Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single Cell RNA Sequencing Identifies an Early Monocyte Gene Signature in Acute Respiratory Distress Syndrome

ABSTRACT: Single Cell RNA Sequencing Identifies an Early Monocyte Gene Signature in Acute Respiratory Distress Syndrome

PROVIDER: PRJNA635353 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR11855222_1.fastq.gz	Fastqsanger.gz
	SRR11855222_2.fastq.gz	Fastqsanger.gz
	SRR11855223_1.fastq.gz	Fastqsanger.gz
	SRR11855223_2.fastq.gz	Fastqsanger.gz
	SRR11855224_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 28

Similar Datasets

Single Cell RNA Sequencing Identifies an Early Monocyte Gene Signature in Acute Respiratory Distress Syndrome

Project description:The acute respiratory distress syndrome (ARDS) results from overwhelming pulmonary inflammation. We used single cell RNA sequencing to probe ARDS at a higher resolution for insights into ARDS pathogenesis. Peripheral blood mononuclear cells of patients with pneumonia and sepsis with early ARDS were compared to that of sepsis patients who did not develop ARDS. Monocyte clusters from ARDS patients revealed multiple distinguishing characteristics in comparison to monocytes from patients without ARDS including down-regulation of SOCS3 expression accompanied by a pro-inflammatory signature with up-regulation of multiple type I IFN-induced genes, especially in CD16+ cells. These data show that monocytes of ARDS patients up-regulate expression of genes not just restricted to those associated with inflammation. Together, our findings identify molecules that are likely involved in ARDS pathogenesis that may inform biomarker and therapeutic development.

2020-07-10 | GSE151263 | GEO

Enhanced T cell-monocyte interation allievates malaria-associated acute respiratory distress syndrome : Bulk RNA-seq

Project description:Malaria-associated acute respiratory distress syndrome (MA-ARDS) is a severe manifestation of malaria with high mortality and no effective treatment. IFN-γ, a key regulator of immunity, plays a role in both promoting and suppressing malaria infection, though its effects on specific cell types remain unclear. In this study, we show that IFN-γ directly enhances CD8+ T cell proliferation, cytotoxicity, and cytokine production in a MA-ARDS mouse model. In IFNGR1-deficient T cells, IFN-γ deficiency led to increased CD8+ expression on Ly6c+ monocytes, enhancing their phagocytic ability. These findings highlight the role of T cell IFN-γ signaling in modulating monocyte function and suggest targeting this pathway could improve T cell-based therapies for MA-ARDS

2025-10-01 | GSE279789 | GEO

Prediction of Mortality In Acute Respiratory Distress Syndrome

Project description:Acute Respiratory Distress Syndrome (ARDS) continues to have a high mortality. The objective of this study is to understand the differences in disease biology between survivors and non-survivors by characterizing BALF protein expression profiles in individual ARDS subjects.

2018-10-24 | PXD002672 | Pride

Enhanced T cell-monocyte interation allievates malaria-associated acute respiratory distress syndrome : Bulk RNA-seq

Project description:Enhanced T cell-monocyte interation allievates malaria-associated acute respiratory distress syndrome : Bulk RNA-seq

| PRJNA1174695 | ENA

Repair of Acute Respiratory Distress Syndrome in COVID-19 by Stromal Cells (REALIST-COVID trial).

Project description:Mesenchymal stromal cells are a potential therapeutic for Acute Respiratory Distress Syndrome due to COVID-19, with pleiotropic immunomodulatory and reparative properties.This study investigated the safety and efficacy of ORBCEL-C (CD362 enriched umbilical cord-derived Mesenchymal Stromal Cells) in this patient population.

2023-06-20 | GSE231660 | GEO

Single cell RNA sequencing identifies an early monocyte gene signature in acute respiratory distress syndrome.

