Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Anti-Inflammatory Effects of Budesonide in Human Fetal Lung

ABSTRACT: Rationale. Lung inflammation in premature infants contributes to development of bronchopulmonary dysplasia (BPD), a chronic lung disease with long-term sequelae. Pilot studies administering budesonide suspended in surfactant have found reduced BPD without apparent adverse effects as occur with systemic dexamethasone therapy. Objectives. To determine effects of budesonide on differential genes expression in human fetal lung

ORGANISM(S): Homo sapiens

PROVIDER: GSE83888 | GEO | 2016/06/30

SECONDARY ACCESSION(S): PRJNA327261

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Anti-Inflammatory Effects of Budesonide in Human Fetal Lung

Project description:Rationale. Lung inflammation in premature infants contributes to development of bronchopulmonary dysplasia (BPD), a chronic lung disease with long-term sequelae. Pilot studies administering budesonide suspended in surfactant have found reduced BPD without apparent adverse effects as occur with systemic dexamethasone therapy. Objectives. To determine effects of budesonide on differential genes expression in human fetal lung Methods. We prepared RNA from 3 samples of human fetal lung at 23 weeks gestation before (preculture, PC) and after 4 days culture as explants with (Bud) or without (Way) budesonide (30 nM) and performed RNAseq on the 9 samples.

2016-06-30 | E-GEOD-83888 | biostudies-arrayexpress

Surfactant plus budesonide decreases lung and systemic responses to injurious ventilation in preterm sheep

Project description:Background: Intratracheal budesonide mixed with surfactant has been investigated as an alternative to decrease lung injury and prevent bronchopulmonary dysplasia in preterm infants. However, possible systemic effects are not known. Our goal was identify systemic effects of intra-tracheal instilled budesonide by transcriptome analysis of the brain and lung in a preterm lamb model of mechanical ventilation. Methods: We performed RNA-sequencing of the fetal periventricular white matter and liver from preterm sheep after treatment with intratracheal budesonide mixed with surfactant or surfactant alone followed by mechanical ventilation. Unventilated animals were used as controls. mRNA profiles were generated from polyA selected RNA using Illumina platform. Read sequences were aligned to the sheep genome (Oar 4.0) using Bowtie2 followed read counts using featureCounts. We performed differential expression analysis using EdgeR. Results: We identified large and significant gene expression genes both in the liver and in the priventricular white matter in animals treated with budesonide+surfactant compared to surfactant alone and unventilated animals. There were complexes synergies and antagonism of effect of ventilation and budesonide on gene expression. Ventilation induced inflammatory signaling in the periventricular white matter and liver which was partially antagonized by budesonide. Budesonide also suppressed developmental pathways in the periventricular white matter. Conclusions: Intratracheal budesonide had systemic effects including suppression of developmental pathways in the brain. These effects could have clinical implication in affecting the neurodevelopmental outcomes of preterm newborns.

2019-11-26 | GSE131195 | GEO

Choriodecidual Infection Downregulates Angiogenesis and Morphogenesis Pathways in Fetal Lungs from Macaca Nemestrina

Project description:Intrauterine exposure to amniotic fluid (AF) cytokines is thought to predispose to bronchopulmonary dysplasia (BPD). We evaluated the effects of GBS exposure on RNA expression in fetal lung tissue to determine early molecular pathways associated with fetal lung injury that may progress to BPD.

2013-04-23 | GSE39029 | GEO

Post-transcriptional regulation of necroptosis gene EIF2AK2 in peripheral blood of bronchopulmonary dysplasia

Project description:Bronchopulmonary dysplasia (BPD) remains the most frequent chronic lung disease among infants, which involves multifactorial pathogenesis. Necroptosis represents a caspase-independent mode of programmed cell death, and its deregulation associates with lung diseases, but the mechanisms of necroptosis during BPD are indistinct. This work was conducted for unveiling the post-transcriptional regulatory mechanisms of necroptosis in BPD.

2024-02-21 | GSE219156 | GEO

Lung resident mesenchymal stromal cells reveal transcriptional dynamics of lung

Project description:We report the correlation between lung-derived neonatal MSCs and 2 clinical variables among preterm newborns: corrected gestational age (CGA) at collection and the severity of bronchopulmonary dysplasia (BPD)

2018-11-15 | GSE106910 | GEO

Remarkable Lung Heterogeneity at Single-Cell Resolution and the Role of Sex as a Biological Variable in Neonatal Hyperoxic Lung Injury

Project description:The goal of the project was to delineate sex-specific differences in the neonatal lung exposed to postnatal hyperoxia to model the pathophysiologic mechanisms in the human disease; bronchopulmonary dysplasia (BPD).

