Ontology highlight
ABSTRACT:
PROVIDER: PRJNA938570 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR23615500_1.fastq.gz | Fastqsanger.gz | |||
| SRR23615500_2.fastq.gz | Fastqsanger.gz | |||
| SRR23615501_1.fastq.gz | Fastqsanger.gz | |||
| SRR23615501_2.fastq.gz | Fastqsanger.gz | |||
| SRR23615502_1.fastq.gz | Fastqsanger.gz |
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Project description:Abstract<br>BACKGROUND: Gene expression profiling (GEP) in cells obtained from peripheral blood has demonstrated to be a very useful approach for biomarker discovery and for studying molecular pathogenesis of prevalent diseases. While there is limited literature availble on gene expression markers associated to Chronic Obstructive Pulmonary Disease (COPD), the transcriptomic picture associated to critical respiratory illness in this disease is not known to the present moment. <br>RESULTS: By using Agilent microarray chips, we have profiled gene expression signatures in whole blood of 28 COPD patients hospitalized with distinct degree of respiratory compromise.12 of them needed of admission to the ICU, while 16 were admitted to the Respiratory Medicine Service. GeneSpring GX 11.0 software was used for performing statistical comparison of transcript levels between ICU and non ICU patients. Ingenuity pathway analysis 8.5 (IPA) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) were employed to select, annotate and visualize genes by function and pathway (gene ontology). T-test evidenced 1501 genes differentially expressed between ICU and non ICU patients. IPA and KEGG analysis of the most representative biological functions revealed that ICU patients showed increased levels of neutrohil gene transcripts, being [cathepsin G (CTSG)], [elastase, neutrophil expressed (ELANE)], [proteinase 3 (PRTN3)], [myeloperoxidase (MPO)], [cathepsin D (CTSD)], [defensin, alpha 3, neutrophil-specific (DEFA3)], azurocidin 1 (AZU1)], [bactericidal/permeability-increasing protein (BPI)] the most representative ones. Proteins codified by these genes form part of the azurophilic granules of neutrophils and are involved in both antimicrobial defence and tissue damage. This ?neutrophil signature? was paralleled by necessity of advanced respiratory and vital support, and presence of bacterial infection.<br>CONCLUSION: study of transcriptomic signatures in blood suggests a central role of neutrophil proteases in COPD patients with critical respiratory illness. Measurement / modulation of the expression of these genes could represent an option for clinical monitoring and treatment of severe COPD exacerbations. <br><br>Keywords: COPD, critical, expression, gene, microarray, neutrophil, proteases.<br><br>
2013-03-12 | E-MEXP-3589 | biostudies-arrayexpress
Project description:To determine gene expression changes that contribute to the development of COPD among smokers using high-throughput RNA sequencing in the peripheral blood of COPD patients. Total RNA sequencing was investigated by prospectively collecting lung function test results and whole blood samples from smokers who visited the outpatient department of respiratory medicine at three hospitals since 2020. This study confirmed gene expression differences in non-coding RNA in COPD patients according to the degree of airflow limitation through RNA-Seq transcriptome analysis. These results may provide valuable predictive resources for future COPD research.
2024-04-17 | GSE240656 | GEO
Project description:Mucus accumulation is a key feature of respiratory diseases such as cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). This is associated with goblet cell metaplasia and mucin overexpression, which can be induced by the increased activity of neutrophil elastase. The aim of the study was to characterization of mucus and epithelial cell proteomics in a porcine pancreatic elastase (PPE) mouse model of COPD/CF. The major proteins detected in mucus plugs obtained from PPE-treated mice included mucins Muc5ac and Muc5b, mucus-related proteins Clca1, Fcgbp, and Bpifb1. These proteins were upregulated in bronchoalveolar lavage (BAL) fluid and epithelial cells in mice exposed to elastase. Similar changes were found in BAL fluid of COPD patients.
2018-10-22 | PXD006770 | Pride
Project description:Chronic obstructive pulmonary disease (COPD) collectively refers to chronic and progressive lung diseases causing not fully reversible limitations in airflow. COPD patients are at high risk for severe respiratory symptoms upon influenza virus infection. Airway epithelial cells provide the first-line antiviral defense, but whether their susceptibility and response to influenza virus infection changes in COPD has not been elucidated. Therefore, this study aimed to i) compare the susceptibility of COPD- and control-derived airway epithelium to influenza virus, and ii) assess protein changes during influenza virus infection by quantitative proteomics. Fluorescent stainings confirmed expression of human- and avian-type influenza virus receptors in primary human bronchial epithelial cells (phBECs) from COPD patients (n=4) and controls (n=3) differentiated at the air-liquid interface. Subjects were closely matched in age, sex, and smoking history and, for COPD-derived phBECs, included stage II (n=2), stage III (n=1) and stage IV (n=1). Proteomics of fully differentiated phBECs pre- and post-influenza A virus infection with A/Puerto Rico/8/34 (PR8) revealed no significant differences between GOLD stage II/ III COPD (n=3) and control phBECs in terms of flu receptor expression, cell type composition, virus replication, or protein profile pre- and post-infection. In contrast, COPD GOLD stage IV phBECs (n=1) showed a distinct pattern of flu receptor expression and a typical COPD phenotype as assessed by a literature-derived panel of 20 proteins and quantification of cell type composition. Independent of health state, proteomics showed a robust antiviral response to influenza virus infection, as well as upregulation of several novel influenza virus-regulated proteins.
