Gene expression profile at single cell level of clinical mild to moderate COPD
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ABSTRACT:
PROVIDER: PRJNA1173543 | ENA |
REPOSITORIES: ENA
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Project description:The research included a cohort of 11 patients who were diagnosed with mild or moderate COPD, as well as a control group of 7 individuals who were matched for age.
2024-10-18 | GSE279570 | GEO
Project description:Rationale: Chronic Obstructive Pulmonary Disease (COPD) is associated with a complex pulmonary and systemic immune response. Objective: To characterize and relate the lung tissue and circulating blood network immune response in COPD. Methods: Lung tissue and circulating blood samples were simultaneously obtained from COPD patients (current smokers n=28 and former smokers n=16) and controls (current smokers n=9 and non-smokers n=12) undergoing thoracic surgery. We used flow cytometry to assess the immune cell composition, Affymetrix arrays to determine whole lung mRNA expression, and Weighted Gene Co-expression Network Analysis (WGCNA) to characterize and compare the pulmonary and systemic immune responses in patients and controls. Results: In lung tissue of current smokers with COPD (vs. non-smokers and former smokers with COPD) we observed a significant increase in the proportion of intermediated phenotype macrophages (Mphage) expressing both M1 and M2 markers, whereas that of M1 Mphage (pro-inflammatory) and CD4+ and CD8+ T-lymphocytes were decreased. These changes were not mirrored in circulating blood but WGCNA identified three modules of co-expressed genes that related, respectively to: (1) the total proportion of lung Mphage (extracellular matrix and angiogenesis genes) ; (2) active smoking (T cell and apoptosis related genes); and, (3) severity of airflow limitation (cilium organization genes). Conclusions: In mild/moderate COPD, the main pulmonary immune cell alterations relate to current smoking, involve changes in the proportion of Mphage and T cells and are associated with changes in whole lung tissue transcriptome. These cellular pulmonary changes are not mirrored in the systemic circulation.
2018-07-01 | GSE103174 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE33336: Development of microRNA expression signature for emphysema in COPD patients GSE33337: miRNA changes in mild and moderate emphysema correlate with target gene expression in vivo and in vitro [target gene expression data] Refer to individual Series
2012-05-31 | E-GEOD-33338 | biostudies-arrayexpress
Project description:The variations of psycho- and physiological deficits caused by TBI correlate with the degree of brain injury. However, the objective stratification of TBI is yet elusive. A modified closed-head injury Marmarou model was used based on the release of a 500 gram steel slug on top of the rat skull from a height of 100 cm or 120 cm to induce differential injury models for mild TBI and moderate TBI, respectively. The skull was covered by a helmet to mimic the warfighter’s condition in theater. The hippocampus was at the focal point of injury, and the cerebellum, was susceptible to diffused shock (secondary injury). The HC-CB axis coordinates visuomotor performance, which is known to be vulnerable to TBI. The rats that received moderate TBI showed deficient visuomotor performance by the Barnes maze test for longer time periods than those inflicted with mild TBI. The time resolved and HC-CB specific transcriptomic analysis focused on genes that enabled discrimination of mild from moderate TBI at 14d post injury which is equivalent to nearly 1.5 years of human lifetime. The functional analysis elucidated an active healing mechanism in the HC exposed to mild TBI. In contrast, moderate TBI caused delayed healing and active cell death in the HC. In conclusion, the graded brain injuries differentially implicated the HC-CB axis, despite the use of a helmet to reduce the impact. Time resolved functional dynamics informed the distinct consequences of mild vs. moderate TBI.
