene expression, bacterial colonization and NEC sensitivity. We conclude that short-term, prenatal intra-amniotic inflammation is unlikely to exert marked effects on intestinal immune development in preterm neonates beyond the immediate neonatal period.
2019-10-25 | GSE139366 | GEO
Project description:Preterm birth is often predisposed by chorioamnionitis (CA) and CA affects the fetal gut and lungs via intra-amniotic (IA) inflammation, thus accentuating the proinflammatory effects of preterm birth. It is not known if IA inflammation also affects other perfusion-sensitive organs (e.g., kidneys) before and after preterm birth. Using preterm pigs as model for preterm infants, we hypothesized that CA induces fetal and neonatal renal dysfunctions that can intially be detected via plasma proteome, partly explaining the frequent renal dysfunction in preterm infants. Fetal pigs (88% gestation) were given an IA dose of lipopolysaccharide (LPS, 1 mg/kg, n=28), delivered preterm by cesarean section three days later, and compared with controls (CON, n=26) at birth and postnatal day five. Plasma proteome and protein markers of inflammatory pathways were evaluated.
2021-03-25 | PXD014619 | Pride
Project description:Using RNA-sequencing (RNA-Seq and miRNA-Seq), we analyzed paired villous trophoblast and decidual basalis transcriptomes of 15 women pregnant with singleton gestations grouped as follows: (1) spontaneous preterm birth (PTB) in the setting of amniocentesis-proven intra-amniotic infection (IAI) and histological chorioamnionits (n=5; GA median [range]: 26 [25-31] weeks); (2) spontaneous idiopathic preterm birth (iPTB, n=5, GA: 32 [30-33] weeks); and (3) term normal pregnancy, that delivered a heathy infant by cesarean section in the absence of labor (n=5; GA: 39 [38-39] weeks).
2016-06-14 | GSE73713 | GEO
Project description:Using RNA-sequencing (RNA-Seq and miRNA-Seq), we analyzed paired villous trophoblast and decidual basalis transcriptomes of 15 women pregnant with singleton gestations grouped as follows: (1) spontaneous preterm birth (PTB) in the setting of amniocentesis-proven intra-amniotic infection (IAI) and histological chorioamnionits (n=5; GA median [range]: 26 [25-31] weeks); (2) spontaneous idiopathic preterm birth (iPTB, n=5, GA: 32 [30-33] weeks); and (3) term normal pregnancy, that delivered a heathy infant by cesarean section in the absence of labor (n=5; GA: 39 [38-39] weeks).
2016-06-14 | GSE73712 | GEO
Project description:Using RNA-sequencing (RNA-Seq and miRNA-Seq), we analyzed paired villous trophoblast and decidual basalis transcriptomes of 15 women pregnant with singleton gestations grouped as follows: (1) spontaneous preterm birth (PTB) in the setting of amniocentesis-proven intra-amniotic infection (IAI) and histological chorioamnionits (n=5; GA median [range]: 26 [25-31] weeks); (2) spontaneous idiopathic preterm birth (iPTB, n=5, GA: 32 [30-33] weeks); and (3) term normal pregnancy, that delivered a heathy infant by cesarean section in the absence of labor (n=5; GA: 39 [38-39] weeks). The primary goal of this study was to identify differentially expressed transcripts and illuminate molecular mechanisms distinguishing IAI-associated PTBs from spontaneous PTBs in the absence of IAI. We further compared iPTB specimens to term specimens to determine genes differentially regulated with advancing gestational age and following spontaneous PTB without IAI. Finally, we determined transcripts selectively expressed in either the villous trophoblast or decidua basalis in each clinical context. Raw data for this series are not available because consent forms do not allow for public access to raw data.
2016-06-14 | E-GEOD-73713 | biostudies-arrayexpress
Project description:Using RNA-sequencing (RNA-Seq and miRNA-Seq), we analyzed paired villous trophoblast and decidual basalis transcriptomes of 15 women pregnant with singleton gestations grouped as follows: (1) spontaneous preterm birth (PTB) in the setting of amniocentesis-proven intra-amniotic infection (IAI) and histological chorioamnionits (n=5; GA median [range]: 26 [25-31] weeks); (2) spontaneous idiopathic preterm birth (iPTB, n=5, GA: 32 [30-33] weeks); and (3) term normal pregnancy, that delivered a heathy infant by cesarean section in the absence of labor (n=5; GA: 39 [38-39] weeks). The primary goal of this study was to identify differentially expressed transcripts and illuminate molecular mechanisms distinguishing IAI-associated PTBs from spontaneous PTBs in the absence of IAI. We further compared iPTB specimens to term specimens to determine genes differentially regulated with advancing gestational age and following spontaneous PTB without IAI. Finally, we determined transcripts selectively expressed in either the villous trophoblast or decidua basalis in each clinical context. Raw data for this study are not available because consent forms do not allow for public access to raw data.
2016-06-14 | E-GEOD-73712 | biostudies-arrayexpress
Project description:Placental insufficiency is implicated in the intrauterine infection-associated spontaneous preterm birth. Using a mouse model of LPS-induced intrauterine inflammation that leads to preterm delivery, RNA-seq study was performed in the placenta at gestational day 17 to assess the transcriptome changes.
2020-11-27 | GSE151728 | GEO
Project description:Distinct processes govern the transition from myometrial quiescence to activation during both term and preterm labor. We sought the specific gene sets responsible for initiating term and preterm labor, along with a core set of effector genes necessary for labor independent of gestational age and the underlying trigger. The Effector Gene Set consisted of 49 genes present in both preterm and term labor but absent from non-labor samples. 122 genes were specific to preterm labor (Preterm Initiator Set) and 229 to term labor (Term Initiator Set). The Term Initiator and the Effector Sets reflected predominantly inflammatory processes. Surprisingly, the Preterm Initiator Gene Set reflected molecular and biological events almost exclusive of inflammation. Preterm and term labor differ dramatically in their unique, initiator gene profiles, suggesting alternative pathways underlie these events. Inflammatory processes are ubiquitous to the Term Initiator and the Effector Gene Sets, supporting the idea term parturition is an inflammatory process. The absence of inflammatory processes in the Preterm Initiator Set suggests inflammation is secondary to processes triggering spontaneous preterm birth, and could explain the lack of therapeutic efficacy associated with anti inflammatory/antibiotic regimens. Experiment Overall Design: Myometrial gene expression was analyzed from samples obtained at term (n=6) or preterm (n=6) with and without labor using cDNA microarrays. Patients in preterm labor all had intra amniotic inflammation. Gene sets were generated using logical operations within a functional mapping tool (MetaCoreâ¢, GeneGo, St. Joseph, MI). Relevant gene sets were validated with quantitative real-time polymerase chain reaction.
2008-10-26 | E-GEOD-9159 | biostudies-arrayexpress