Single-cell RNA Sequencing of Human Esophageal Epithelium in Homeostasis and Allergic Inflammation
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ABSTRACT:
PROVIDER: PRJNA828562 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR18839868.fastq.gz | Fastqsanger.gz | |||
| SRR18839869.fastq.gz | Fastqsanger.gz | |||
| SRR18839870.fastq.gz | Fastqsanger.gz | |||
| SRR18839871.fastq.gz | Fastqsanger.gz | |||
| SRR18839872.fastq.gz | Fastqsanger.gz |
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Project description:Bulk RNA Sequencing of Human Esophageal Epithelium in Homeostasis and Allergic Inflammation
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Project description:To investigate gene expression signature of the human esophageal epithelium we performed FACS sorting of the basal and the suprabasal layers from the esophageal biopsies based on the expression of podoplanin and E-cadherin.
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Project description:To investigate gene expression signature of the human esophageal epithelium at the homeostatic and inflammatory conditions we performed scRNAseq on the human esophageal biopsies obtained from the healhy patients, patients with active eosinophilic esophagitis (EoE) and patients in the remission.
2022-06-15 | GSE201153 | GEO
Project description:Eosinophilic esophagitis (EoE) is a chronic, allergic inflammatory disease of the esophageal mucosa. Although type 2 cytokines are predominant, targeting type 2 inflammation alone is not always effective for all patients. In EoE patients, the transcriptional profiling of esophageal biopsy reveals upregulation of type I and II interferon (IFN) response, dysregulated immune signaling, and downregulation of esophageal-specific genes. However, further investigation is needed to examine the gene expression changes in esophageal epithelium because it plays an important role in EoE. To investigate the upregulation of Interferon Stimulated Genes (ISGs) in EoE esophageal epithelium, we isolated epithelial cells from active EoE patients and non-EoE controls. We performed bulk RNA sequencing to analyze the epithelial-specific transcriptome in EoE. Unsupervised hierarchical clustering of the most variable genes differentiated the active EoE biopsies from non-EoE controls. Gene set enrichment analysis identified IFN-γ response as the most significant upregulated pathway.
2024-02-26 | GSE234973 | GEO
Project description:The esophagus is protected from the hostile environment by a stratified epithelium, which renews rapidly. Homeostasis of this epithelium is ensured by a rare population of stem cells in the basal layer: Keratin 15+ (Krt15+) cells. However, little is known about the molecular mechanisms regulating their distinct features, namely self-renewal, potency, and epithelial regeneration. Achaete-Scute Family BHLH Transcription Factor 2 (ASCL2) is strongly upregulated in Krt15+ stem cells and is known to contribute to stem cell maintenance in other tissues. Herein, we investigated the role of ASCL2 in maintaining homeostasis under normal and stress conditions in the esophageal epithelium. ASCL2 overexpression severely dysregulated cell differentiation and cell fate. Proliferation was also reduced due potentially to a blockage in the G1 phase of the cell cycle or an induction of quiescence. Mass spectrometry analysis confirmed alterations in several proteins associated with differentiation and cell cycle. In addition, overexpression of ASCL2 enhanced resistance to radiation and chemotherapeutic drugs. Overall, these results denoted the role of ASCL2 as a key regulator of the proliferation-differentiation equilibrium in the esophageal epithelium.
2024-05-24 | PXD039477 | Pride
Project description:Hippo signaling regulates the homeostasis of multiple organs. Mst1 and Mst2 (Mst1/2) are critical components of the Hippo signaling pathway. Here, we utilized RNA sequencing to determine the transcriptional change in the esophageal epithelium upon Mst1/2 deletion. The analysis of gene expression profiles allows us to understand the role of Mst1/2 in the regulation of various biological processes in the esophageal epithelium.
