Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA297708 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:miRNA-Seq of human placenta: spontaneous preterm birth in the presence of intra-amniotic infection/inflammation and controls
| PRJNA297709 | 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: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: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:Preterm birth is a leading cause of neonatal mortality and lacks an effective therapy. Ascending microbial infections from the lower genital tract lead to infection of the placenta, amniotic fluid and fetus causing preterm birth or stillbirth. Directly in the path of an ascending infection is the cervical mucus plug (CMP), a dense mucoid structure in the cervical canal with potential antimicrobial properties. In this study, we aimed to define the components of CMP responsible for antimicrobial activity against a common lower genital tract organism associated with preterm birth and stillbirths, namely Group B Streptococcus (GBS). Using a quantitative proteomic approach, we identified antimicrobial factors in CMPs that were collected from healthy human pregnancies. This study aims to provide new insight into how the human CMP may limit ascending bacterial infection.
2018-02-09 | PXD008600 | Pride