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Siglec-1−/FSClow alveolar macrophages exhibit pro-inflammatory phenotypes in chronic obstructive pulmonary disease

ABSTRACT: Siglec-1−/FSClow alveolar macrophages exhibit pro-inflammatory phenotypes in chronic obstructive pulmonary disease

PROVIDER: PRJNA819427 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18466143_1.fastq.gz	Fastqsanger.gz
	SRR18466143_2.fastq.gz	Fastqsanger.gz
	SRR18466144_1.fastq.gz	Fastqsanger.gz
	SRR18466144_2.fastq.gz	Fastqsanger.gz
	SRR18466145_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Siglec-1−/FSClow alveolar macrophages exhibit pro-inflammatory phenotypes in chronic obstructive pulmonary disease

Project description:Alveolar macrophages (AMs) in patients with chronic obstructive pulmonary disease (COPD) orchestrate persistent inflammation in the airway, however, sub-populations of alveolar macrophages predominantly participating in chronic inflammation have been poorly characterised. We recently reported that Siglec-1 was involved in recognition and engulfment of non-typeable Haemophilus influenzae and that the expression of Siglec-1 on AMs was decreased in COPD lung tissues. Here, based on the expression of Siglec-1 and the intensity of forward scattergram (FSC) using flow cytometry, we identified three subsets present in alveolar macrophages: Siglec-1+/FSChi, Siglec-1−/FSChi, Siglec-1−/FSClow subsets. The Siglec-1−/FSClow subset increased in number in the lungs of COPD subjects. RNA-sequencing revealed that the Siglec-1−/FSClow subset exhibited pro-inflammatory and protease-producing phenotypes compared to other two subsets. Clinically, a decrease in the intensity of Siglec-1 expression in macrophages of induced sputum from COPD subjects was correlated with exacerbation rates in prospective four years. Collectively Siglec-1− AMs showed the pro-inflammatory properties and that their emergence in COPD airways was a risk factor in exacerbation. The Siglec-1−/FSClow subset might serve as “pathogenic macrophages” which could lead to poor clinical outcomes for patients with COPD

2025-03-24 | GSE199345 | GEO

Comparing murine lung resident alveolar Siglec-F(high) macrophages to CD11b(high) macrophages following bleomycin injury

Project description:Macrophages (MΦ) have been shown to contribute to fibrogenesis, however the underlying mechanisms and specific MΦ subsets involved remain unclear. Lung MΦ can be divided into two subsets: Siglec-Fhi resident alveolar MΦ and CD11bhi MΦ that primarily arise from immigrating monocytes. RNA-seq analysis was performed to compare these MΦ subsets during fibrosis. CD11bhi MΦ, not Siglec-Fhi MΦ, expressed high levels of pro-fibrotic chemokines and growth factors.

2018-02-05 | GSE94699 | GEO

Gene expression profiles of Siglec-14/THP-1 and Siglec-5/THP cell lines, with or without NTHi stimulation

Project description:Acquisition of a new strain of non-typeable Haemophilus influenzae (NTHi) is often associated with exacerbation of chronic obstructive pulmonary disease (COPD). We have previously reported that COPD patients who are homozygous null for SIGLEC14 gene is less susceptible to COPD exacerbation than those who have wild-type allele with functional SIGLEC14 gene. In order to gain insight into the mechanism behind the COPD exacerbation, and to find new clues that may lead to the discovery of objective biomarker of COPD exacerbation, Siglec-14/THP-1 and Siglec-5/THP-1 cell lines, which mimic monocytes from homozygous wild-type and homozygous SIGLEC14-null person, respectively, were incubated with or without NTHi, and their gene expression profiles were compared by using Affymetrix Human Genome U133 Plus 2.0 Array. Four samples (2 cell lines x 2 conditions) were analyzed. No replicates were made.

2014-08-04 | E-GEOD-47929 | biostudies-arrayexpress

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

Project description: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.

2020-04-17 | GSE130928 | GEO

Gene expression profiles of Siglec-14/THP-1 and Siglec-5/THP cell lines, with or without NTHi stimulation

2014-08-04 | GSE47929 | GEO

Gene expression in liver tissues derived from wild-type and Siglec-E-deficient mice at 55 weeks of age

Project description:We show that mice lacking Siglec-E, the main member of the CD33rSiglec family, exhibit reduced survival. Removal of Siglec-E causes the development of exaggerated signs of aging at the molecular, structural, and cognitive level. We found that accelerated aging was related both to an unbalanced ROS metabolism, and to a secondary impairment in detoxification of reactive molecules, ultimately leading to increased damage to cellular DNA, proteins and lipids. Taken together, our data suggest that CD33rSiglecs co-evolved in mammals to achieve a better management of oxidative stress during inflammation, which in turn reduces molecular damage and extends lifespan. Total RNA obtained from liver tissues from two wild-type and three Siglec-E-deficient mice

2016-01-15 | E-GEOD-64760 | biostudies-arrayexpress

Type-I interferon inducible genes 26 weeks after mCMV infection in Siglec-H wt and Siglec-H ko mice and their non infected controls

Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-Î± in vitro and that Siglec-H ko mice produce more IFN-Î± after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease. For microarray experiments gene expression profiles of total splenic cells from two wt and Siglec-H ko mice 26 weeks after infection with luciferase expressing murine Cytomegalovirus (5x105 pfu) or from two uninfected wt and Siglec-H ko control mice were analyzed

2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of the Effect of GM-CSF on the Transcriptomes of Alveolar and Exudative Lung Macrophages from Influenza-infected C57BL/6 Mice

Project description:The transcriptomes of FACS-sorted siglec-F+ alveolar macrophages and siglec-f- CD11b+ exudative macrophages from inducible airway GM-CSF over-expressing transgenic mice (DTGM) were compared to non-inducible littermate controls during influenza A virus infection.

2018-01-12 | GSE109099 | GEO

Siglec-3 (CD33) and Siglec-8 ligands

Project description:Identification of human brain ligand for the microglial inhibitory receptors Siglec-3 (CD33) and Siglec-8

2022-03-07 | PXD032064 | JPOST Repository

Human Obstructive and Non-obstructive Hypertrophic Cardiomyopathy Disease Mechanisms

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2022-01-01 | GSE181764 | GEO

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