Development of gene expression signatures for neonatal tissues of mice with Usp10 gene knockout
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE198574 | GEO | 2022/03/15
REPOSITORIES: GEO
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Project description:Development of gene expression signatures for neonatal tissues of mice with Usp10 gene knockout
| PRJNA816059 | ENA
Project description:Bacterial pulmonary infections are a major cause of morbidity and mortality in neonates, with less severity in older children (juveniles). Previous studies demonstrated that CD4+ T cells in the mouse lung, whose primary responsibility is coordinating the immune response foreign pathogens, are differentially methylated in neonates compared with juveniles. Nevertheless, the effect of this differential methylation on CD4+ T cell gene expression and response to infection remains unclear. We treated E. coli-infected neonatal (4-day-old) and juvenile (13-day-old) mice with decitabine (DAC), a DNA methyltransferase inhibitor with broad-spectrum DNA demethylating activity, and performed simultaneous genome-wide DNA methylation and transcriptional profiling on lung CD4+ T cells. Juvenile and neonatal mice experienced differential demethylation in response to DAC treatment, with larger methylation differences observed in neonates. By cross-filtering differentially expressed genes between juveniles and neonates with those sites that were demethylated in neonates, we found that interferon-responsive genes such as Ifit1 are the most down-regulated methylation-sensitive genes in neonatal mice. DAC treatment shifted neonatal lung CD4+ T cells toward a gene expression program similar to that of juveniles. Following lung infection with E. coli, lung CD4+ T cells in neonatal mice exhibit epigenetic repression of important host defense pathways, which are activated by inhibition of DNA methyltransferase activity to resemble a more mature profile.
2022-12-22 | GSE214488 | GEO
Project description:Bacterial pulmonary infections are a major cause of morbidity and mortality in neonates, with less severity in older children (juveniles). Previous studies demonstrated that CD4+ T cells in the mouse lung, whose primary responsibility is coordinating the immune response foreign pathogens, are differentially methylated in neonates compared with juveniles. Nevertheless, the effect of this differential methylation on CD4+ T cell gene expression and response to infection remains unclear. We treated E. coli-infected neonatal (4-day-old) and juvenile (13-day-old) mice with decitabine (DAC), a DNA methyltransferase inhibitor with broad-spectrum DNA demethylating activity, and performed simultaneous genome-wide DNA methylation and transcriptional profiling on lung CD4+ T cells. Juvenile and neonatal mice experienced differential demethylation in response to DAC treatment, with larger methylation differences observed in neonates. By cross-filtering differentially expressed genes between juveniles and neonates with those sites that were demethylated in neonates, we found that interferon-responsive genes such as Ifit1 are the most down-regulated methylation-sensitive genes in neonatal mice. DAC treatment shifted neonatal lung CD4+ T cells toward a gene expression program similar to that of juveniles. Following lung infection with E. coli, lung CD4+ T cells in neonatal mice exhibit epigenetic repression of important host defense pathways, which are activated by inhibition of DNA methyltransferase activity to resemble a more mature profile.
2022-12-22 | GSE214489 | GEO
Project description:We sought to determine the impact of chorioamnionitis exposure on the neonatal monocyte H3K4me3 histone modification landscape over the course of fetal and neonatal immune system development using ChIP-seq. H3K4me3 ChIP-seq was performed on umbilical cord blood purified CD14+ monocytes from healthy and chorioamnionitis-exposed extremely preterm neonates (under 30 weeks gestation), late preterm neonates (30-36 weeks gestation), and term neonates (37+ weeks gestation).
2018-08-01 | GSE111873 | GEO
Project description:Expression profiling by microarray was used with a murine listeriosis model to better understand increased susceptibility of preterm neonates to infection. We used DNA microarray to identify genes that were differentially expressed in liver of adult and neonatal Balb/c mice after listeriosis infection.
2013-06-01 | GSE45051 | GEO
Project description:Immaturity of alveolar macrophages (AMs) around birth contributes to the susceptibility of newborns to lung disease. However, the molecular features differentiating neonatal and mature, adult AMs are poorly understood. Here we identify the unique transcriptomes and enhancer landscapes of neonatal and adult AMs. While the core AM signature was similar, adult AMs expressed higher levels of genes involved in lipid metabolism, while neonatal AMs expressed a largely proinflammatory gene profile. Open enhancer regions identified by ATAC-seq contained motifs for nuclear receptors, MITF, and STAT in adult AMs and AP-1 and NF-kB in neonatal AMs. Intranasal LPS activated a similar innate immune response in both neonates and adults, with higher basal expression of inflammatory genes in neonates. The lung microenvironment drove many of the distinguishing gene expression and open chromatin characteristics of neonatal and adult AMs. Neonatal AMs retained high expression of some proinflammatory genes, suggesting the differences in neonatal AMs result from both inherent cell properties and environmental influences.
