Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Alveolar macrophage immunometabolism and lung function impairment in smoking and chronic obstructive pulmonary disease

ABSTRACT: Background: Metabolic plasticity involving shifts between mitochondrial respiration and glycolysis is emerging as a crucial component of efficient innate immune cell responses. Alveolar macrophages (AMs), the most abundant antigen-presenting cells in the lung, are dramatically increased in the lungs of patients with chronic obstructive pulmonary disease (COPD). However, COPD AMs exhibit dysfunctional responses to infection with lower phagocytic ability and impairment of mitochondrial reactive oxygen species (ROS) generation. Little is known about the mitochondrial function or respiration of these cells and whether alterations in their mitochondrial or glycolytic activities may contribute to the pathogenesis of COPD.

ORGANISM(S): Homo sapiens

PROVIDER: GSE130928 | GEO | 2020/04/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Epigenetic reprogramming of airway macrophages drives polarization and inflammation in muco-obstructive lung disease (RNA_Treat)

Project description:Lung diseases, such as cystic fibrosis and COPD, are characterized by mucus obstruction and chronic airway inflammation, but their mechanistic link remains poorly understood. Here, we focused on the role of the mucostatic airway microenvironment on epigenetic reprogramming of airway macrophages (AM) and resulting transcriptomic and phenotypical changes. Using a muco-obstructive mouse model (Scnn1b-transgenic), we identified epigenetically controlled, differentially regulated pathways and transcription factors involved in inflammatory responses and macrophage polarization. Ex vivo stimulation of wild-type AMs with mucus induced gene expression changes, comparable with those observed in AMs from Scnn1b-transgenic mice. Functionally, AMs from Scnn1b-transgenic mice displayed impaired efferocytosis, phagocytosis and excessive inflammatory responses upon lipopolysaccharide challenge, mediated through enhanced Irf1 activity and expression. Our data show that mucostasis induces epigenetic reprogramming of AMs, leading to changes favoring tissue damage and disease progression. Targeting of these altered AMs may support therapeutic approaches in patients with muco-obstructive lung diseases.

2021-09-10 | GSE154806 | GEO

Epigenetic reprogramming of airway macrophages drives polarization and inflammation in muco-obstructive lung disease (RNA_BL)

2021-09-10 | GSE154805 | GEO

Epigenetic reprogramming of airway macrophages drives polarization and inflammation in muco-obstructive lung disease (ATAC_BL)

2021-09-10 | GSE154804 | GEO

Epigenetic reprogramming of airway macrophages drives polarization and inflammation in muco-obstructive lung disease (ATAC_Treat)

2021-09-10 | GSE154807 | GEO

Epigenetic reprogramming of airway macrophages drives polarization and inflammation in muco-obstructive lung disease (WGBS_BL)

2021-09-10 | GSE154803 | GEO

Alveolar macrophage immunometabolism and lung function impairment in smoking and chronic obstructive pulmonary disease

Project description:Alveolar macrophage immunometabolism and lung function impairment in smoking and chronic obstructive pulmonary disease

| PRJNA541954 | ENA

Lung proteomic biomarkers associated with chronic obstructive pulmonary disease

Project description:Identifying protein biomarkers for chronic obstructive pulmonary disease (COPD) has been challenging. Most previous studies have utilized individual proteins or pre-selected protein panels measured in blood samples. To identify COPD protein biomarkers by applying comprehensive mass spectrometry proteomics in lung tissue samples. We utilized mass spectrometry proteomic approaches to identify protein biomarkers from 152 lung tissue samples representing COPD cases and controls.

2022-01-07 | PXD024124 | Pride

Chronic obstructive pulmonary disease

Project description:Diaphragm muscles in Chronic Obstructive Pulmonary Disease (COPD) patients undergo an adaptive fast to slow transformation that includes cellular adaptations. This project studies the signaling mechanisms responsible for this transformation. Keywords: other

2003-07-16 | GSE475 | GEO

Alveolar Macrophage Immunometabolism and Lung Function Impairment in Smoking and Chronic Obstructive Pulmonary Disease.

Project description: Not available

| S-EPMC7068819 | biostudies-literature

Chronic obstructive pulmonary disease (COPD)

Project description:Chronic obstructive pulmonary disease (COPD) Metagenome

| PRJNA647843 | ENA