E-GEOD-40885
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: PRJNA175261
PROVIDER: E-GEOD-40885 | ExpressionAtlas | 2015-09-30
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:Data expression in alveolar macrophages induced by lipopolysaccharide in humans
| PRJNA175261 | ENA
Project description:Rationale: Lipopolysaccharide (LPS) is ubiquitous in the environment. Inhalation of LPS has been implicated in the pathogenesis and/or severity of several lung diseases, including pneumonia, chronic obstructive pulmonary disease and asthma. Alveolar macrophages are the main resident leukocytes exposed to inhaled antigens. Objectives: To obtain insight into which innate immune pathways become activated within human alveolar macrophages upon exposure to LPS in vivo. In seven healthy humans sterile saline was instilled into a lung segment by bronchoscope, followed by instillation of LPS into the contralateral lung. Six hours later a bilateral bronchoalveolar lavage was performed and whole-genome transcriptional profiling was done (Affymetrix HG-U133 Plus 2.0) on purified alveolar macrophages, comparing cells exposed to saline or LPS from the same individuals.
2012-09-15 | E-GEOD-40885 | biostudies-arrayexpress
Project description:Alveolar macrophages are the first line of defense against pathogens in the lungs of all mammalian species and therefore may constitute an appropriate therapeutic target cell in the treatment and prevention of opportunistic airway infections. Analysis of alveolar macrophages from several species has revealed a unique cellular phenotype and transcriptome, presumably linked to their distinct airway environment and function in host defense. The current study extends these findings to the horse. Firstly, the transcriptome of equine alveolar macrophages was compared to that of equine peritoneal macrophages. This comparison revealed the differential basal expression of 451 genes. Gene expression analysis revealed an alternative macrophage polarisation profile in alveolar macrophages and a hybrid macrophage activation profile in peritoneal macrophages, a phenomenon potentially attributable to a degree endotoxin tolerance. Secondly, the change in gene expression profile of equine AMs following lipopolysaccharide stimulation was investigated. This revealed a significant change in the expression of 240 genes, including well known upregulated inflammatory genes.
2016-06-06 | GSE69871 | GEO
Project description:Rationale: Lipopolysaccharide (LPS) is ubiquitous in the environment. Inhalation of LPS has been implicated in the pathogenesis and/or severity of several lung diseases, including pneumonia, chronic obstructive pulmonary disease and asthma. Alveolar macrophages are the main resident leukocytes exposed to inhaled antigens. Objectives: To obtain insight into which innate immune pathways become activated within human alveolar macrophages upon exposure to LPS in vivo.
2012-09-15 | GSE40885 | GEO
Project description:Expression data from human alveolar macrophages (AMs)
| PRJNA786547 | ENA
Project description:The proteasome is a central regulatory hub for intracellular signaling by degrading numerous signaling mediators. Immunoproteasomes are specialized types of proteasomes known to be involved in shaping adaptive immune responses, but their role for innate immune signaling is elusive. Here, we analyzed immunoproteasome function for polarization of alveolar macrophages which are highly specialized tissue macrophages of the alveolar surface of the lung. Classical activation (M1 polarization) of primary alveolar macrophages by LPS/IFNγ transcriptionally induced all three immunoproteasome subunits LMP2, LMP7, and MECL-1. In contrast, IL-4 triggered alternative (M2) activation was accompanied by posttranscriptional upregulation of LMP2 and LMP7. Accordingly, immunoproteasome activity increased in M1 cells, and to some extent under M2 conditions. Analyzing the polarization capability from LMP7 deficient mice revealed no effect on the LPS/IFNγ triggered M1 profile, but uncovered a distorted M2 profile for IL-4 stimulated LMP7-/- alveolar macrophages as characterized by increased M2 marker gene expression and CCL17 cytokine release. This shift in immunoproteasome-dependent M2 polarization was accompanied by amplified AKT/STAT6 activation and IRF4 expression in LMP7-/- alveolar macrophages. IL-13 stimulation of LMP7 deficient cells induced a similar M2 skewed profile and IL4Rα protein expression was generally elevated in LMP7-/- alveolar macrophages, indicating that amplified IL4R signaling in immunoproteasome defective cells may contribute to augmented M2 polarization. Importantly, treatment with an LMP7-specific proteasome inhibitor recapitulated the findings of genetic LMP7 inactivation. Our results thus suggest a novel role of immunoproteasome function for regulating innate immune function of macrophages by limiting IL4R expression and signaling. Expression data of M0 and M2 macrophages derived from Lmp7 k.o. and control animals
2016-06-29 | E-GEOD-72000 | biostudies-arrayexpress
Project description:To reveal early responses to one of septic agents, lipopolysaccharide (LPS), in tissue resident macrophages, we isolated Kupffer cells as well as alveolar macrophages from bolus LPS-injected mice at 1 and 4 hours (hr) of early time points and performed quantitative RNA sequencing
2018-12-27 | GSE108553 | GEO
Project description:Macrophages are key immune cells in tissues that are able to adapt their metabolic phenotype in response to different stimuli. Lysine deacetylases are important enzymes for regulating inflammatory gene expression and their inhibitors have anti-inflammatory effects in models of chronic obstructive pulmonary disease (COPD). We hypothesized that these anti-inflammatory effects may be driven by or associated with metabolic changes in macrophages. To validate this hypothesis, we used an unbiased and a targeted proteomic approach to investigate metabolic enzymes and LC- and GC-MS to quantify metabolites in combination with functional parameters in primary murine alveolar-like macrophages after lipopolysaccharide (LPS)-induced activation with and without lysine deacetylase inhibitors. We found that lysine deacetylase inhibitor treatment resulted in reduced production of inflammatory mediators such as TNF-α and IL-1β. However, only minor changes in macrophage metabolism were observed, as only one of the deacetylase inhibitors slightly increased mitochondrial respiration. However, lysine deacetylase inhibition specifically enhanced expression of proteins involved in ubiquitination, and this may be a potential driver of the anti-inflammatory effects of lysine deacetylase inhibitors. Our data illustrate that a multi-omics approach is necessary to gain a better understanding of how macrophages interact with cues from their environment. More detailed insight into the molecular mechanisms of KDAC inhibition is needed and investigating ubiquitination seems a promising next step. This is important as conventional anti-inflammatory drugs like corticosteroids have low effectiveness in many patients and novel therapeutic strategies are urgently needed.
2024-02-21 | PXD040933 | Pride
Project description:Expression data from murine lung derived alveolar macrophages
| PRJNA539917 | ENA