Homo sapiens
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-8823
PROVIDER: PRJNA102147 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Mononuclear phagocytes play an important role in the removal of apoptotic cells by expressing cell surface receptors that recognize and remove apoptotic cells. Based on the knowledge that cigarette smoking is associated with increased lung cell turnover, we hypothesized that alveolar macrophages (AM) of normal cigarette smokers may exhibit enhanced expression of apoptotic cell removal receptor genes. AM obtained by bronchoalveolar lavage of normal non-smokers (n=11) and phenotypic normal smokers (n=13, 36 +/- 6 pack per year) were screened for mRNA expression of all known apoptotic cell removal receptors using Affymetrix HG-U133 Plus 2.0 chips with TaqMan RT-PCR confirmation. Of the 14 known apoptotic receptors expressed, only MER Tyrosine Kinase (MERTK), a transmembrane tyrosine kinase receptor, was significantly up-regulated in smokers. MERTK expression was then assessed in AM of smokers vs nonsmokers by TaqMan RT-PCR, immunohistochemistry, Western and flow analysis. Smoker AM had up-regulation of MERTK mRNA levels (smoker vs non-smoker, 3.6-fold by microarray, p<0.003; 9.5-fold by TaqMan RT-PCR, p<0.02). Immunohistochemistry demonstrated a qualitative increase in MERTK protein expression on AM of smokers. Increased protein expression of MERTK on AM of smokers was confirmed by Western and flow analyses (p< 0.007 and p< 0.0002, respectively). MERTK, a cell surface receptor that recognizes apoptotic cells, is expressed on human AM, and its expression is up-regulated in AM of cigarette smokers. This may reflect an increased demand for removal of apoptotic cells in smokers, an observation with implications for the development of chronic obstructive pulmonary disease (COPD), a disorder associated with dysregulated apoptosis of lung parenchymal cells. Experiment Overall Design: Alveolar macrophages were obtained from bronchoalveolar lavage.
2008-10-18 | E-GEOD-8823 | biostudies-arrayexpress
Project description:Mononuclear phagocytes play an important role in the removal of apoptotic cells by expressing cell surface receptors that recognize and remove apoptotic cells. Based on the knowledge that cigarette smoking is associated with increased lung cell turnover, we hypothesized that alveolar macrophages (AM) of normal cigarette smokers may exhibit enhanced expression of apoptotic cell removal receptor genes. AM obtained by bronchoalveolar lavage of normal non-smokers (n=11) and phenotypic normal smokers (n=13, 36 ± 6 pack-yr) were screened for mRNA expression of all known apoptotic cell removal receptors using Affymetrix HG-U133 Plus 2.0 chips with TaqMan RT-PCR confirmation. Of the 14 known apoptotic receptors expressed, only MER Tyrosine Kinase (MERTK), a transmembrane tyrosine kinase receptor, was significantly up-regulated in smokers. MERTK expression was then assessed in AM of smokers vs nonsmokers by TaqMan RT-PCR, immunohistochemistry, Western and flow analysis. Smoker AM had up-regulation of MERTK mRNA levels (smoker vs non-smoker, 3.6-fold by microarray, p<0.003; 9.5-fold by TaqMan RT-PCR, p<0.02). Immunohistochemistry demonstrated a qualitative increase in MERTK protein expression on AM of smokers. Increased protein expression of MERTK on AM of smokers was confirmed by Western and flow analyses (p< 0.007 and p< 0.0002, respectively). MERTK, a cell surface receptor that recognizes apoptotic cells, is expressed on human AM, and its expression is up-regulated in AM of cigarette smokers. This may reflect an increased demand for removal of apoptotic cells in smokers, an observation with implications for the development of chronic obstructive pulmonary disease (COPD), a disorder associated with dysregulated apoptosis of lung parenchymal cells. Keywords: Comparison of gene expression in alveolar macrophages of normal non-smokers and normal smokers.
2008-08-01 | GSE8823 | GEO
Project description:Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. Mertk is an efferocytosis receptor involved in the recognition and removal of apoptotic debris by macrophages and other phagocytic cells. Here we show that Mertk negatively regulates the clearance of S. pneumoniae, as measured by the greater number of viable bacteria in the lung of wild type vs. Mertk-/- mice 24 hours post-inoculation. The impaired clearance observed in wild type mice was associated with a greater number of neutrophils in the bronchoalveolar lavage (BAL) and lower concentration of IFNγ in the BAL fluid; however, similar enhancement of clearance was observed in Mertk-/- mice receiving neutralizing IFNγ antibody. Mertk is highly expressed on alveolar macrophages. Transcriptomic changes observed in primary Mertk-/- alveolar macrophages were associated with leukocyte activation, cellular motility, and response to stimulus. Mertk deficiency similarly enhanced proinflammatory gene expression in S. pneumoniae-stimulated alveolar macrophages in vitro and in pneumonic lung tissue. Thus, Mertk contributes to alveolar macrophage homeostasis through the receptor’s immunomodulatory role. Naive Mertk-/- alveolar macrophages appear primed for an inflammatory response to S. pneumoniae leading to greater cell motility, improved bacterial killing and enhancement of other innate immune cells through the production of inflammatory mediators.