2022-07-05 | GSE196926 | GEO
Project description:RATIONALE: In a mouse model of maternal transmission of asthma risk (J. Immunol 170:1683, 2003), baby mice of asthmatic (As), but not normal (Nrm), mothers show increased susceptibility to allergy. We previously showed that adoptive transfer to normal baby mice of dendritic cells (DCs) harvested from asthma-susceptible but allergen-naïve neonates reproduces the increased susceptibility to asthma. Hence, the maternal effect is mediated by altered neonatal DCs, which skew immune responses towards a pro-allergic Th2 phenotype. To identify potential molecular mechanisms, we performed epigenomic profiling of isolated neonatal DCs. METHODS: BALB/c mice were sensitized by 2 i.p. injections of ovalbumin (OVA) in alum and repeatedly challenged with OVA aerosols (As) prior to mating with normal males. Purified splenic CD11c+ DCs of 14-day old allergen-naïve offspring from these As and control Nrm mothers were isolated using magnetic beads. Methylation profiles of genomic DNA were obtained using Switchgear epigenomic chip arrays. After normalization and background correction analysis using significance analysis for microarrays (SAM) and ANOVA was performed. RESULTS: We identified 300 to 6000 (depending on stringency) chromosomal regions with significantly different methylation status, (2 â 10 fold). Clustering methods and pathway analysis identified several interrelated gene groups that merit further study. CONCLUSION: Maternal asthma causes multiple significant epigenetic changes in neonatal dendritic cells. Keywords: Dendritic cells, genomic DNA, DNA methylation, allergy, asthma The analysis includes 9 samples of genomic DNA from isolated splenic CD11c+ dendritic cells (>95% pure) per group. The two groups are neonates born to mothers with induced allergy to ovalbumin, and normal control neonates. All neonates are genetically and environmentally identical, and allergen-naive.
2010-06-24 | E-GEOD-13380 | biostudies-arrayexpress
Project description:Expression profiling by microarray was used with a murine listeriosis model to better understand increased susceptibility of preterm neonates to infection. We used DNA microarray to identify genes that were differentially expressed in liver of adult and neonatal Balb/c mice after listeriosis infection. A murine listeriosis model was established. The methods for culturing and counting the Listeria monocytogenes (strain CNL 85/163) had been described in previous publications. The Listeria was injected intraperitoneally using a 1-mL U-100 insulin syringe with a 30 gauge needle. Doses of Listeria monocytogenes used were based on work by our laboratory showing that similar bacterial colony counts were obtained with 4.2 x 10^5 total Listeria per adult mouse and 150 Listeria per gram for 3 to 5 day old neonatal mice. In neonatal mice, great care was taken to void deep intraperitoneal injection towards the viscera, or across the central abdominal vessels. At specified time points, liver was removed upon animal sacrifice and immediately flash frozen in liquid nitrogen and stored at -80 degrees Centigrade. Three adult mice and three neonatal mice were used at each time point.
2013-06-01 | E-GEOD-45051 | biostudies-arrayexpress
Project description:Neonates are intrinsically defective at creating memory CD8+ T cells in response to infection with intracellular pathogens. Here we investigated differential of small RNAs, transcription factors, and chemokine receptors regulation in neonates as compared to adults before and during infection. We found that prior to infection, naïve cells have a different expression profile for many microRNAs, and gene targets of these microRNAs show widespread expression differences. These targets and other changes in gene expression in naïve cells result in neonatal cells that get activated more easily, express chemokine receptors that home to sites of infection, and are less protected from apoptosis during contraction. As a result, changes in neonatal naïve cells drive effector cell terminal differentiation at the expense of creating long-lived memory cells. total RNAs were sequenced from adult and neonatal CD8+ T cells before and during infection
2015-09-24 | E-GEOD-65922 | biostudies-arrayexpress
Project description:Paracrine effects mediated by exosomes contribute to the major regenerative functions of cell therapies after myocardial injuries. Early neonatal mammals retain a transient regeneration capacity after heart injury, which reminds us to explore the cardioprotective and regenerative potency of plasma exosomes from neonatal mouse (npEXO). Therefore, we isolated plasma exosomes from neonatal mice and performed proteomic analysis.
2022-12-13 | PXD038805 |