Mammalia strain:Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB18141 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR567792.fastq.gz | Fastqsanger.gz | |||
| DRR567793.fastq.gz | Fastqsanger.gz | |||
| DRR567794.fastq.gz | Fastqsanger.gz | |||
| DRR567795.fastq.gz | Fastqsanger.gz | |||
| DRR567796.fastq.gz | Fastqsanger.gz |
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Project description:Activated eosinophils is a major cell type to be mainly involved in allergic diseases. Recent studies also indicated that eosinophils play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD), especially asthma-COPD overlap and/or eosinophil COPD. The aim of this study is to clarify cellular characters of human eosinophils in patients with asthma-COPD overlap and/or eosinophil COPD.
2024-06-20 | PXD052550 | JPOST Repository
Project description:The role of eosinophilic inflammation in chronic obstructive pulmonary disease (COPD) pathogenesis is unknown and is probably different than in asthma. The molecular processes underlying the differences between eosinophils from asthma and COPD have not been studied. The study group included 5 patients with asthma and 4 patients with COPD. The RNA-Seq data analysis identified 26 differentially expressed genes between COPD and asthma (according to adjusted p-value). In total, 6 genes were up-regulated (CCL3L1, CCL4L2, SERPINB2, PRSS21, GPR82) and 20 were down-regulated (e.g. JUN, IFITM3, DUSP1, GNG7, ZNF107, BCL6) in peripheral eosinophils of COPD patients compared to asthma. Biological processes associated with down-regulated genes were cell differentiation, positive regulation of RNA metabolic process. The genes associated with signaling of IL-4 and IL-13 pathway were down-regulated in COPD eosinophils compared to asthma. Peripheral eosinophils from COPD and asthma patients present different transcriptomic profiles suggesting their different function in pathobiology of both obstructive airway diseases.
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Project description:RNA-seq comparison of coding RNA expression in blood eosinophils from patients with severe allergic eosinophilic asthma treated with mepolizumab with those of healthy controls and matched severe asthmatic patients receiving omalizumab.
2021-12-17 | E-MTAB-10190 | biostudies-arrayexpress
Project description:Global expression pattern in eosinophils in various conditions such as eosinophilic asthma, hypereosinophilic dermatological diseases, parasitosis and pulmonary aspergillosis. Eosinophil were isolated from peripheral blood by FACS from 4 hypereosinophilic conditions: eosinophilic asthma (4 replicates), hypereosinophilic dermatological diseases (3 replicates), parasitosis (3 replicates) and pulmonary aspergillosis (4 replicates).
2015-12-10 | E-GEOD-65239 | biostudies-arrayexpress
Project description:Severe asthma is a clinically and physiologically heterogeneous disease. Benralizumab is a monoclonal antibody which binds the alpha chain of the interleukin-5 receptor and used for severe eosinophilic asthma worldwide. However, not all eosinophilic asthma patients will benefit from benralizumab due to heterogeneity of this disease. Therefore, we performed comprehensive gene expression analysis of whole blood cells that examine severe asthma disease heterogeneity in response to benralizumab. This study is the first to perform comprehensive transcriptome analysis of whole blood cells to identify transcriptomic endotypes of severe asthma clusters that correlate with benralizumab response. The identified transcriptomic endotypes of severe asthma clusters are associated with gene signatures of eosinophils and neutrophilis.
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Project description:Patients with chronic obstructive pulmonary disease (COPD) having higher blood eosinophil levels exhibit worse lung function and more severe emphysema, implying the potential role of eosinophils in emphysema development. However, the specific mechanism underlying eosinophil-mediated emphysema development is not fully elucidated. In this study, single-cell RNA sequencing was used to identify eosinophil subgroups in mouse models of asthma and emphysema and analyze their functions. Analysis of the accumulated eosinophils revealed differential transcriptomes between the mouse lungs of elastase-induced emphysema and ovalbumin-induced asthma., Eosinophil depletion alleviated elastase-induced emphysema. Notably, eosinophil-derived cathepsin L (CTSL) degraded the extracellular matrix (ECM), causing emphysema in the pulmonary tissue. Eosinophils were positively correlated with serum CTSL levels, which were increased in patients with emphysema than in those without emphysema. Collectively, these results suggest that CTSL expression in eosinophils plays an important role in ECM degradation and remodeling and is related to emphysema in patients with COPD. Therefore, eosinophil-derived CTSL may serve as a potential therapeutic target for patients with emphysema.
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Project description:Eosinophils represent key cells driving inflammatory processes in asthma and eosinophilic esophagitis (EoE). Eosinophils migration and activation in disease is orchestrated by a myriad of molecules among which prostaglandin D2, the cognate ligand of CRTH2, and interleukin 5 play a crucial role. In clinical studies with CRTH2 antagonists and anti-IL-5 antibodies, a reduction of the number of eosinophils in disease tissue of asthma and EoE patients was demonstrated, validating the pharmacological effects on eosinophils migration. In contrast, activation of eosinophils through IL5 or CRTH2 receptor has not been studied to the same extent. Understanding the molecular CRTH2 and IL5 activation bias in disease would provide a better assessment of pharmacological intervention, or the need for a combination therapy, to block eosinophils efficiently. We performed gene expression profiling studies with isolated human eosinophils to compare the molecular signatures of CRTH2 and IL5 receptor activation. Furthermore we employed gene set enrichment analysis to query the eosinophils activation bias in asthma and EoE. We observed that activation of CRTH2 and IL5 on human eosinophils shared a large part of the molecular response but also present distinct molecular signatures. Remarkably, FADS1, involved in the synthesis of prostaglandin D2, was identified as a specific CRTH2-induced gene that is counter-regulated by IL5, potentially representing a feedback loop between CRTH2 and IL5 receptor. In silico use of the identified gene signatures and FADS1 demonstrated an enrichment of the IL5 activation signature in lung tissue of asthma patients, whereas esophagus tissue of EoE patients presented a CRTH2 bias.
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Project description:Global expression pattern in eosinophils in various conditions such as eosinophilic asthma, hypereosinophilic dermatological diseases, parasitosis and pulmonary aspergillosis.
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Project description:Memory helper T cells provide long-lasting host defeMemory helper T cells provide long-lasting host defense against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders. against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2 hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders.
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Project description:This study identifies differentially expression genes in the sputum of people with eosinophilic, neutrophilic and paucigranulocytic asthma. A selection of markers identified using this microarray were further validated using qPCR on a wider sample set. Gene expression profiles were generated from induced sputum samples from 47 asthma patients and were grouped by the inflammatory phenotype assigned using sputum cell counts into neutrophilic asthma (n=12), eosinophilic asthma (n=17) and paucigranulocytic asthma (n=18). RNA was extracted, amplified and hybridised to Illumina Sentrix HumanRef-8 Version 2 Expression BeadChips, and genes that were differentially expressed between asthma inflammatory phenotypes were compared.
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