Isolated alveolar macrophages
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE2125 | GEO | 2005/10/04
SECONDARY ACCESSION(S): PRJNA91735
REPOSITORIES: GEO
Similar Datasets
Project description:This series represents isolated alveolar macrophages from human subjects.
2008-06-12 | E-GEOD-2125 | biostudies-arrayexpress
Project description:This series represents alveolar macrophages from a mouse model of emphysema, deletion of the integrin beta6 Keywords: parallel sample
2005-12-31 | GSE2255 | GEO
Project description:Purpose: The goal of this study is to investigate the alteration of gene expression pattern of alveolar macrophages by allergen challenge in human asthmatics. Method: By using subsegmental bronchial provocation with allergen (SBP-AG) protocol, we obtained BAL fluids, before and 48 hours after allergen challenge in the subjects enrolled in the protocol. Alveolar macrophages were purified from the BAL fluids and total RNA was isolated. Next-generation sequencing data were generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the human genome and identified 29,691 transcripts in the macrophage mRNAs. Among them, the change in the expression profiles of 37 transcripts were statistically significant. Conclusions: It has been well accepted that Th2 cytokine enriched environment transforms the phenotype of macrophages into alternatively activated form. However, the details of a genome-wide gene expression profiles of macrophages were not well investigated. Using RNA-seq technology, we provided comprehensive data of macrophage gene expression profiles in allergic lung inflammation. Our data could offer a framework to study biologic functions of alternatively activated macrophage in chronic inflammatory diseases. mRNA profiles of alveolar macrophages obtained from asthmatics, before and after allergen challenge.
2015-04-01 | E-GEOD-65039 | biostudies-arrayexpress
Project description:Human alveolar macrophages and monocyte derived macrophages were compared using genome-wide transcriptional profiling.
2012-09-19 | E-TABM-1206 | biostudies-arrayexpress
Project description:Mild asthmatics who met the criteria of the IRB approved protocol of Sub-segmental Bronchial Provocation with Allergen were recruited. The subjects were challenged with sensitive allergen through bronchoscopy. Bronchoalveolar lavage (BAL) fluids were collected before and at 48 hours after allergen challegen. From the BAL fluids, alveolar macrophages were purifed and their RNA was extracted. Total 138 genes including five house keeping genes were evaluated. Two samples of alveolar macrophages from single subject, before and 48 hours after allergen challenge, were directly compared in terms of the expression of inflammatory, chemokine, cytokine genes and their receptor genes.
2014-02-01 | E-GEOD-54585 | biostudies-arrayexpress
Project description:The objective of the overall study was to determine the effects of oral vitamin D supplementation on alveolar macrophages from human subjects. In this substudy, subjects treated with vitamin D (intervention group) in paired analysis had small, but significant effects on immune-related differential gene expression pre versus post supplementation. In this study, we obtained alveolar macrophages by bronchoalveolar lavage of subjects before and after a 3 month vitamin D trial. RNA for the array was obtained shortly after bronchoscopy. Randomized Controlled Trial: This is a substudy of paired samples of subjects treated with vitamin D. Each sample was studied once. 22 individuals were studied.
2014-04-08 | E-GEOD-56583 | biostudies-arrayexpress
Project description:This series represents mature CD4+ lymphocytes with high and low expression of integrin α4β7 isolated from human subjects. Keywords = lymphocyte, integrin α4β7 , differential gene expression, microarray Keywords: parallel sample
2004-02-13 | GSE1039 | GEO
Project description:Cigarette smoking is the leading cause of emphysema in the United States. Alveolar macrophages play a critical role in the inflammation-mediated remodeling of the lung parenchyma in emphysema. However, the exact gene pathways and the role of DNA methylation in moderating this pathological transformation are not known. In order to more exactly understand this process, we compared genome-wide expression and methylation signatures of alveolar macrophages isolated from heavy smokers with those isolated from non-smoking controls. We found enrichment of differential methylation in genes from immune system and inflammatory pathways as determined by standard pathway analysis. Consistent with recent findings, significant methylation changes were particularly enriched in the areas flanking CpG islands (CpG shores). Analysis of matching gene expression data demonstrated a parallel enrichment for changes in immune system and inflammatory pathways. We conclude that alveolar macrophages from the lungs of smokers demonstrate coordinated changes in DNA methylation and gene expression that link to inflammation pathways. We suggest that further studies of DNA methylation in immune and inflammation-related gene expression are needed to understand the pathogenesis of emphysema and other smoking-related diseases. Expression analysis of 13 smokers vs. 10 non-smokers on the Affymetrix Exon Array. This submission represents the expression component of the study.