2025-03-04 | GSE210550 | GEO
Project description:Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. Mertk is an efferocytosis receptor involved in the recognition and removal of apoptotic debris by macrophages and other phagocytic cells. Here we show that Mertk negatively regulates the clearance of S. pneumoniae, as measured by the greater number of viable bacteria in the lung of wild type vs. Mertk-/- mice 24 hours post-inoculation. The impaired clearance observed in wild type mice was associated with a greater number of neutrophils in the bronchoalveolar lavage (BAL) and lower concentration of IFNγ in the BAL fluid; however, similar enhancement of clearance was observed in Mertk-/- mice receiving neutralizing IFNγ antibody. Mertk is highly expressed on alveolar macrophages. Transcriptomic changes observed in primary Mertk-/- alveolar macrophages were associated with leukocyte activation, cellular motility, and response to stimulus. Mertk deficiency similarly enhanced proinflammatory gene expression in S. pneumoniae-stimulated alveolar macrophages in vitro and in pneumonic lung tissue. Thus, Mertk contributes to alveolar macrophage homeostasis through the receptor’s immunomodulatory role. Naive Mertk-/- alveolar macrophages appear primed for an inflammatory response to S. pneumoniae leading to greater cell motility, improved bacterial killing and enhancement of other innate immune cells through the production of inflammatory mediators.
2025-03-04 | GSE210549 | GEO
Project description:Streptococcus pneumoniae is the leading cause of community-acquired pneumonia. Mertk is an efferocytosis receptor involved in the recognition and removal of apoptotic debris by macrophages and other phagocytic cells. Here we show that Mertk negatively regulates the clearance of S. pneumoniae, as measured by the greater number of viable bacteria in the lung of wild type vs. Mertk-/- mice 24 hours post-inoculation. The impaired clearance observed in wild type mice was associated with a greater number of neutrophils in the bronchoalveolar lavage (BAL) and lower concentration of IFNγ in the BAL fluid; however, similar enhancement of clearance was observed in Mertk-/- mice receiving neutralizing IFNγ antibody. Mertk is highly expressed on alveolar macrophages. Transcriptomic changes observed in primary Mertk-/- alveolar macrophages were associated with leukocyte activation, cellular motility, and response to stimulus. Mertk deficiency similarly enhanced proinflammatory gene expression in S. pneumoniae-stimulated alveolar macrophages in vitro and in pneumonic lung tissue. Thus, Mertk contributes to alveolar macrophage homeostasis through the receptor’s immunomodulatory role. Naive Mertk-/- alveolar macrophages appear primed for an inflammatory response to S. pneumoniae leading to greater cell motility, improved bacterial killing and enhancement of other innate immune cells through the production of inflammatory mediators.
2025-03-04 | GSE210548 | GEO
Project description:Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages in Response to the In Vivo Oxidant Stress of Cigarette Smoking The oxidant burden of cigarette smoking induces lung cell dysfunction, and play a significant role in the pathogenesis of lung disease. Two cell populations directly exposed to the oxidants in cigarette smoke are the small airway epithelium and alveolar macrophages. Of these, the epithelium appears to be more vulnerable to smoking, becoming disordered in differentiation, repair and function, while alveolar macrophages become activated, without becoming diseased. In this context, we asked: for the same individuals, what is the baseline trancriptome of oxidant-related genes in small airway epithelium compared to alveolar macrophages and do the responses of the transcriptome of these 2 cell populations differ substantially to inhaled cigarette smoke? To address these questions we used microarray gene expression and TaqMan analysis to assess the gene expression profile of known oxidant-related genes in paired samples recovered by bronchoscopy from small airway epithelium and alveolar macrophages from the same healthy nonsmokers and normal smokers. Of the 155 oxidant-related genes surveyed, 122 (77%) were expressed in both cell populations in nonsmokers. However, of the genes expressed by both cell populations, oxidant related gene expression levels were higher in alveolar macrophages (67 genes, 43%) than small airway epithelium (37 genes, 24%). There were more oxidant-related genes uniquely expressed in the small airway epithelium (17%), than in alveolar macrophages (5%). In healthy smokers, the majority of oxidant-related genes were expressed in both cell populations, but there were marked differences in the numbers of oxidant-related genes that smoking up- or down-regulated. While smoking up-regulated 15 genes (10%) and down-regulated 7 genes (5%) in the small airway epithelium, smoking had far less effect on alveolar macrophages [only 4 (3%) genes up-regulated, and only 1 (0.6%) down-regulated]. Only a small number of smoking responsive oxidant-related genes overlapped between the two cell types (2 up-regulated, and no down-regulated genes). Consistent with this observation, pathway analysis of smoking-responsive genes in the small airway epithelium showed oxidant-related pathways dominated, but in alveolar macrophages immune-response pathways dominated. Thus, the responses of the oxidant-related transcriptome of cells with an identical genome and exposed to the same oxidant stress of cigarette smoking are very different, with responses of oxidant-related genes of alveolar macrophages far more subdued than that of small airway epithelium, consistent with the clinical observation that, while the small airway epithelium is vulnerable, alveolar macrophages are not "diseased" in response to the oxidant stress of cigarette smoking. Gene expression profiles of known oxidant-related genes in paired samples recovered by bronchoscopy from small airway epithelium and alveolar macrophages from the same healthy nonsmokers and normal smokers.
