Multi-Omics Analysis of Pain/Stress Impact on Neurodevelopment in Preterm Infants
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ABSTRACT:
PROVIDER: PRJNA842139 | ENA |
REPOSITORIES: ENA
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Project description:Multi-Omics Analysis of Pain/Stress Impact on Neurodevelopment in Preterm Infants
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Project description:We procured peripheral whole blood from ten healthy preterm infants and ten preterm infants with bronchopulmonary dysplasia
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Project description:We procured PBMCs whole blood from five HC preterm infants and five preterm infants with BPD. PBMCs were extracted using a density gradient centrifugation method. Initially, 10ml of peripheral blood was mixed with an equal volume of physiological saline, then carefully layered onto Ficoll solution (T10124, from Shangbao Biotech Co., Ltd., Shanghai). After centrifugation at 2,000 rpm for 20 minutes, the cells stratified due to differences in density, with PBMCs positioned between the red blood cells and plasma. Subsequently, the intermediate layer containing PBMCs was gently collected, washed several times with physiological saline to remove residual medium and red blood cells, and finally, PBMCs were isolated and collected through centrifugation.
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Project description:We conducted a prospective cohort study with independent Discovery and Validation cohorts, to formulate predictive biomarkers for Bronchopulmonary Dysplasia in extremely preterm infants. Tracheal aspirate samples were collected at birth from extremely preterm infants. Exosomes were extracted from tracheal aspirates and total RNA was extracted from these exosomes from individual samples. miRNA profiling for all ~ 800 miRNAs was conducted on each sample by nanostring platform. This study found that a distinct airway exosomal miRNA sigrature at birth (decreased miR 876-3p) predicts future development of severe Bronchopulmonary Dysplasia in extremely preterm infants.
2017-12-29 | GSE108604 | GEO
Project description:Preterm infants are highly susceptible to sustained lung inflammation, which may be triggered by exposure to multiple environmental cues such as supplemental oxygen (O2) and infections. The underlying mechanisms are still poorly understood. The hypothesis of this study is that dysregulated macrophage activation is a key feature leading to inflammation-mediated development of bronchopulmonary dysplasia (BPD) in preterm infants.
Cord blood samples of preterm infants (n=14) and term infants (n=19) as well as peripheral blood from healthy adults (n=17) were collected. Age-dependent differences in immune responses of monocyte-derived Mä from preterm infants were characterized and compared to term infants and adults after lipopolysaccharide (LPS) exposure.
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Project description:This study measured the cytokine, cellular and transcriptomic response to RSV and compared these between preterm and term infants CBMC responses
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Project description:Host immune responses during late-onset sepsis (LOS) in very preterm infants are poorly characterised due to a complex and dynamic pathophysiology and challenges in working with small available blood volumes. We present here an unbiased transcriptomic analysis of whole peripheral blood from very preterm infants at the time of LOS. RNA-Seq was performed on peripheral blood samples (6 – 29 days postnatal age) taken at the time of suspected LOS from very preterm infants <30 weeks gestational age. Infants were classified based on blood culture positivity and elevated C-reactive protein concentrations as having confirmed LOS (n=5), possible LOS (n=4) or no LOS (n=9). Bioinformatics and statistical analyses performed included pathway over-representation and protein-protein interaction network analyses. Plasma cytokine immunoassays were performed to validate differentially expressed cytokine pathways.The blood leukocyte transcriptional responses of infants with confirmed LOS differed significantly from infants without LOS (1,317 differentially expressed genes). However, infants with possible LOS could not be distinguished from infants with no LOS or confirmed LOS. Transcriptional alterations associated with LOS included genes involved in pathogen recognition (mainly TLR pathways), cytokine signalling (both pro-inflammatory and inhibitory responses), immune and haematological regulation (including cell death pathways), and metabolism (altered cholesterol biosynthesis). At the transcriptional-level cytokine responses during LOS were characterised by over-representation of IFN-α/β, IFN-γ, IL-1 and IL-6 signalling pathways and up-regulation of genes for inflammatory responses. Infants with confirmed LOS had significantly higher levels of IL-1α and IL-6 in their plasma. Blood responses in very preterm infants with LOS are characterised by altered host immune responses that appear to reflect unbalanced immuno-metabolic homeostasis.
2020-06-03 | GSE138712 | GEO
Project description:16S rRNA gene profiling of preterm infants
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Project description:Staphylococcus (S.) epidermidis is one of the most common nosocomial coagulase-negative staphylococci infections in preterm infants. The clinical signs of infection are often unspecific and identification of novel markers to complement the current diagnosis is needed. In this study, we investigated proteomic alterations in the neonatal mouse brain following S. epidermidis infection and in the blood in preterm infants. We identified lipocalin 2 (LCN2) as a crucial protein associated with cerebrovascular changes and astrocyte reactivity in mice. While astrocytes were activated in S. epidermidis infected mice, LCN2 protein expression in the brain was associated with endothelial cells but not astrocyte reactivity. By combining weighted gene co-expression analysis and differential expression approaches, we further identified that LCN2 protein was linked to blood C-reactive protein levels in a cohort of preterm infants born <28 weeks of gestation. Blood LCN2 levels were associated with similar alterations of cytokines and chemokines in both infected mice and human preterm infants with increased levels of CRP. The present experimental and clinical study indicates that LCN2 might be a suitable additional marker of preterm infection/inflammation associated with cerebrovascular changes and neuroinflammation.
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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 the relationship between gestational age (GA), birth weight and estímate blood cell-type composition in premature infants and to elucidate early epigenetic biomarkers associated with BPD. Cord blood DNA from preterm neonates that went on to develop BPD (n = 14) or not (nonBPD, n = 93) was applied to Illumina 450K methylation arrays. Using DNA methylation analysis of cord blood DNA, we investigated association of GA and birth weight with the estimated distribution of cord blood cell types, particularly the nucleated red blood cell (NRBC) in a pilot-size cohort of preterm infants with or without BPD. We describe changes in methylation-based estimates of blood cell-type composition in relation to GA and birth weight. After adjusting for covariates (GA, birth weight, cell type proportions, etc.) we identify differentially methylated CpGs and genes associated with BPD.
2022-05-05 | GSE188949 | GEO