2020-12-31 | GSE131435 | GEO
Project description:Chronic obstructive pulmonary disease (COPD) is a progressive and irreversible chronic inflammatory lung disease. The abnormal inflammatory response of the lung, mainly to cigarette smoke, causes multiple cellular and structural changes affecting all of its compartments, which leads to disease progression. The molecular mechanisms underlying these pathological changes are still not fully understood The aim of this study was to identify genes and molecular pathways potentially involved in the pathogenesis of COPD Peripheral lung tissue samples from moderate COPD patients, smokers and nonsmokers were obtained. All patients were undergoing lung resection for localized carcinomas. RNA was extracted and processed for further hybridization on Affymetrix microarrays
2016-08-25 | E-GEOD-37768 | biostudies-arrayexpress
Project description:Purpose: Identify whole lung gene expression patterns in a house dust mite model of mild/moderate asthma Methods: Lung gene expression profiles of 10 week old BALB/c female mice were generated by ribosome-depleted, 150 nt, paired-end, stranded RNA-seq with Illumina HiSeq v4. Sequence reads that passed quality filters after trimming were analyzed with Sailfish-cir to identify linear RNAs and circular RNAs. Differential expression of linear RNAs was assessed with Deseq2 . QRT–PCR validation was performed using TaqMan and SYBR Green methods. Results: 100 million sequence reads per sample were mapped to the mouse genome (build mm10) using Sailfish-cir to identify linear and circular RNA transcripts. Pathway analysis of differentially expressed genes identified upregulation of gene sets for human asthma, mouse lung allergic inflammation, Muc5ac regulated genes and smooth muscle genes after allergic sensitization. Gene level exppression in each asthma-related pathway was reduced by the miR-145 antagonist. The miR-145 antagonist and several nontargeting oligos also upregulated interferon signaling pathways suggesting a general antiinflammatory effect of LNA/DNA oligos in the lung. Conclusions: Lung-directed delivery of LNA/DNA oligonucleotides with cationic lipid nanoparticles is an efffective means to prevent inflammatory gene expression in a house dust mite model of mild/moderate asthma.
2019-06-06 | GSE132263 | GEO
Project description:To define the role of microRNAs and their mRNA targets in emphysema severity in COPD patients. We performed Agilent human miRNA oligo arrays (8x15K array, Part No. G4470A, Agilent Technologies) based on miRBase V9.1 on lung tissues from 9 mild and 20 moderate emphysema lungs obtained from patients undergoing curative resection for lung cancer. We identified 5 miRNAs and two of those were tested and validated technically using qRT-PCR. The predicted mRNA targets for the five miRNAs were identified in MSigDB using GSEA and their expression were negatively correlated in exvivo lung mRNA expression profile obtained from GEO datasets (GSE17770 and GSE1650). Increasing the expression of one of the miRNA target, miR-34c in BEAS-2B and HFL 1 cell lines resulted in the downregulation of 50 TargetScan and Pictar predicted targets of miR-34c.
2012-05-31 | E-GEOD-33337 | biostudies-arrayexpress
Project description:Host transcriptomic profiling of COVID-19 patients with mild, moderate, and severe clinical outcomes
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Project description:Hand, foot and mouth disease (HFMD), caused by enterovirus 71 (EV71), presents mild to severe disease, and sometimes fatal neurological and respiratory manifestations. However, reasons for the severe pathogenesis remain undefined. To investigate this, infection and viral kinetics of EV71 isolates from clinical disease (mild, moderate and severe) from Sarawak, Malaysia, were characterized in human rhabdomyosarcoma (RD), neuroblastoma (SH-SY5Y) and peripheral blood mononuclear cells (PBMCs). High resolution transcriptomics was used to decipher EV71-host interactions in PBMCs. Ingenuity analyses revealed similar pathways triggered by all EV71 isolates, although the extent of activation varied. Importantly, several pathways were found to be specific to the severe isolate, including triggering receptor expressed on myeloid cells 1 (TREM-1) signaling. Depletion of TREM-1 in EV71-infected PBMCs with peptide LP17 resulted in decreased levels of pro-inflammatory genes, and reduced viral loads for the moderate and severe isolates. Mechanistically, this is the first report describing the transcriptome profiles during EV71 infections in primary human cells, and the involvement of TREM-1 in the severe disease pathogenesis, thus providing new insights for future treatment targets.
2020-03-16 | GSE135964 | GEO
Project description:miRNA expression in tracheal aspirates in mild/moderate and severe BPD
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