2024-02-26 | GSE248501 | GEO
Project description:Despite the well-recognized role of IL-13–induced transcriptional responses in allergic inflammation, the epigenetic mechanisms driven by IL-13 have not been well defined. We interrogated the transcriptional and epigenetic signatures of IL-13-induced epithelial responses focusing on the chromatin activation marks H3K4me3, H3K9Ac, and H3K27Ac. ChIP-sequencing analysis revealed that IL-13–inducible genes were epigenetically poised for induction and continued to accumulate epigenetic changes in response to IL-13. By intersecting the transcriptome and the epigenome of the IL-13 response, we identified neurotrophic tyrosine kinase receptor 1 (NTRK1) as a major target of IL-13 in epithelial cells. Using eosinophilic esophagitis as a model system for human allergic inflammation, we found that NTRK1 was dramatically induced in inflamed esophageal biopsies, and downstream mediators of NTRK1 signaling were elevated in diseased tissue. The NTRK1 ligand nerve growth factor (NGF) was constitutively expressed in control and disease states, indicating that induction of the receptor by IL-13 limited pathway activation. In epithelial cells, NGF and IL-13 synergistically induced transcription and secretion of the key eosinophil chemoattractant CCL26 (eotaxin-3). In summary, we demonstrate that IL-13–mediated allergic responses are epigenetically driven and identify NTRK1 as a novel epigenetic and transcriptional target of IL-13 that uniquely contributes to allergic inflammation. Human esophageal epithelial cell line TE-7 was stimulated with IL-13 at 100 ng/ml for 2 hr, 6 hr and 24 hr and subjected to RNA-sequencing. In parallel, TE-7 cells were induced with IL-13 for 6 hr and subjected to ChIP-sequencing analysis for H3K4me3, H3K9Ac and H3K27Ac activating chromatin marks.
2015-04-09 | E-GEOD-57637 | biostudies-arrayexpress
Project description:Many esophageal diseases arise in the context of chronic inflammation, but the role that esophageal epithelial cells play in initiating inflammation remains poorly understood. Since the IKKβ/NF-κB and STAT3 pathways are critical signaling hubs that drive inflammatory-mediated responses, we aimed to identify how these two pathways regulate gene expression in esophageal epithelial cells. In this study, we performed RNA-Seq analysis on esophageal epithelium from mice with overexpression of constitutively active Ikkb and/or loss of Stat3 specifically in esophageal epithelial cells.
2021-04-01 | GSE154129 | GEO
Project description:MicroRNAs (miRNAs) exert powerful effects on immunity through coordinate regulation of multiple target genes in a wide variety of cells. Group 2 innate lymphoid cells (ILC2s) are tissue sentinel mediators of allergic inflammation. We established the physiological requirements for miRNAs in ILC2 homeostasis and immune function, and compared the global miRNA repertoire of resting and activated ILC2s and T helper type 2 (TH2) cells. Mice lacking the miR-17~92 cluster in ILC2s displayed reduced lung inflammation following exposure to the natural allergen papain. Moreover, miR-17~92-deficient ILC2s exhibited defective growth and cytokine expression in response to IL-33 and TSLP in vitro. The miR-17~92 cluster member miR-19a promoted IL-13 production and inhibited expression of several target genes, including SOCS1 and A20, signaling inhibitors that limit IL-13 production. These findings establish miRNAs as important regulators of ILC2 biology, reveal overlapping but non-identical miRNA-regulated gene expression networks in ILC2s and TH2 cells, and reinforce the therapeutic potential of targeting miR-19 to alleviate pathogenic allergic responses .
2017-11-02 | GSE96934 | GEO
Project description:Background: In asthma, airway epithelium remodeling can already be detected during childhood, and epithelial cells are more susceptible to virus and oxidative stress. Their exact role in natural history and severity of children allergic respiratory disease remains however surprisingly unexplored. Aim: To analyze dysfunctions of epithelium in dust mite allergic respiratory disease (rhinitis ± asthma) in children. Methods: Expression profilings of nasal epithelial cells collected by brushing were performed on Affymetrix Hugene 1.0 ST arrays. All allergic patients were sensitized to dust mite. 19 patients had an isolated allergic rhinitis (AR). 14 patients had AR associated with asthma. Patients were compared to 12 controls, their severity and control being assessed according to NAEPP and ARIA criteria. Infections by respiratory viruses were excluded by real-time PCR measurements. Results: 61 probes were able to distinguish allergic rhinitis children from healthy controls. A majority of these probes was under the control of Th2 cytokines, as evidenced by parallel experiments performed on primary cultures of nasal epithelial cells. In uncontrolled asthmatic patients, we observed not only an enhanced expression of these Th2-responsive transcripts, but also a down-regulation of interferon-responsive genes. Conclusion: Our study identifies a Th2 driven epithelial phenotype common to all dust mite allergic children. Besides, it suggests that epithelium is involved in the severity of the disease. Expression profiles observed in uncontrolled asthmatic patients suggest that severity of asthma is linked at the same time to atopy and to impaired viral response. Nasal epithelium gene expression profiling of dust mite allergic children with isolated rhinitis, rhinitis associated with asthma and controls. 38 samples classified in 4 categories : 14 isolated rhinitis (R), 6 rhinitis with uncontrolled asthma (UA), 7 rhinitis with controlled asthma (CA) and 11 healthy subjects (C )
2012-01-05 | E-GEOD-19187 | biostudies-arrayexpress