Project description:Acute respiratory distress syndrome (ARDS) results from overwhelming pulmonary inflammation. Prior bulk RNA sequencing provided limited insights into ARDS pathogenesis. We used single cell RNA sequencing to probe ARDS at a higher resolution. PBMCs of patients with pneumonia and sepsis with early ARDS were compared with those of sepsis patients who did not develop ARDS. Monocyte clusters from ARDS patients revealed multiple distinguishing characteristics in comparison with monocytes from patients without ARDS, including downregulation of SOCS3 expression, accompanied by a proinflammatory signature with upregulation of multiple type I IFN-induced genes, especially in CD16+ cells. To generate an ARDS risk score, we identified upregulation of 29 genes in the monocytes of these patients, and 17 showed a similar profile in cells of patients in independent cohorts. Monocytes had increased expression of RAB11A, known to inhibit neutrophil efferocytosis; ATP2B1, a calcium pump that exports Ca2+ implicated in endothelial barrier disruption; and SPARC, associated with processing of procollagen to collagen. These data show that monocytes of ARDS patients upregulate expression of genes not just restricted to those associated with inflammation. Together, our findings identify molecules that are likely involved in ARDS pathogenesis that may inform biomarker and therapeutic development.

| S-EPMC7406263 | biostudies-literature

Small RNA-Seq of plasma-derived exosomes from Acute Respiratory Distress Syndrome patients and healthy subjects

Project description:Despite a significant progress in the treatment of Acute Respiratory Distress Syndrome (ARDS), our ability to identify early patients and predict outcome remains limited. In this study, we aimed to characterize small RNA content of plasma exosomes from ARDS patients in order to identify potential diagnostic biomarkers of the disease. For the first time, we profiled miRNA expression levels in plasma-derived exosomes from ARDS patients (n=8) compared to healthy subjects (n=10) by small RNA-seq. It allowed us to identify 12 exosomal miRNAs differentially expressed in ARDS context (padj<0.05).

2021-01-19 | E-MTAB-9991 | biostudies-arrayexpress

Differentiating children with sepsis with and without acute respiratory distress syndrome using proteomics

Project description:Both sepsis and acute respiratory distress syndrome (ARDS) rely on imprecise clinical definitions leading to heterogeneity, which has contributed to negative trials. Because circulating protein/DNA complexes have been implicated in sepsis and ARDS, we aimed to develop a proteomic signature of DNA-bound proteins to discriminate between children with sepsis with and without ARDS. We performed a prospective case-control study in 12 children with sepsis with ARDS matched to 12 children with sepsis without ARDS on age, severity of illness score, and source of infection. We performed co-immunoprecipitation and downstream proteomics in plasma collected ≤ 24 h of intensive care unit admission. Expression profiles were generated, and a random forest classifier was used on differentially expressed proteins to develop a signature which discriminated ARDS. The classifier was tested in six independent blinded samples. Neutrophil and nucleosome proteins were over-represented in ARDS, including two S100A proteins, superoxide dismutase (SOD), and three histones. Random forest produced a 10-protein signature that accurately discriminated between children with sepsis with and without ARDS. This classifier perfectly assigned six independent blinded samples as having ARDS or not. We validated higher expression of the most informative discriminating protein, galectin-3-binding protein, in children with ARDS. Our methodology has applicability to isolation of DNA-bound proteins from plasma. Our results support the premise of a molecular definition of ARDS, and give preliminary insight into why some children with sepsis, but not others, develop ARDS.

2024-02-14 | PXD049377 | Pride

Lung collapse and respiratory distress in neonatal cloned cows is caused by surfactant homeostasis disorders

Project description:Respiratory distress is one of the major causes of the high mortality rate in neonatal cloned animals. Although some therapeutic methods have been used to improve the survival of cloned neonatal animals, the mechanisms of their neonatal respiratory distress lacked thorough investigation. Pathological analyses including necropsy and histology were implemented to determine the precise disease phenotypes, by which not fully dilated lungs, alveolar collapse and thickened alveolar walls were detected in neonatal cloned cows dying of respiratory distress compared to naturally conceived neonatal cows. In addition, we compared mRNA expression profiles between the two groups and differentially expressed genes (DEGs) have been achieved. Based on DEGs, GO and KEGG pathway enrichment analyses were performed, which showed that processes and pathways associated with surfactant homeostasis were significantly enriched between the two groups (p < 0.05).

2019-10-14 | GSE88912 | GEO

Temporal Changes in MicroRNA Expression in Blood Leukocytes from Patients with the Acute Respiratory Distress Syndrome

Project description:MicroRNA (miRNA) control gene transcription by binding to and repressing the translation of messenger RNA (mRNA). Their role in the acute respiratory distress syndrome (ARDS) is undefined. Blood leukocytes from 51 patients enrolled in a prior randomized trial of corticosteroids for ARDS were analyzed. After screening eight patients with microarrays for increased miRNA expression, 25 miRNAs were selected for further analysis using RT-PCR in all 51 patients on days 0, 3 and 7.

2017-08-22 | GSE83630 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data