2022-12-29 | PXD031461 | Pride
Project description:Rationale: Multiciliated cell (MCC) loss/dysfunction is common in the small airways of patients with COPD but it is unclear if this contributes to COPD lung pathology. Objectives: To determine whether loss of MCCs causes a COPD-like phenotype in mice and explore a potential role for the transcription factor p73 in COPD. Methods: p73floxE7-E9 mice were crossed with Shh-Cre mice to generate mice lacking MCCs in the airway epithelium. The resulting p73airway mice were analyzed using electron microscopy, flow cytometry, morphometry, forced oscillation technique, and single-cell RNA sequencing. Further, the effects of cigarette smoke on p73 transcript and protein expression were examined using in vitro and in vivo models and in studies including airway epithelium from smokers and COPD patients. Measurements and Main Results: Loss of functional p73 in the respiratory epithelium resulted in a near-complete absence of MCCs in p73airway mice. In adulthood, these mice spontaneously developed neutrophilic inflammation and emphysema-like lung remodeling and had progressive loss of secretory cells. Exposure of normal airway epithelium cells to cigarette smoke rapidly and durably suppressed p73 expression in vitro and in vivo. Further, TP73 mRNA expression was reduced in the airways of current smokers (n=82) compared to former smokers (n=69) and p73-expressing MCCs were reduced in the small airways of COPD patients (n=11) compared non-COPD controls (n=12). Conclusions: Loss of functional p73 in murine airway epithelium results in the absence of MCCs and promotes COPD-like lung pathology. In smokers and patients with COPD, loss of p73 may contribute to MCC loss or dysfunction.
2023-11-20 | GSE240096 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is a heterogenous respiratory disease mainly caused by smoking. Respiratory infections constitute a major risk factor for acute worsening of COPD symptoms or COPD exacerbation. Mitochondrial functionality, which is crucial for the execution of physiologic functions of metabolically active cells, is impaired in airway epithelial cells (AECs) of COPD patients as well as smokers. However, the potential contribution of mitochondrial dysfunction in AECs to progression of COPD, infection-triggered exacerbations in AECs and a potential mechanistic link between mitochondrial and epithelial barrier dysfunction is unknown to date. In this study, we used an in vitro COPD exacerbation model based on AECs exposed to cigarette smoke extract (CSE) followed by infection with Streptococcus pneumoniae (Sp). The levels of oxidative stress, as an indicator of mitochondrial stress were quantified upon CSE and Sp. The expression of proteins associated with mitophagy, mitochondrial content and biogenesis as well as mitochondrial fission and fusion was quantified upon CSE and Sp. Transcriptional AEC profiling was performed to identify the potential changes in innate immune pathways and correlate them with mitochondrial function. We found that CSE exposure substantially altered mitochondrial function in AECs by suppressing mitochondrial complex protein levels, reducing mitochondrial membrane potential and increasing mitochondrial stress and mitophagy. Moreover, CSE-induced mitochondrial dysfunction correlated with reduced enrichment of genes involved in apical junctions and innate immune responses to Sp, particularly type I interferon responses. Together, our results demonstrated that CSE-induced mitochondrial dysfunction may contribute to impaired innate immune responses to Sp and may thus trigger COPD exacerbation.
2022-05-27 | GSE197751 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) and squamous cell lung carcinoma (SCC) are both smoking-related diseases. Interestingly, COPD itself is a risk factor for SCC, and this is independent of smoking history. Inferring from this knowledge, it is plausible to assume that patients with COPD may have a different gene expression profile in normal bronchial epithelium and in SCC. To test this hypothesis, we compared gene expression profiles in bronchial epithelium and in SCC from patients with and without COPD. Gene expression profiles were generated using whole human genome oligo microarrays for 28 laser microdissected histologically normal bronchial epithelium samples (10 without COPD, 18 with COPD) and 35 laser microdissected SCC samples (17 without COPD, 18 with COPD). We found no significant differences in gene expression levels between normal bronchial epithelium from patients with and without COPD. Remarkably, 374 genes were differentially expressed in SCC obtained from patients with or without COPD; 295 showed a higher expression level in SCC from patients with COPD and 79 genes showed higher expression levels in SCC from patients without COPD. Genes related to mitochondrial localization (n=44) and genes located on chromosomal arm 5q (n=34) were significantly overrepresented. For both categories, all genes showed a higher expression level in SCC from patients with COPD than from those without COPD. In conclusion, SCC from patients with COPD show a different gene expression profile compared to SCC from patients without COPD. This suggests that COPD related factors affect the gene expression signature in SCC.
2009-02-01 | GSE12472 | GEO
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