2011-09-11 | E-GEOD-13931 | biostudies-arrayexpress
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.
2012-10-02 | GSE34517 | GEO
Project description:Cigarette smoking is the leading cause of the respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). While the pathogenesis of COPD is complex, there is abundant evidence that alveolar macrophages (AM) play an important role. Based on the concept that COPD is a slow-progressing disorder likely involving multiple mediators released by AM activated by cigarette smoke, the present study focuses on the identification of previously unrecognized genes that may be linked to early events in the molecular pathogenesis of COPD, as opposed to factors associated with the presence of disease. To accomplish this, microarray analysis using Affymetrix microarrays was used to carry out an unbiased survey of the differences in gene expression profiles in the AM of phenotypically normal, ~20 pack-yr smokers compared to healthy non-smokers. Although smoking did not alter the global gene expression pattern of AM, 75 genes were modulated by smoking, with 40 genes up-regulated and 35 down-regulated in the AM of smokers compared to non-smokers. Most of these genes belong to the functional categories of immune/inflammatory response, cell adhesion and extracellular matrix, proteolysis and antiproteolysis, lysosomal function, antioxidant-related, signal transduction and regulation of transcription. Of these 75 genes, 69 have not been previously recognized to be up- or down-regulated in alveolar macrophages in association with smoking or COPD, including genes coding for proteins belonging to all of the above categories, and others belonging to various functional categories or of unknown function. These observations suggest that gene expression responses of alveolar macrophages associated with the stress of cigarette smoking are more complex than previously thought, and offer a variety of new insights into the complex pathogenesis of smoking-induced lung diseases. Experiment Overall Design: 5 non smokers and 5 smokers Experiment Overall Design: Alveolar macrophages were obtained from bronchoalveolar lavage
2007-09-06 | E-GEOD-3212 | biostudies-arrayexpress
Project description:Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%. 4 never smokers and 4 active smokers were recruited for the study. After bronchoalveolar lavage and RNA isolation, gene expression was measured using Affymetrix Human Exon 1.0 ST arrays.
2012-10-02 | E-GEOD-34517 | biostudies-arrayexpress
Project description:Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages in Response to the In Vivo Oxidant Stress of Cigarette Smoking The oxidant burden of cigarette smoking induces lung cell dysfunction, and play a significant role in the pathogenesis of lung disease. Two cell populations directly exposed to the oxidants in cigarette smoke are the small airway epithelium and alveolar macrophages. Of these, the epithelium appears to be more vulnerable to smoking, becoming disordered in differentiation, repair and function, while alveolar macrophages become activated, without becoming diseased. In this context, we asked: for the same individuals, what is the baseline trancriptome of oxidant-related genes in small airway epithelium compared to alveolar macrophages and do the responses of the transcriptome of these 2 cell populations differ substantially to inhaled cigarette smoke? To address these questions we used microarray gene expression and TaqMan analysis to assess the gene expression profile of known oxidant-related genes in paired samples recovered by bronchoscopy from small airway epithelium and alveolar macrophages from the same healthy nonsmokers and normal smokers. Of the 155 oxidant-related genes surveyed, 122 (77%) were expressed in both cell populations in nonsmokers. However, of the genes expressed by both cell populations, oxidant related gene expression levels were higher in alveolar macrophages (67 genes, 43%) than small airway epithelium (37 genes, 24%). There were more oxidant-related genes uniquely expressed in the small airway epithelium (17%), than in alveolar macrophages (5%). In healthy smokers, the majority of oxidant-related genes were expressed in both cell populations, but there were marked differences in the numbers of oxidant-related genes that smoking up- or down-regulated. While smoking up-regulated 15 genes (10%) and down-regulated 7 genes (5%) in the small airway epithelium, smoking had far less effect on alveolar macrophages [only 4 (3%) genes up-regulated, and only 1 (0.6%) down-regulated]. Only a small number of smoking responsive oxidant-related genes overlapped between the two cell types (2 up-regulated, and no down-regulated genes). Consistent with this observation, pathway analysis of smoking-responsive genes in the small airway epithelium showed oxidant-related pathways dominated, but in alveolar macrophages immune-response pathways dominated. Thus, the responses of the oxidant-related transcriptome of cells with an identical genome and exposed to the same oxidant stress of cigarette smoking are very different, with responses of oxidant-related genes of alveolar macrophages far more subdued than that of small airway epithelium, consistent with the clinical observation that, while the small airway epithelium is vulnerable, alveolar macrophages are not "diseased" in response to the oxidant stress of cigarette smoking.
2011-09-12 | GSE13931 | GEO