Targeted ileal transcriptomic analysis in paediatric IBDs.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA644629 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We employed contemporary targeted autoimmune RNA sequencing (HTG molecular diagnostics, Autoimmune panel) to ileal tissue derived from 96 paediatric IBD, Crohn's disease, Ulcerative colitis patients and controls. Weighted-gene-co-expression-network-analysis (WGCNA) was performed and differentially expressed genes (DEGs) were determined. We integrated clinical data to determine co-expression modules associated with time to relapse.
2021-05-12 | GSE153974 | GEO
Project description:Crohn’s disease arises through host-environment interaction, with abnormal gene expression resulting from disturbed pathway activation or response to bacteria. Single cell RNA-sequencing of ileal tissue from 2 paediatric Crohn’s disease patients was performed, identifying populations of CD8+ effector memory T cells (CD8+ Tem), memory B-cells, monocytes, epithelial cells and plasma cells within the ileal tissue. Specialised epithelial cells driving differential expression of S100A8 and S100A9 and associated with defence to bacterium were identified, as well as IL17-signalling associated pathways in monocyte and epithelial cell populations.
2021-05-12 | GSE153866 | GEO
Project description:Transcriptomic evidence of lung repair in paediatric ARDS survival
| PRJNA928385 | ENA
Project description:This SuperSeries is composed of the following subset Series: GSE6217: Microarray analysis of V. cholerae genes differentially expressed in 12 h rabbit ileal loop fluid GSE24405: Microarray analysis of V. cholerae genes differentially expressed in 8 h rabbit ileal loop mucus GSE24406: Microarray analysis of V. cholerae genes differentially expressed in 12 h rabbit ileal loop mucus GSE24407: Microarray analysis of V. cholerae genes differentially expressed in 8h rabbit ileal loop fluid Refer to individual Series
2010-09-28 | E-GEOD-24408 | biostudies-arrayexpress
Project description:Management of terminal ileal Crohn's disease (CD) is difficult due to fibrotic prognosis and failure to achieve mucosal healing. A limited number of synchronous analyses have been conducted on the transcriptome and microbiome in unpaired terminal ileum tissues. Therefore, our study focused on the transcriptome and mucosal microbiome in terminal ileal tissues of CD patients with the aim of determining the role of cross-talk between the microbiome and transcriptome in the pathogenesis of terminal ileal CD. Mucosa-attached microbial communities were significantly associated with segmental inflammation status. Interaction-related transcription factors (TFs) are the panel nodes for crosstalk between the gene patterns and microbiome for terminal ileal CD. The transcriptome and microbiome in terminal ileal CD can be different related to local inflammatory status, and specific differentially expressed genes (DEGs) may be targeted for mucosal healing. TFs connect gene patterns with the microbiome by reflecting environmental stimuli and signals from microbiota.
2021-04-08 | GSE171244 | GEO
Project description:Purpose: To uncover differentially-regulated transcripts and pathways/biological processes in newly-diagnosed, pediatric Crohn's disease in comparison to healthy controls. Methods: Intestinal epithelial cells were dissociated from ileal endoscopic biopsies, and stored at -80C in RNAlater. The polyA RNA fraction was purified, and single-end, 50 bp reads were sequenced and aligned to the Hg19 genome using the TopHat2 aligner. Differential analysis was performed using Bioconductor packages including edgeR, where significance was defined as p<0.05 and fold change>2. Results: We obtained 15788 reasonably-expressed transcripts that were included in differential analyses. Conclusions: Our study characterizes the dysregulation of intestinal epithelial cells in treatment-naïve Crohn's disease using RNA sequencing for transcriptomic profile of cells obtained through ileal endoscopic biopsies.
2018-10-30 | GSE117875 | GEO
Project description:Acute myeloid leukaemia (AML) affects children and adults of all ages. AML remains one of the major causes of death in children with cancer and for children with AML relapse is the most common cause of death. By modelling AML in vivo we demonstrate that AML is discriminated by the age of the cell of origin. Young cells give rise to myeloid, lymphoid or mixed phenotype acute leukaemia, whereas adult cells give rise exclusively to AML, with a shorter latency. Unlike adult, young AML cells do not remodel the bone marrow stroma. Transcriptional analysis distinguishes young AML by the upregulation of immune pathways. Analysis of human paediatric AML samples recapitulates a paediatric immune cell interaction gene signature, highlighting two genes, RGS10 and FAM26F as prognostically significant. This work advances our understanding of paediatric AML biology, and provides murine models that offer the potential for developing paediatric specific therapeutic strategies.