2022-10-25 | GSE211356 | GEO

Urine Proteomics for Noninvasive Monitoring of Biomarkers in Bronchopulmonary Dysplasia

Project description:Current techniques to diagnose and/or monitor critically ill neonates with bronchopulmonary dysplasia (BPD) require invasive sampling of body fluids, which can affect the health status of these frail neonate. We tested our hypotheses 1) it is feasible to use early urine samples from extremely low gestational age newborns at risk for bronchopulmonary dysplasia for proteomics, and 2) urine proteomics can confirm previously identified proteins and biomarkers associated with BPD without invasive sample collection. We developed a robust high throughput urine proteomics methodology that requires only 50 microliters of urine. We validated the methodology on urine collected within 72 hours of birth. Urine samples were collected from extremely low gestational age newborns (ELGANS) (gestational age (26 + 1.2) weeks) admitted to a single Neonatal Intensive Care Unit(NICU); half of whom eventually developed BPD, while the other half served as controls. Our high throughput urine proteomics approach clearly identified several BPD-associated changes in the urine proteome recapitulating expected blood proteome changes. Interestingly, sixteen identified urinary proteins are known targets of drugs approved by the Food and Drug Administration (FDA). Urine proteomics can be used for prediction of BPD risk. In addition to identifying numerous proteins implicated in BPD pathophysiology, previously found in invasively collected blood, tracheal aspirate, and broncho-alveolar lavage, urine proteomics also suggested novel potential therapeutic targets. Ease of access to urine for sequential proteomic evaluations could also allow for longitudinal monitoring of disease progression and impact of therapeutic intervention.

2022-04-04 | PXD028895 | Pride

Proteome analysis of a human donor cohort to study bronchopulmonary dysplasia

Project description:Bronchopulmonary Dysplasia (BPD) is a disease of prematurity related to the arrest of normal lung development. The objective of this study was to perform whole lung proteomics to identify proteins and pathways differentially regulated in BPD in early childhood. The proteomes of biopsies from pediatric human donors aged 1.3 to 3 years were classified based on history of prematurity and histopathologic severity of "Healed" BPD [hBPD] (N=3) and "Established" BPD [eBPD] (N=3) with respective full term age-matched controls (N=6). Samples were analyzed using aTMT16plex labelling strategy. Code employed to perform the statistics is available at https://github.com/GeremyClair/Proteome_analysis_of_a_human_donor_cohort_to_study_bronchiopulmonary_displasia

2023-03-15 | MSV000091493 | MassIVE

Cord blood gene expression profiles of bronchopulmonary dysplasia in preterm infants

Project description:Bronchopulmonary dysplasia (BPD) is a lung disease in premature infants characterized by impaired pulmonary development which persists into later life. While advances in neonatal care have improved survival rates of premature infants, cases of BPD haves been increased. Therapeutic options are limited for prevention and treatment. This study was designed to explore differentially expressed genes associated with BPD. Cord blood mRNA from preterm neonates that went on to develop BPD (n = 6) or not (nonBPD, n = 17) was applied to Illumina HumanHT-12 arrays, we identify differentially expressed genes associated with BPD.

2022-05-05 | GSE188944 | GEO

Pulmonary immune cell transcriptome changes in double-hit model of BPD induced by chorioamnionitis and postnatal hyperoxia

Project description:Preterm infants with bronchopulmonary dysplasia (BPD) have lifelong increased risk of respiratory morbidities associated with environmental pathogen exposure and underlying mechanisms are poorly understood. The resident immune cells of the lung play vital roles in host defense. However, the effect of perinatal events associated with BPD on pulmonary-specific immune cells is not well understood. We used a double-hit model of BPD induced by prenatal chorioamnionitis followed by postnatal hyperoxia, and performed global transcriptome analysis of all resident pulmonary immune cells. This is the first comprehensive report delineating transcriptomic changes in resident immune cells of the lung in a translationally relevant double-hit model of BPD.

2021-01-19 | GSE161836 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data