2011-02-03 | E-GEOD-27002 | biostudies-arrayexpress
Project description:Purpose: The goal of this study is to investigate the alteration of gene expression pattern of alveolar macrophages by allergen challenge in human asthmatics. Method: By using subsegmental bronchial provocation with allergen (SBP-AG) protocol, we obtained BAL fluids, before and 48 hours after allergen challenge in the subjects enrolled in the protocol. Alveolar macrophages were purified from the BAL fluids and total RNA was isolated. Next-generation sequencing data were generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 75 million sequence reads per sample to the human genome and identified 29,691 transcripts in the macrophage mRNAs. Among them, the change in the expression profiles of 37 transcripts were statistically significant. Conclusions: It has been well accepted that Th2 cytokine enriched environment transforms the phenotype of macrophages into alternatively activated form. However, the details of a genome-wide gene expression profiles of macrophages were not well investigated. Using RNA-seq technology, we provided comprehensive data of macrophage gene expression profiles in allergic lung inflammation. Our data could offer a framework to study biologic functions of alternatively activated macrophage in chronic inflammatory diseases.
2015-04-01 | GSE65039 | GEO
Project description:The glutathione S-transferase (GST) gene family codes for enzymes that detoxify xenobiotics by catalyzing the conjugation of xenobiotics to glutathione. Based on reports that inherited copy number variations (CNV) in the genome modulate some GST expression levels and with the knowledge that cigarette smoke contains >3000 xenobiotics, and that the small airway epithelium and alveolar macrophages are involved early in the pathogensis of smoking-induced lung disease, we asked: do germline CNVs modulate GST expression level in the small airway epithelium and alveolar macrophages? Affymetrix HG U133 Plus 2.0 microarrays were used to survey GST gene expression in the small airway epithelium and alveolar macrophages obtained by bronchoscopic brushings from current smokers (n=35) and nonsmokers (n=35). The CNV genotypes of these 70 subjects were determined by Affymetrix Human SNP array 5.0 chips. Sixteen % of subjects had deletions of both GSTM1 alleles. These deletions were associated with reduced GSTM1 mRNA levels in both the small airway epithelium (p<10-7) and alveolar macrophages (p<0.05). Thirty % of subjects had homozygous deletions of GSTT1 with concomitant reduced mRNA levels in both small airway epithelium and alveolar macrophages (p<10-7). In contrast, genes flanking the CNV regions of both GST genes showed no difference in expression level among subjects with and without the GST deletions (p>0.3). Interestingly, GSTT2B, a duplicate gene of GSTT2, exhibited homozygous deletion in blood in 27% of subjects and was not expressed in small airway epithelium in the remainder of subjects but was expressed in alveolar macrophages of heterozygotes and wild type subjects, proportionate to genotype (p<10-3). These data demonstrate that highly prevalent CNV deletions of genes critical to ameliorating smoking-associated xenobiotic-induced damage in the lung can result in significant modulation of the gene expression levels, with the linear relationship of genotype to expression level suggesting minimal compensation of gene expression levels in heterozygotes consistent with GST polymorphisms playing a role in the risk for development of smoking-induced lung disease.
2019-08-26 | GSE20250 | GEO