2018-11-04 | GSE122066 | GEO
Project description:Acute myeloid leukaemia (AML) affects children and adults of all ages. AML remains one of the major causes of death in children with cancer and for children with AML relapse is the most common cause of death. Here, by modelling AML in vivo we demonstrate that AML is discriminated by the age of the cell of origin. Young cells give rise to myeloid, lymphoid or mixed phenotype acute leukaemia, whereas adult cells give rise exclusively to AML, with a shorter latency. Unlike adult, young AML cells do not remodel the bone marrow stroma. Transcriptional analysis distinguishes young AML by the upregulation of immune pathways. Analysis of human paediatric AML samples recapitulates a paediatric immune cell interaction gene signature, highlighting two genes, RGS10 and FAM26F as prognostically significant. This work advances our understanding of paediatric AML biology, and provides murine models that offer the potential for developing paediatric specific therapeutic strategies.
2018-06-14 | GSE107662 | GEO
Project description:Constitutive signalling pathway activation is a key feature of primary tumours and cancer cell lines. The regulation of gene expression changes may be via both genomic and epigenetic means, and understanding the mechanisms by which signal transduction may be activated can provide rational targets for therapeutic intervention. We have previously carried out DNA copy and expression profiling on a unique panel of five paediatric glioma cell lines, and have noted only a limited influence of gene amplification on gene expression. In the present study we have extended our work to include a measure of global methylation changes as well as micro RNA profiling in the same cell lines. We noted various instances of signalling pathway activation associated with specific hypermethylation or miRNA regulation of gene expression at various effectors also observed in primary paediatric tumours. These data provide evidence for the multifaceted nature of gene expression changes in paediatric high grade glioma, and identify novel targets for targeted therapy in this treatment refractory disease.
2010-12-03 | E-TABM-858 | biostudies-arrayexpress
Project description:Background: Patients with paediatric-onset systemic lupus erythematosus (SLE) often present with more severe clinical courses than adult-onset patients. Although genome-wide DNA methylation (DNAm) profiling has been performed in adult-onset SLE patients, parallel data on paediatric-onset SLE are not available. Therefore, we undertook a genome-wide DNAm study in paediatric-onset SLE patients across multiple blood cell lineages. Methods: The DNAm profiles of four purified immune cell lineages were compared in 16 Chinese patients with paediatric-onset SLE and 13 healthy controls using the Illumina HumanMethylationEPIC BeadChip. The DNAm dataset consisted of 145 samples, including data from CD4+ T cells, CD8+ T cells, B cells, neutrophils and whole blood. Results: Genome-wide DNAm analysis revealed considerable variation in DNAm levels across samples, and as expected, clustering occurred by cell type rather than disease status. Comparison of DNAm in whole blood and within each independent cell lineage identified a consistent pattern of loss of DNAm at 21 CpG sites overlapping 15 genes, which represented a robust, disease-specific DNAm signature for paediatric-onset SLE in our cohort. This DNAm signature shows considerable overlap with that identified in our adult-onset SLE patient cohort, predominantly showing a loss of DNAm and enrichment in genes involved in type I interferon signalling in SLE, regardless of the age of onset. In addition, cell lineage-specific changes, involving both loss and gain of DNAm, were observed in both novel genes and genes with well-described roles in SLE pathogenesis. Conclusion: The SLE-specific DNAm signature has the potential to develop into a diagnostic biomarker for SLE, which is particularly important for paediatric-onset patients, as diagnosing SLE in children can be challenging. This study also highlights the importance of studying DNAm changes in different immune cell lineages rather than only whole blood, since cell type-specific DNAm changes facilitated the elucidation of the cell type-specific molecular pathophysiology of SLE.
2019-02-19 | GSE118144 | GEO