Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA371496 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5233872_1.fastq.gz | Fastqsanger.gz | |||
| SRR5233872_2.fastq.gz | Fastqsanger.gz | |||
| SRR5233873_1.fastq.gz | Fastqsanger.gz | |||
| SRR5233873_2.fastq.gz | Fastqsanger.gz | |||
| SRR5233874_1.fastq.gz | Fastqsanger.gz |
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Project description:We report the global pattern of ileal gene expression in a cohort of 359 treatment-naïve pediatric Crohn Disease, Ulcerative Colitis patients and controls. We focus on genes with consistent altered expression in inflamed and unaffected ileum of CD [ileal-involved CD (iCD) and non-invloved ileal CD (cCD)], but not in the ileum of ulcerative colitis or control.
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Project description:Purpose: To clarify the biological processes underlying variation in disease location and antimicrobial sero-reactivity across age-of onset in pediatric Crohn disease. Methods: We characterize the ileal global pattern of gene expression using single-end, 50bp RNA-sequencing using the Illumina HiSeq2000 in 304 treatment-naïve pediatric Crohn patients and non-IBD controls. Reads were quantified using Kallisto with Gencodev23 annotations. For all analyses, data were stratified by patient age-of-onset. Results: Performing differential analysis of all reasonably-expressed transcripts (TPM>5 in ≥5 samples, with significance defined as FDR-corrected p-value<0.05 and fold change≥1.5), we identify a robust gene signature with higher expresison of an immune gene set in older patients (≥10 years at diagnosis) compared to younger patients (<10 years at diagnosis), and a decrease in expression of antimicrobial Paneth cell-derived α-defensins. Conclusion: We provide evidence for maturation of mucosal Th1 immune response and loss of epithelial antimicrobial α-defensins with increasing age-of-onset.
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Project description:Samples for microarray analysis were derived from terminal ileum and colonic tissues from probands with Crohn´s disease and Ulcerative Colitis and control patients, respectively. IBD tissue biopsies from non-inflamed regions 10 cm distant from pathological areas were selected. To minimize inter-individual differences in gene expression and to enrich for IBD-specific transcriptional events, 2.5 µg of total RNA from terminal ileum and colon transversum from four individuals of each patient and control group were used for pooling. Keywords = IBD Keywords = Crohn´s disease Keywords = Ulcerative Colitis Keywords: other
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Project description:Long non-coding RNA (lncRNA) mechanisms in gut inflammation are poorly understood. Tissue-specificity of lncRNAs linked to patient outcomes may direct interventions with fewer off-target effects. Using 693 mucosal samples, we prioritize lncRNAs linked with ulcerative colitis (UC) course and define an atlas of lncRNAs expressed along the gastrointestinal tract dysregulated in celiac duodenum, Crohn Disease ileum, and UC rectum using independent test and validation cohorts.
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Project description:Objective: Long non-coding RNAs (lncRNA) regulate gene transcription and diverse cellular functions. We previously defined a novel core inflammatory and metabolic ileal gene signature in treatment naïve pediatric Crohn Disease (CD), however, genome-wide characterization of lncRNA expression was lacking. We now extend our analyses to define a more comprehensive view that includes lncRNA. Design: Using RNAseq, we performed a systematic profiling of lncRNAs and protein-coding genes expression in 177 ileal biopsies. Co-expression analysis was used to identify functions and tissue-specific expression. RT-PCR was used to test lncRNAs regulation by IL-1β in Caco-2 enterocytes model. Results: We characterize a widespread dysregulation of 459 lncRNA in the ileum of treatment naïve pediatric CD patients. Unsupervised and supervised classifications using the 459 lncRNA showed comparable patients’ grouping as the 2160 dysregulated protein-coding genes, linking lncRNA to CD pathogenesis. Co-expression and functional annotation enrichment analyses across several tissues and cell types showed that the up-regulated LINC01272 is associated with a myeloid pro-inflammatory signature while the down-regulated HNF4A-AS1 exhibits association with an epithelial metabolic signature. We further validated expression and regulation of prioritized lncRNA upon IL-1β exposure in differentiated Caco-2 cells. Finally, we identified significant correlations between LINC01272 and HNF4A-AS1 expression and more severe mucosal injury. Conclusion: We define differentially expressed lncRNA in the ileum of treatment naive pediatric CD. We show lncRNA utility to correctly classify disease or healthy states and demonstrate their regulation in response to an inflammatory signal. These lncRNA, after mechanistic exploration, may serve as potential new targets for RNA-based interventions.
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