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E-GEOD-40885

ABSTRACT: Data expression in alveolar macrophages induced by lipopolysaccharide in humans

OTHER RELATED OMICS DATASETS IN: PRJNA175261

PROVIDER: E-GEOD-40885 | ExpressionAtlas | 2015-09-30

REPOSITORIES: ExpressionAtlas

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			Action	DRS
	E-GEOD-40885-analysis-methods.tsv	Tabular
	E-GEOD-40885-atlasExperimentSummary.Rdata	Rdata
	E-GEOD-40885-configuration.xml	Xml
	E-GEOD-40885-percentile-ranks.tsv	Tabular
	E-GEOD-40885.condensed-sdrf.tsv	Tabular

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Homo sapiens

Project description:Data expression in alveolar macrophages induced by lipopolysaccharide in humans

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Data expression in alveolar macrophages induced by lipopolysaccharide in humans

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

Equus caballus

Project description:Expression data from lipopolysaccharide treated and untreated equine alveolar macrophages and basal comparison with peritoneal macrophages

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Project description:Expression data from canine alveolar macrophages

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Expression data from lipopolysaccharide treated and untreated equine alveolar macrophages and basal comparison with peritoneal macrophages

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.

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Data expression in alveolar macrophages induced by lipopolysaccharide in humans

2012-09-15 | GSE40885 | GEO

Immunoproteasome dysfunction augments alternative polarization of alveolar macrophages

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/IFNÎ³ 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/IFNÎ³ 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 IL4RÎ± 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

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Project description:Within the human lung, interplay between alveolar epithelial cells and resident macrophages shape lung development and function in both health and disease. To study these processes, we devised a strategy for co-culturing hPSC-derived alveolar epithelial organoids and induced macrophages to form functional environment, which we name alveolar assembloids (AlvAssemb). By scRNAseq and functional analysis of AlvAssemb, we identified alveolar type 2-like cells that produced GM-CSF, a response associated with tissue adaptation of macrophages, and that resident alveolar macrophage-like cells secreted interleukin-1β and interleukin-6, a core immune response function, and expressed genes required for surfactant metabolism. Remarkably, in response to alveolar epithelial injury, we found that macrophage-like cells within AlvAssemb efficiently eliminated damaged cells and absorbed oxidized lipids. Moreover, in response to lipopolysaccharide exposure and Mycobacterium tuberculosis infection, we found that core features of the human respiratory defense response were replicated in AlvAssemb. These findings support that AlvAssemb could serve as a valuable platform to investigate human lung development and pathology.

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Genome-wide transcriptional profiles of Kupffer cells and alveolar macrophages from naïve and LPS-injected mice

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

Expression data from human alveolar macrophages (AMs)

Project description:Expression data from human alveolar macrophages (AMs)

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