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Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

ABSTRACT: Lung myeloid dendritic cells isolated from emphysema but not healthy subjects induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung myeloid dendritic cells from healthy or emphysema subjects. These genes may play crucial roles in directing Th1 and Th17 cells differentiation.

ORGANISM(S): Homo sapiens

PROVIDER: GSE26296 | GEO | 2011/01/01

SECONDARY ACCESSION(S): PRJNA135059

REPOSITORIES: GEO

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Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

Project description:Lung myeloid dendritic cells isolated from emphysema but not healthy subjects induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung myeloid dendritic cells from healthy or emphysema subjects. These genes may play crucial roles in directing Th1 and Th17 cells differentiation. Total mRNA was extracted from lung myeloid dendritic cells isolated from lungs of three healthy controls and three emphysema patients.

2011-01-01 | E-GEOD-26296 | biostudies-arrayexpress

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses. Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups. There were three replicates in each group.

2015-09-05 | E-GEOD-72734 | biostudies-arrayexpress

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

2015-09-05 | GSE72734 | GEO

Homo sapiens

Project description:Genome-wide analysis of lung myeloid dendritic cells gene expression from healthy or emphysema subjects

| PRJNA135059 | ENA

Single-cell RNAseq of the human normal and emphysema lung

Project description:To study emphysema, we conduct single-cell RNAseq of the human healthy and emphysema lung using 10X genomics scRNAseq technique.

2023-02-13 | GSE196638 | GEO

Epigenetic stabilization of DC and DC precursor classical activation by TNFalpha drives protective T-cell polarization

Project description:We report that TNFalpha mediated dendritic cell priming via alterations in histone 3 lysine 4 trimethylation (H3K4me3) sustains lasting protective Th1/Th17 responses during invasive Cryptococcus neoformans pulmonary infection. Cryptococcus neoformans pulmonary infection results in increased global lung dendritic cell H3K4me3 over naive lung dendritic cells. Blockage of TNFalpha during Cryptococcus neoformans pulmonary infection results in decreased H3K4me3 at sites crucial to protective Th1/Th17 responses.

2018-08-15 | GSE118543 | GEO

Emphysema Lung Tissue Gene Expression Profiling

Project description:Gene expression profiling of lung tissue from undiseased (NML), 'usual' emphysema (EML), and Alpha-1 Antitrypsin Deficiency-related emphysema (ADL). Keywords = Emphysema Keywords = COPD Keywords = Alpha-1 Antitrypsin Deficiency Keywords: ordered

2004-06-01 | GSE1122 | GEO

Transcription profiling of human lung tissue from severe emphysema versus normal or mild emphysema human patients

Project description:Comparison of severely emphysematous tissue removed at lung volume reduction surgery to that of normal or mildly emphysematous lung tissue resected from smokers with nodules suspicious for lung cancer. Data obtained from the 18 patients with severe emphysema and 12 patients with mild/no emphysema. Research may provide insights into the pathogenetic mechanisms involved in chronic obstructive pulmonary disease (COPD).

2007-08-13 | E-GEOD-1650 | biostudies-arrayexpress

Expression Profiling Identifies Genes Involved in Emphysema

Project description:Chronic obstructive pulmonary disease (COPD) is a major public health problem. The aim of this study was to identify genes involved in emphysema severity in COPD patients. Gene expression profiling was performed on total RNA extracted from non-tumor lung tissue from 30 smokers with emphysema. Class comparison analysis based on gas transfer measurement was performed to identify differentially expressed genes. Genes were then selected for technical validation by quantitative reverse transcriptase-PCR (qRT-PCR) if also represented on microarray platforms used in previously published emphysema studies. Genes technically validated advanced to tests of biological replication by qRT-PCR using an independent test set of 62 lung samples. Class comparison identified 98 differentially expressed genes (p<0.01). Fifty-one of those genes had been previously evaluated in differentiation between normal and severe emphysema lung. qRT-PCR confirmed the direction of change in expression in 29 of the 51 genes and 11 of those validated, remaining significant at p<0.05. Biological replication in an independent cohort confirmed the altered expression of eight genes, with seven genes differentially expressed by greater than 1.3 fold, identifying these as candidate determinants of emphysema severity. Gene expression profiling of lung from emphysema patients identified seven candidate genes associated with emphysema severity including COL6A3, SERPINF1, ZNHIT6, NEDD4, CDKN2A, NRN1 and GSTM3.

2009-09-21 | GSE17770 | GEO

Eosinophils promote lung emphysema via CTSL

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.

2023-10-17 | GSE237749 | GEO

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